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  • CLASSES

    Corticosteroids, Inhalant
    Ophthalmological Corticosteroids
    Systemic Corticosteroid Combinations
    Systemic Corticosteroids, Plain

    DEA CLASS

    Rx

    DESCRIPTION

    Synthetic long-acting glucocorticoid; little to no mineralocorticoid activity; superior ability to penetrate CNS; useful for cerebral edema; roughly 20—30 times more potent than hydrocortisone and 5—7 times more potent than prednisone.

    COMMON BRAND NAMES

    AK-Dex, Baycadron, CUSHINGS SYNDROME DIAGNOSTIC, Decadron, DexPak Jr TaperPak, DexPak TaperPak, DoubleDex, Maxidex, Ozurdex, Simplist Dexamethasone, Solurex, Zema-Pak, ZoDex, ZonaCort 11 Day, ZonaCort 7 Day

    HOW SUPPLIED

    AK-Dex/Decadron/Dexamethasone/Dexamethasone Sodium Phosphate Auricular (Otic) Drops: 0.1%
    AK-Dex/Decadron/Dexamethasone/Dexamethasone Sodium Phosphate Auricular (Otic) Sol: 0.1%
    AK-Dex/Decadron/Dexamethasone/Dexamethasone Sodium Phosphate Ophthalmic Drops: 0.1%
    AK-Dex/Decadron/Dexamethasone/Dexamethasone Sodium Phosphate Ophthalmic Sol: 0.1%
    Baycadron/Decadron/Dexamethasone Oral Elixir: 0.5mg, 5mL
    CUSHINGS SYNDROME DIAGNOSTIC/Decadron/Dexamethasone/DexPak Jr TaperPak/DexPak TaperPak/Zema-Pak/ZoDex/ZonaCort 11 Day/ZonaCort 7 Day Oral Tab: 0.5mg, 0.75mg, 1mg, 1.5mg, 2mg, 4mg, 6mg
    Decadron/Dexamethasone/Dexamethasone Sodium Phosphate/DoubleDex/Simplist Dexamethasone/Solurex Intra-Articular Inj Sol: 1mL, 4mg, 10mg
    Decadron/Dexamethasone/Dexamethasone Sodium Phosphate/DoubleDex/Simplist Dexamethasone/Solurex Intralesional Inj Sol: 1mL, 4mg, 10mg
    Decadron/Dexamethasone/Dexamethasone Sodium Phosphate/DoubleDex/Simplist Dexamethasone/Solurex Intramuscular Inj Sol: 1mL, 4mg, 10mg
    Decadron/Dexamethasone/Dexamethasone Sodium Phosphate/DoubleDex/Simplist Dexamethasone/Solurex Intravenous Inj Sol: 1mL, 4mg, 10mg
    Decadron/Dexamethasone/Dexamethasone Sodium Phosphate/DoubleDex/Simplist Dexamethasone/Solurex Soft Tissue Inj Sol: 1mL, 4mg, 10mg
    Dexamethasone Oral Sol: 0.5mg, 1mg, 1mL, 5mL
    Maxidex Ophthalmic Susp: 0.1%
    Ozurdex Intravitreal Imp: 0.7mg

    DOSAGE & INDICATIONS

    For the treatment of adrenocortical function abnormalities, such as adrenocortical insufficiency, congenital adrenal hyperplasia, chronic primary (Addison's disease) or secondary adrenocortical insufficiency, or adrenogenital syndrome.
    Oral dosage (dexamethasone)
    Adults

    Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response. NOTE: Parenteral therapy may be needed in acute insufficiency. Hydrocortisone and cortisone are preferred for these conditions; dexamethasone has no mineralocorticoid properties. Dosages required may be variable.

    Infants, Children, and Adolescents

    0.15 to 0.375 mg/m2/day PO once daily has been recommended for patients with congenital adrenal hyperplasia. Although most experts recommend hydrocortisone as first-line treatment of adrenal insufficiency in pediatric patients whose linear growth is incomplete due to a lower incidence of growth suppression, other authors have stated that dexamethasone may be used safely with close monitoring and individualization of dose based on growth, bone age, and hormone levels. Liquid formulations of dexamethasone are recommended for more precise titration of doses. 0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Parenteral therapy may be needed in acute insufficiency.

    Intravenous or Intramuscular dosage (dexamethasone sodium phosphate)
    Adults

    Initially, 0.5 to 9 mg/day IV or IM, divided every 6 to 12 hours. Adjust according to patient response. NOTE: Hydrocortisone and cortisone are preferred for these conditions; dexamethasone has no mineralocorticoid properties. Dosages required may be variable.

    Infants, Children and Adolescents

    0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.

    For hypothalamic-pituitary-adrenal (HPA) suppression diagnosis (e.g., dexamethasone suppression tests).
    For use as a test for Cushing's syndrome.
    Oral dosage (dexamethasone)
    Adults

    0.5 mg PO every 6 hours for 48 hours. 24-hour urine collections are made for determination of 17-hydroxycorticosteroid excretion. Alternatively, 1 mg PO at 11:00 p.m. with plasma cortisol concentration measured at 8:00 a.m. the following morning.

    Children and Adolescents

    25 to 30 mcg/kg/dose PO (Max: 2 mg/dose PO) given at 11:00 p.m. with a plasma cortisol concentration measured at 8:00 a.m. the following morning. A plasma cortisol concentration of less than 5 mcg/dL occurs in normal individuals but not those with Cushing's syndrome. Measure a dexamethasone concentration concurrently with the cortisol concentration to ensure adequacy of the dexamethasone dose.

    For use as a test to distinguish Cushing's syndrome secondary to pituitary ACTH excess from Cushing's syndrome secondary to other causes.
    Oral dosage (dexamethasone)
    Adults

    2 mg PO every 6 hours for 48 hours. 24-hour urine collections are made for determination of 17-hydroxycorticosteroid excretion.

    Children and Adolescents

    120 mcg/kg/dose PO (Max: 8 mg/dose PO) given at 11:00 p.m. with a plasma cortisol concentration measured at 8:00 a.m. the following morning. A decrease in the morning cortisol of 20% or more from baseline had a 97.5% sensitivity and 100% specificity in distinguishing patients with Cushing's disease from those with primary adrenal disorders in a retrospective study (n = 125, age 3 to 18 years). Measure a dexamethasone concentration concurrently with the cortisol concentration to ensure adequacy of the dexamethasone dose. Alternatively, a 2 day test consisting of 30 mcg/kg/day PO on day 1 and 120 mcg/kg/day PO on day 2, each given in 4 divided doses, has been recommended. Cortisol concentrations are suppressed in patients with pituitary Cushing's syndrome after the larger dose but not the smaller dose; cortisol concentrations are not suppressed after dexamethasone in patients with adrenocorticotropic hormone-independent Cushing syndrome.

    For the treatment of allergic conditions, such as acute anaphylaxis, anaphylactoid reactions, anaphylactic shock, angioedema, acute noninfectious laryngeal edema, drug hypersensitivity reactions, or serum sickness reactions.
    For acute anaphylaxis or anaphylactoid reactions.
    Oral dosage (dexamethasone) and Intramuscular dosage (dexamethasone sodium phosphate)
    Adults

    4 to 8 mg IM as a single dose on day 1. Then change to oral therapy, 1.5 mg PO twice daily on days 2 and 3; then 0.75 mg PO twice daily on day 4; then 0.75 mg PO once daily on days 5 and 6, then discontinue.

    For anaphylactic shock.
    Intravenous dosage (dexamethasone sodium phosphate)
    Adults

    Various dosage regimens have been used. 1 to 6 mg/kg IV or 40 mg IV every 4 to 6 hours while shock persists. Alternatively, 20 mg IV injection followed by an IV infusion of 3 mg/kg over 24 hours.

    For the systemic treatment of other allergic disorders including angioedema, acute noninfectious laryngeal edema, drug hypersensitivity reactions, or serum sickness.
    Oral dosage (dexamethasone)
    Adults

    Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response.

    Infants, Children, and Adolescents

    0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.

    Intravenous or Intramuscular dosage (dexamethasone sodium phosphate)
    Adults

    Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust according to patient response.

    Infants, Children, and Adolescents

    0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.

    For the treatment of cerebral edema associated with primary or metastatic brain tumor, craniotomy, or head injury.
    For treatment of cerebral edema in pediatric patients.
    Intravenous and Intramuscular dosage (dexamethasone sodium phosphate)
    Infants, Children, and Adolescents

    Initially, 1 to 1.5 mg/kg/dose IV, then 1 to 1.5 mg/kg/day IV in divided doses every 3 to 4 hours was used in conjunction with hyperventilation, control of body temperature, barbiturates, and continuous intracranial and arterial pressure monitoring in pediatric patients with severe head injury (n = 24, age 3 months to 14 years). 0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved dosage range. Adjust according to patient response. Use is not a substitute for neurosurgical evaluation and definitive management such as neurosurgery, etc.

    Oral dosage (dexamethasone)
    Infants, Children, and Adolescents

    0.02 to 0.3 mg/kg/day PO or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response. Use is not a substitute for neurosurgical evaluation and definitive management such as neurosurgery, etc.

    Intravenous or Intramuscular dosage (dexamethasone sodium phosphate injection)
    Adults

    10 mg IV or IM as a single dose, followed by 4 mg IV or IM every 6 hours, until symptoms subside, then reduce dosage. A response should be seen within 12 to 24 hours, and a gradual dose reduction begun after 2 to 4 days, reducing over another 5 to 7 days. Replace with oral dosage as soon as possible. For palliative maintenance therapy when oral therapy is not feasible, 2 mg IM or IV can be given 2 to 3 times per day, if needed. Use is not a substitute for neurosurgical evaluation and definitive management such as neurosurgery, etc.

    Oral dosage (dexamethasone)
    Adults

    For cerebral edema, 1 to 3 mg PO three times daily, can follow parenteral therapy; then, taper off over a period of 5 to 7 days. For palliative management of recurrent or inoperable brain tumors, maintenance with 2 mg PO given 2 or 3 times daily may be effective.

    For the treatment of complicated or disseminated pulmonary tuberculosis infection (i.e., tuberculous meningitis and pericarditis) as adjunctive therapy in combination with antituberculous therapy.
    Oral dosage (dexamethasone)
    Adults

    The FDA-labeled initial dose is 0.75 to 9 mg/day PO depending on the disease severity. Adjunctive corticosteroid therapy has been shown to improve survival for patients with tuberculosis involving the CNS and pericardium, but has not been universally recommended by guidelines for all forms of tuberculosis. For meningitis, the Infectious Diseases Society of America (IDSA) recommends 12 mg/day PO for the initial 3 weeks, with doses tapered during the next 3 weeks. Alternatively for CNS infections in HIV patients, a dose of 0.3 to 0.4 mg/kg/day PO for 2 to 4 weeks, then taper by 0.1 mg/kg/week until 0.1 mg/kg/day PO, then reduce to 4 mg/day PO and taper by 1 mg/week for a total duration of approximately 12 weeks. Initial doses in clinical trials for tuberculosis in general have ranged from 2.25 to 16 mg/day IV or IM for 4 to 8 weeks; many trials were prior to the use of rifampin, which may decrease bioavailability and increase plasma clearance of corticosteroids. A meta-analysis suggests that steroid use may reduce mortality in all forms of tuberculosis which may be influenced by genetic variation at the LTA4H gene.

    Children and Adolescents weighing at least 25 kg

    12 mg/day PO for the initial 3 weeks, with doses tapered during the next 3 weeks is recommended by the Infectious Diseases Society of America (IDSA). The American Academy of Pediatrics (AAP) suggests initial steroid therapy for 4 to 6 weeks, then appropriately taper doses. 0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range.

    Children and Adolescents weighing less than 25 kg

    8 mg/day PO for the initial 3 weeks, with doses tapered during the next 3 weeks is recommended by the Infectious Diseases Society of America (IDSA). The American Academy of Pediatrics (AAP) suggests initial steroid therapy for 4 to 6 weeks, then appropriately taper doses. 0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range.

    Intravenous or Intramuscular dosage (dexamethasone sodium phosphate)
    Adults

    The FDA-labeled initial dose is 0.5 to 9 mg/day IV or IM depending on disease severity. Adjunctive corticosteroid therapy has been shown to improve survival for patients with tuberculosis involving the CNS and pericardium, but has not been universally recommended by guidelines for all forms of tuberculosis. For meningitis, the Infectious Diseases Society of America (IDSA) recommends 12 mg/day IV or IM for the initial 3 weeks, with doses tapered during the next 3 weeks. Alternatively for CNS infections in HIV patients, a dose of 0.3 to 0.4 mg/kg/day IV or IM for 2 to 4 weeks, then taper by 0.1 mg/kg/week until 0.1 mg/kg/day PO, then 4 mg/day PO and taper by 1 mg/week for a total duration of approximately 12 weeks. Initial doses in clinical trials for tuberculosis in general have ranged from 2.25 to 16 mg/day IV or IM for 4 to 8 weeks; many trials were prior to the use of rifampin, which may decrease bioavailability and increase plasma clearance of corticosteroids. A meta-analysis suggests that steroid use may reduce mortality in all forms of tuberculosis which may be influenced by genetic variation at the LTA4H gene.

    Children and Adolescents weighing at least 25 kg

    12 mg/day IV or IM for the initial 3 weeks, with doses tapered during the next 3 weeks is recommended by the Infectious Diseases Society of America (IDSA). The American Academy of Pediatrics (AAP) suggests initial steroid therapy for 4 to 6 weeks, then appropriately taper doses. 0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range.

    Children and Adolescents weighing less than 25 kg

    8 mg/day IV or IM for the initial 3 weeks, with doses tapered during the next 3 weeks is recommended by the Infectious Diseases Society of America (IDSA). The American Academy of Pediatrics (AAP) suggests initial steroid therapy for 4 to 6 weeks, then appropriately taper doses. 0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range.

    For the treatment of kidney transplant rejection in conjunction with other immunosuppressants or for the treatment of acute graft-versus-host disease (GVHD).
    Intravenous or Intramuscular dosage (dexamethasone sodium phosphate solution for injection)
    Adults

    Initially, 0.5 to 9 mg/day IV or IM, in divided doses. Adjust according to patient response. Renal transplant guidelines recommend corticosteroids for the initial treatment of acute rejection.

    Children and Adolescents

    0.06 to 0.3 mg/kg/day or 1.2 to 10 mg/m2/day IM or IV in divided doses every 6 to 12 hours. Renal transplant guidelines recommend corticosteroids for the initial treatment of acute rejection.

    For the reduction of edema and inflammation associated with selected cases of otitis externa.
    Otic dosage (using dexamethasone sodium phosphate ophthalmic solution)
    Adults, Adolescents, and Children

    Instill 3 or 4 drops (ophthalmic solution) into the aural canal 2 to 3 times per day. When a favorable response is obtained, reduce dosage gradually and eventually discontinue. If preferred, the aural canal may be packed with a gauze wick saturated with solution. Keep the wick moist with solution and remove from the ear after 12 to 24 hours. May repeat as needed at the discretion of the prescriber. There is no specific otic solution preparation; use ophthalmic solution. Used for steroid responsive inflammatory conditions of the external auditory meatus, such as allergic otitis externa, selected purulent and nonpurulent infective otitis externa when the hazard of steroid use is accepted to decrease edema and inflammation.

    For the treatment of pruritus and inflammatory effects of corticosteroid-responsive dermatologic disorders, including dermatitis, alopecia areata, atopic dermatitis, bullous dermatitis herpetiformis, contact dermatitis (including Rhus dermatitis due to poison ivy, poison oak, poison sumac), discoid lupus erythematosus, eczema, exfoliative dermatitis, granuloma annulare, keloids, lichen planus, lichen simplex chronicus or neurodermatitis, necrobiosis lipoidica diabeticorum, pemphigus, polymorphous light eruption, plaque psoriasis, cutaneous T-cell lymphoma (CTCL) or mycosis fungoides, severe seborrheic dermatitis, urticaria, and severe erythema multiforme or Stevens-Johnson syndrome.
    For systemic treatment of inflammatory and allergic dermatoses (e.g., severe dermatitis, psoriasis, or exfoliative dermatitis, erythema multiforme, or Stevens-Johnson syndrome).
    Oral dosage (dexamethasone)
    Adults

    Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response.

    Children and Adolescents

    0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.

    Intravenous or Intramuscular dosage (dexamethasone sodium phosphate injection solution)
    Adults

    Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust according to patient response.

    Children and Adolescents

    0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.

    For intralesional or soft-tissue treatment of specific corticosteroid-responsive skin or soft-tissue lesions.
    Intralesional or Soft Tissue dosage (dexamethasone sodium phosphate injection solution)
    Adults

    The 4 mg/mL injection strength may be used for intralesional and soft tissue administration. Doses range from 0.2 mg to 4 mg injected as a single dose at the appropriate site. For soft tissue injections a dose of 2 to 4 mg is recommended. Usually employed when condition to be treated is limited to 1 or 2 sites. Dosage dependent upon degree of inflammation, size, disease state, and location of affected area. Repeat doses may be given from once every 3 to 5 days to once every 2 to 3 weeks. Examples of conditions where intralesional dosage is used include keloids, localized hypertrophic, infiltrated, inflammatory lesions (e.g., lichen planus, psoriatic plaques, granuloma annulare, and lichen simplex chronicus or neurodermatitis), discoid lupus erythematosus, necrobiosis lipoidica diabeticorum, and alopecia areata.

    For adjunctive therapy in the treatment of rheumatic disorders including acute gouty arthritis, ankylosing spondylitis, rheumatoid arthritis, juvenile rheumatoid arthritis (JRA)/juvenile idiopathic arthritis (JIA), post-traumatic osteoarthritis, synovitis of osteoarthritis, and for psoriatic arthritis; or for the treatment of acute episodes or exacerbation of nonrheumatic inflammatory conditions including acute and subacute bursitis, epicondylitis, acute non-specific tenosynovitis, and cystic tumors of an aponeurosis tendon (ganglia).
    Oral dosage (dexamethasone)
    Adults

    Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response.

    Infants, Children, and Adolescents

    0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.

    Intravenous or Intramuscular dosage (dexamethasone sodium phosphate injection solution)
    Adults

    Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust maintenance dosage according to patient response.

    Infants, Children, and Adolescents

    0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.

    Intra-Articular or Intrasynovial injection dosage (dexamethasone sodium phosphate injection solution)
    Adults

    Dosage ranges from 2 to 4 mg for large joints and 0.8 to 1 mg for small joints. Injection into intervertebral joints should not be attempted at any time and hip joint injection cannot be recommended as an office procedure. Intrasynovial should be employed only when affected areas are limited to 1 or 2 sites. May repeat from once every 3 to 5 days to once every 2 to 3 weeks.

    Intralesional or Soft Tissue dosage (dexamethasone sodium phosphate injection solution)
    Adults

    The 4 mg/mL injection strength may be used for intralesional and soft tissue administration. Doses range from 0.2 mg to 4 mg injected as a single dose at the appropriate site. For soft tissue and bursal injections a dose of 2 to 4 mg is recommended. Ganglia require a dose of 1 to 2 mg. A dose of 0.4 to 1 mg is used for injection into tendon sheaths. Usually employed when condition to be treated is limited to 1 or 2 sites. Dosage dependent upon degree of inflammation, size, disease state, and location of affected area. Repeat doses may be given from once every 3 to 5 days to once every 2 to 3 weeks.

    For the treatment of hematologic disorders such as secondary thrombocytopenia in adults, autoimmune hemolytic anemia, erythroblastopenia, congenital hypoplastic anemia, and thrombocytopenia associated with immune thrombocytopenia/idiopathic thrombocytopenic purpura (ITP).
    Oral dosage (dexamethasone)
    Adults

    Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. For many conditions, the dosing of corticosteroids is highly variable. Adjust according to patient response. In an open study of 10 patients with ITP, pulse dosing produced a sustained improvement in platelet count with a total daily dose of 40 mg/day PO for 4 consecutive days out of each 28 day cycle for 6 consecutive cycles.

    Children and Adolescents

    0.024 to 0.34 mg/kg/day PO or 0.66 to 10 mg/m2/day PO, given in 2 to 4 divided doses. For many conditions, the dosing of corticosteroids is highly variable. Adjust according to patient response.

    Intramuscular or Intravenous dosage (dexamethasone sodium phosphate)
    Adults

    Initially, 0.5 to 9 mg/day IV or IM, given in 2 to 4 divided doses. For many conditions, the dosing of corticosteroids is highly variable. Adjust according to patient response.

    Children

    0.06 to 0.3 mg/kg/day or 1.2 to 10 mg/m2/day IV or IM in divided doses every 6 to 12 hours. For many conditions, the dosing of corticosteroids is highly variable. Adjust according to patient response.

    For the treatment of acute asthma† exacerbation.
    Oral dosage
    Adults

    Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response. Use parenteral dexamethasone dosage for severe respiratory conditions or those compromising the airway.

    Infants, Children, and Adolescents

    0.6 mg/kg/dose PO as a single dose or once daily for 2 days (Max: 16 mg/dose). Administer dexamethasone parenterally for severe respiratory conditions or those compromising the airway. Single or 2-day oral dexamethasone regimens have shown similar efficacy, less vomiting, and improved compliance when compared to a 5-day course of oral prednisone or prednisolone. Use of dexamethasone for greater than 2 days may increase the potential for metabolic side effects. The National Asthma Education and Prevention Program guidelines recommend prednisone, prednisolone, or methylprednisolone as the systemic corticosteroids of choice for moderate to severe asthma exacerbations; however, other corticosteroids, such as dexamethasone, given in equipotent daily doses are likely to be as effective. FDA approved initial dose range: 0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses; however, this range is significantly lower than the range used in clinical practice.

    Intravenous or Intramuscular dosage (dexamethasone sodium phosphate)
    Adults

    Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust according to patient response.

    Infants, Children, and Adolescents

    0.6 mg/kg/dose IV or IM as a single dose (Max: 16 mg/dose). Single-dose regimens ranging from 0.3 to 1.7 mg/kg/dose (Max: 36 mg/dose) have been reported. In a study of young children with moderate exacerbations, a single day regimen of parenteral dexamethasone resulted in similar efficacy as a 5-day course of oral prednisolone. Although the National Asthma Education and Prevention Program guidelines recommend prednisone, prednisolone, or methylprednisolone as the systemic corticosteroids of choice for the management of moderate to severe asthma exacerbations, they state that other corticosteroids, such as dexamethasone, given in equipotent daily doses are likely to be as effective. FDA approved dose range: 0.5 to 9 mg per day IV or IM is the FDA-approved initial dosage range depending on the condition being treated; however, higher doses are often used in clinical practice.

    For the treatment of hypercalcemia related to sarcoidosis or cancer, or for the treatment of nonsuppurative thyroiditis, or for severe cases of myasthenia gravis not controlled by antimyasthenic agents alone.
    For the treatment of hypercalcemia related to cancer or for the treatment of nonsuppurative thyroiditis in pediatric patients.
    Oral dosage
    Infants, Children, and Adolescents

    0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.

    Intravenous and Intramuscular dosage
    Infants, Children, and Adolescents

    0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.

    Oral dosage (dexamethasone)
    Adults

    Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. For many conditions, the dosing of corticosteroids is highly variable. Adjust to patient response.

    For the treatment of nephrotic syndrome to induce diuresis or decrease proteinuria.
    Oral dosage
    Adults

    Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response until urine is protein-free, then slowly taper as indicated. Some patients may require long-term dosing.

    Infants, Children, and Adolescents

    0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.

    For the treatment of Hodgkin's disease.
    Oral dosage
    Adults and Children

    Dosages vary depending upon the chemotherapy protocol. Common doses include 1.5 to 6 mg/m2/day PO for 8 to 21 days or 8 mg PO every 8 hours for 10 days.

    For the treatment of non-Hodgkin's lymphoma (NHL).
    For the palliative treatment of NHL.
    Oral dosage
    Adults

    initial, 0.75 to 9 mg orally daily; dose is dependent on the disease being treated and should be individualized based on patient response. Maintenance therapy may be given; use the lowest dose that produces an adequate clinical response. Taper dexamethasone gradually in patients on long-term therapy; do not abruptly stop therapy in these patients.

    Infants, Children, and Adolescents

    initial, 0.02 to 0.3 mg/kg (0.6 mg to 9 mg/m2) orally daily in 3 or 4 divided doses. Dose is dependent on the disease being treated and should be individualized based on patient response. Maintenance therapy may be given; use the lowest dose that produces an adequate clinical response. Taper dexamethasone gradually in patients on long-term therapy; do not abruptly stop therapy in these patients.

    Intravenous dosage (dexamethasone sodium phosphate injection)
    Adults

    initial, 0.5 to 9 mg IV daily; dose is dependent on the disease being treated and should be individualized based on patient response. Maintenance therapy may be given; use the lowest dose that produces an adequate clinical response. Taper dexamethasone gradually in patients receiving IV therapy for more than a few days; do not abruptly stop therapy in these patients.

    For the treatment of relapsed or refractory, aggressive NHL in transplant eligible patients, in combination with gemcitabine and cisplatin (and rituximab for CD20-positive disease)†.
    Oral dosage
    Adults

    40 mg orally daily on days 1, 2, 3, and 4 in combination with gemcitabine 1,000 mg/m2 IV on days 1 and 8 and cisplatin 75 mg/m2 IV on day 1 (GDP regimen) every 21 days for 2 cycles was evaluated in a randomized, phase III trial (NCIC-CTG LY.12 trial). In patients with CD20-positive lymphoma, rituximab 375 mg/m2 IV was added on day 1 of each treatment cycle (R-GDP regimen). Patients in the trial could receive a third cycle of therapy if they did not achieve a complete or partial response after the second cycle. Patients with CD20-positive lymphoma who received an autologous stem-cell transplant (ASCT) were randomized to receive either rituximab 375 mg/m2 IV every 2 months for 6 cycles or observation starting 28 days post ASCT.

    For the treatment of relapsed or refractory diffuse large B-cell lymphoma in transplant eligible patients, in combination with cisplatin and cytarabine (DHAP regimen) and ofatumumab†.
    Oral or Intravenous dosage
    Adults

    40 mg orally or IV on days 1, 2, 3, and 4 as part of the DHAP regimen with cisplatin 100 mg/m2 as a continuous IV infusion over 24 hours on day 1 and cytarabine 2 grams/m2 IV over 3 hours every 12 hours for 2 doses on day 2 in combination with ofatumumab 1,000 mg IV on days 1 and 8 of cycle 1 then ofatumumab 1,000 mg IV on day 1 of cycles 2 and 3 was evaluated in a randomized, phase III trial (n = 445; the ORCHARRD trial). Cycles were repeated every 21 days for a total of 3 cycles of therapy. Premedication with acetaminophen, diphenhydramine, and an IV glucocorticoid was administered prior to each ofatumumab infusion. If dexamethasone from the DHAP chemotherapy was dosed on the same day as ofatumumab, then the glucocorticoid premedication was omitted and substituted with the 40-mg dose of dexamethasone. Granulocyte colony-stimulating factor use was recommended as follows: filgrastim 5 micrograms (mcg)/kg on days 6 to 13 or pegfilgrastim 6 mg on day 6 on cycles of therapy with no stem-cell mobilization and filgrastim 5 to 10 mcg/kg on days 6 to 13 on cycles of therapy that were followed by stem-cell mobilization. Central nervous system prophylaxis using intrathecal therapy was permitted. Supportive care during treatment consisted of irradiated blood products, oral antibiotics, and antifungal prophylaxis as clinically indicated.

    For the treatment of acute lymphocytic leukemia (ALL).
    Oral dosage (dexamethasone)
    Adults, Adolescents, and Children

    6 to 10 mg/m2/day PO for 14 days as part of induction, consolidation, or intensification combination regimens.

    For the treatment of multiple myeloma.
    For the treatment of multiple myeloma in patients who have received at least 1 prior therapy, in combination with lenalidomide.
    Oral dosage
    Adults

    40 mg PO once daily on days 1 to 4, 9 to 12, and 17 to 20 every 28 days for the first 4 cycles of therapy, and then 40 mg PO once daily on days 1 to 4 every 28 days starting with cycle 5. Given in combination with lenalidomide (25 mg PO once daily on days 1 to 21 of each cycle). Continue or modify dosing based on clinical and laboratory findings. Lenalidomide is FDA approved in combination with dexamethasone for the treatment of multiple myeloma in patients that have failed at least 1 prior therapy.

    For the treatment of patients with newly diagnosed multiple myeloma, in combination with lenalidomide.
    Oral dosage
    Adults 75 years and younger

    40 mg PO once daily on days 1, 8, 15, and 22; administer in combination with lenalidomide (25 mg PO once daily for 21 days followed by 7 days off treatment). Continue 28-day treatment cycles until disease progression in patients who are ineligible for an autologous stem-cell transplantation (ASCT); hematopoietic stem-cell mobilization should occur within four 28-day treatment cycles in patients who are eligible for an ASCT. Lenalidomide is FDA approved in combination with dexamethasone for the treatment of newly diagnosed multiple myeloma.

    Geriatric Adults older than 75 years

    20 mg PO once daily on days 1, 8, 15, and 22; administer in combination with lenalidomide (25 mg PO once daily for 21 days followed by 7 days off treatment). Continue 28-day treatment cycles until disease progression. Lenalidomide is FDA approved in combination with dexamethasone for the treatment of newly diagnosed multiple myeloma.

    For newly diagnosed multiple myeloma as induction therapy prior to autologous stem-cell transplantation, in combination with doxorubicin and vincristine†.
    Oral dosage
    Adults 65 years and younger

    Dexamethasone 40 mg PO daily on days 1 to 4, days 9 to 12, and days 17 to 20 or dexamethasone 40 mg PO daily days 1 to 4 on all cycles, and days 9 to 12 and days 17 to 20 of cycles 1 and 2 only , plus doxorubicin 9 mg/m2/day IV and vincristine 0.4 mg/day IV on days 1 to 4 (VAD regimen). Cycles are repeated every 4 weeks for 3 to 4 cycles as induction therapy prior to autologous stem-cell transplantation. This regimen has been studied in previously untreated multiple myeloma patients. Doxorubicin and vincristine were administered as a continuous IV infusion over 24 hours/day or as a daily IV infusion.

    For newly diagnosed multiple myeloma, in combination with thalidomide.
    Oral dosage
    Adults

    40 mg PO on days 1 to 4, days 9 to 12, and days 17 to 20 of every 28-day treatment cycle plus thalidomide (200 mg PO once daily, given at bedtime and at least 1-hour after the evening meal). Thalidomide is FDA approved in combination with dexamethasone for the treatment of newly diagnosed multiple myeloma.

    For newly diagnosed multiple myeloma as induction therapy prior to autologous stem-cell transplantation, in combination with bortezomib†.
    Oral dosage
    Adults 65 years and younger

    40 mg PO days 1 to 4 during all cycles and on days 9 to 12 for cycles 1 and 2 only, plus bortezomib (1.3 mg/m2 IV on days 1, 4, 8, and 11) repeated every 3 weeks for 4 cycles as induction therapy prior to autologous stem-cell transplantation has been evaluated in newly diagnosed multiple myeloma patients in randomized, phase III studies.

    For newly diagnosed multiple myeloma as induction therapy prior to autologous stem-cell transplantation, in combination with bortezomib and thalidomide†.
    Oral dosage
    Adults 65 years and younger

    Dexamethasone 40 mg PO on days 1, 2, 4, 5, 8, 9, 11, and 12 plus bortezomib (1.3 mg/m2 IV on days 1, 4, 8, and 11) and thalidomide (100 mg PO once daily for the first 14 days during cycle 1 only, and then 200 mg PO once daily thereafter). Regimen is known as the VTD regimen. Repeated every 21 days for 3 cycles prior to a double (tandem) autologous stem-cell transplant (ASCT). Regimen was studied in a multicenter, randomized, phase III study. Patients randomized to induction therapy with VTD also received two 35-day consolidation cycles with VTD (bortezomib 1.3 mg/m2 on days 1, 8, 15, and 22 plus thalidomide 100 mg PO daily and dexamethasone 40 mg PO on days 1, 2, 8, 9, 15, 16, 22, and 23) following the second transplantation. Patients also received maintenance therapy with dexamethasone 40 mg PO on days 1 to 4 every 28 days until relapse or disease progression. Additionally in a randomized, phase III study, dexamethasone 40 mg PO on days 1 to 4 and 9 to 12 plus bortezomib (1.3 mg/m2 on days 1, 4, 8, and 11) and thalidomide (200 mg PO daily after dose escalation as follows in the first cycle: thalidomide 50 mg/day on days 1 to 14 and 100 mg/day on days 15 to 28) repeated every 4 weeks for 6 cycles prior to an ASCT was studied. In this study, patients who received up to 3 years of maintenance therapy (starting 3 months after ASCT) with bortezomib (1.3 mg/m2 IV on days 1, 4, 8, and 11 repeated every 3 months) plus thalidomide (100 mg/day PO) had significantly improved 2-year progression-free survival compared with thalidomide or interferon alfa-2b maintenance therapy.

    For the treatment of multiple myeloma in patients who have received at least 2 prior therapies (including bortezomib and an immunomodulatory agent), in combination with panobinostat and bortezomib.
    Oral dosage
    Adults

    Dexamethasone 20 mg PO on days 1, 2, 4, 5, 8, 9, 11, and 12 during cycles 1 to 8, then dexamethasone 20 mg PO on days 1, 2, 8, and 9 during cycles 9 to 16. Administer in combination with bortezomib (1.3 mg/m2 IV bolus over 3 to 5 seconds on days 1, 4, 8, and 11 in cycles 1 to 8) then bortezomib (1.3 mg/m2 on days 1 and 8 in cycles 9 to 16) and panobinostat (20 mg PO on days 1, 3, 5, 8, 10, and 12). Continue every 21-day treatment cycles for up to 8 cycles; consider giving up to an additional 8 cycles (maximum of 16 treatment cycles) in patients who experience clinical benefit without unresolved severe or medically significant toxicity. Panobinostat is FDA approved in combination with bortezomib and dexamethasone for the treatment of multiple myeloma in patients who have received at least 2 prior therapies (including bortezomib and an immunomodulatory agent). CLINICAL TRIAL DATA: Treatment with panobinostat, bortezomib, and dexamethasone (n = 387; median therapy duration of 5 months) was compared with placebo, bortezomib, and dexamethasone (n = 381; median therapy duration of 6.1 months) in patients with relapsed or relapsed and refractory multiple myeloma who had received 1 to 3 prior therapies in a multinational, randomized, phase III trial (the PANORAMA1 trial). The median patient age was 63 years (range, 56 to 69 years), about 51% of patients had received 1 prior therapy, and approximately 57% of patients had previously received a stem-cell transplantation. Patients with primary refractory or bortezomib refractory disease were ineligible for this study. At a median follow-up time of 6.47 months (interquartile range, 1.81 to 13.47 months), the median progression-free survival time (primary endpoint) was significantly improved in the panobinostat arm (11.99 months) compared with the placebo arm (8.08 months; hazard ratio [HR] = 0.63; 95% CI, 0.52 to 0.76; p < 0.0001). The overall survival (OS) time was not significantly improved in the panobinostat arm (33.64 months vs. 30.39 months; HR = 0.87; 95% CI, 0.69 to 1.1); however, OS data are not mature. Crossover from the placebo arm to the panobinostat arm is not permitted.

    For the treatment of relapsed multiple myeloma in patients who have received 1 to 3 prior lines of therapy, in combination with carfilzomib and lenalidomide.
    Oral and Intravenous dosage
    Adults

    40 mg PO or IV on days 1, 8, 15, and 22 in combination with lenalidomide (25 mg PO once daily for 21 days) and carfilzomib as specified in the protocol. Treatment cycles are repeated every 28 days until disease progression or unacceptable toxicity; maximum of 18 cycles for carfilzomib only. CYCLE 1: carfilzomib 20 mg/m2 IV over 10 minutes on days 1 and 2; if tolerated, increase to a target dose of 27 mg/m2 IV over 10 minutes on days 8, 9, 15, and 16. CYCLES 2 to 12: carfilzomib 27 mg/m2 IV over 10 minutes on days 1, 2, 8, 9, 15, and 16. CYCLES 13 to 18: carfilzomib 27 mg/m2 IV over 10 minutes on days 1, 2, 15, and 16. Dose carfilzomib at a maximum body surface area (BSA) of 2.2 m2; dose adjustment is not necessary for patients with a weight change of 20% or less. NOTE: Carfilzomib is FDA approved in combination with lenalidomide and dexamethasone for the treatment of relapsed multiple myeloma in patients who have received 1 to 3 prior lines of therapy. PREMEDICATION: Give dexamethasone 30 minutes to 4 hours prior to the carfilzomib (on carfilzomib dosing days only). SUPPORTIVE CARE: Give hydration with both oral fluids and IV fluids prior to each carfilzomib dose in cycle 1. Additional IV hydration may be given after the carfilzomib infusion in cycle 1. Oral and/or IV hydration may be continued as needed in subsequent cycles; adjust hydration to individual patient needs. Thromboprophylaxis is recommended. Consider giving an antiviral agent and an antacid medication. CLINICAL TRIAL DATA: In a prespecified interim analysis of a multinational, randomized, open-label, phase III trial (n = 792; the ASPIRE trial), the median progression-free survival time (primary endpoint) was significantly increased with carfilzomib plus lenalidomide/dexamethasone (26.3 months) compared with lenalidomide/dexamethasone alone (17.6 months; hazard ratio [HR] = 0.69; 95% CI, 0.57 to 0.83; p = 0.0001) in patients with relapsed multiple myeloma who had received 1 to 3 prior therapies (age range, 31 to 91 years; median of 2 prior therapies). In this study, some patients had previously received bortezomib (65.8%) and/or lenalidomide (19.8%). The median overall survival (OS) time had not been reached in either study arm at the time of the interim analysis (median follow-up: carfilzomib arm, 32.3 months; lenalidomide/dexamethasone alone, 31.5 months). The estimated 24-month OS rates were 73.3% and 65% in the carfilzomib/lenalidomide/dexamethasone and lenalidomide/dexamethasone arms, respectively (HR = 0.79; 95% CI, 0.63 to 0.99; p = 0.04); prespecified criteria for stopping the study due to OS benefit was not met and this study is ongoing.

    For the treatment multiple myeloma in patients who have received at least 1 prior therapy, in combination with daratumumab and bortezomib.
    Oral or Intravenous dosage
    Adults 75 years or younger

    Daratumumab is FDA approved in combination with bortezomib and dexamethasone for this indication. Dexamethasone 20 mg PO or IV on days 1, 2, 4, 5, 8, 9, 11, and 12 (or 20 mg PO/IV once weekly in patients with a body-mass index less than 18.5, poorly controlled diabetes mellitus, or a prior intolerance to glucocorticoid therapy) repeated every 3 weeks for 8 cycles in combination with daratumumab and bortezomib was evaluated in a multinational, randomized, open-label, phase III trial (n = 498; CASTOR trial). The bortezomib dosage is 1.3 mg/m2 as a subcutaneous injection or IV infusion on days 1, 4, 8, and 11 repeated every 3 weeks for 8 cycles. The daratumumab dosage is 16 mg/kg (actual body weight) IV weekly on weeks 1 to 9 (9 doses), 16 mg/kg IV every 3 weeks on weeks 10 to 24 (5 doses), and then 16 mg/kg IV every 4 weeks starting on week 25 until disease progression. Administer standard pre-and post-infusion medications with daratumumab infusions. Give dexamethasone prior to the daratumumab infusion when these drugs are scheduled on the same day.

    Geriatric Adults over 75 years

    Daratumumab is FDA approved in combination with bortezomib and dexamethasone for this indication. Dexamethasone 20 mg PO/IV once weekly repeated every 3 weeks for 8 cycles in combination with daratumumab and bortezomib was evaluated in a multinational, randomized, open-label, phase III trial (n = 498; CASTOR trial). The bortezomib dosage is 1.3 mg/m2 as a subcutaneous injection or IV infusion on days 1, 4, 8, and 11 repeated every 3 weeks for 8 cycles. The daratumumab dosage is 16 mg/kg (actual body weight) IV weekly on weeks 1 to 9 (9 doses), 16 mg/kg IV every 3 weeks on weeks 10 to 24 (5 doses), and then 16 mg/kg IV every 4 weeks starting on week 25 until disease progression. Administer standard pre-and post-infusion medications with daratumumab infusions. Give dexamethasone prior to the daratumumab infusion when these drugs are scheduled on the same day.

    For the treatment of multiple myeloma in patients who have received at least 1 prior therapy, in combination with daratumumab and lenalidomide.
    Oral or Intravenous dosage
    Adults 75 years or younger

    Daratumumab is FDA-approved in combination with lenalidomide and dexamethasone for this indication. Dexamethasone 40 mg IV/PO once weekly (or 20 mg IV/PO once weekly for patients with a body-mass index less than 18.5) in combination with lenalidomide and daratumumab until disease progression or unacceptable toxicity was evaluated in a multinational, randomized, open-label, phase III trial (n = 569; POLLUX trial). The lenalidomide dosage is 25 mg PO daily on days 1 to 21 repeated every 28 days in patients with creatinine clearance (CrCl) greater than 60 mL/min and 10 mg PO daily on days 1 to 21 repeated every 28 days in patients with a CrCl of 30 to 60 mL/min. The daratumumab dosage is 16 mg/kg (actual body weight) IV weekly on weeks 1 to 8 (8 doses), 16 mg/kg IV every other week on weeks 9 to 24 (8 doses), and then 16 mg/kg IV every 4 weeks starting on week 25 until disease progression. Administer standard pre-and post-infusion medications with daratumumab infusions. In patients receiving full dose dexamethasone, administer as 20 mg IV prior to the daratumumab infusion and then 20 mg PO the next day when these drugs are scheduled on the same week; patients receiving a 20 mg/week dexamethasone dose should receive the entire dose administered prior to the daratumumab infusion.

    Geriatric Adults over 75 years

    Daratumumab is FDA-approved in combination with lenalidomide and dexamethasone for this indication. Dexamethasone 20 mg IV/PO once weekly in combination with lenalidomide and daratumumab until disease progression or unacceptable toxicity was evaluated in a multinational, randomized, open-label, phase III trial (n = 569; POLLUX trial). The lenalidomide dosage is 25 mg PO daily on days 1 to 21 repeated every 28 days in patients with creatinine clearance (CrCl) greater than 60 mL/min and 10 mg PO daily on days 1 to 21 repeated every 28 days in patients with a CrCl of 30 to 60 mL/min. The daratumumab dosage is 16 mg/kg (actual body weight) IV weekly on weeks 1 to 8 (8 doses), 16 mg/kg IV every other week on weeks 9 to 24 (8 doses), and then 16 mg/kg IV every 4 weeks starting on week 25 until disease progression. Administer standard pre-and post-infusion medications with daratumumab infusions. Give dexamethasone prior to the daratumumab infusion when these drugs are scheduled on the same week.

    For the treatment of newly diagnosed multiple myeloma, in combination with bortezomib and lenalidomide†.
    Oral dosage
    Adults

    20 mg orally on days 1, 2, 4, 5, 8, 9, 11, and 12; bortezomib 1.3 mg/m2 IV on days 1, 4, 8, and 11; and lenalidomide 25 mg orally daily on days 1 to 14 repeated every 21 days (VRd regimen) for 8 cycles was evaluated in a randomized, phase III trial (n = 471; SWOG S0777 trial). Following induction therapy, patients received maintenance therapy with lenalidomide 25 mg/day on days 1 to 21 and dexamethasone 40 mg orally on days 1, 8, 15, and 22 repeated every 28 days; the median duration of maintenance therapy was 385 days. All patients received herpes simplex virus prophylaxis and thromboembolic prophylaxis with aspirin 325 mg/day.

    For the treatment of multiple myeloma in patients who have received at least 2 prior therapies including lenalidomide and a proteasome inhibitor, in combination with pomalidomide and daratumumab.
    Oral or Intravenous dosage
    Adults 75 years or younger

    Daratumumab is FDA-approved in combination with pomalidomide and dexamethasone for this indication. Dexamethasone 40 mg IV/PO once weekly (or 20 mg IV/PO once weekly for patients with a body-mass index less than 18.5) in combination with pomalidomide (4 mg PO daily on days 1 to 21 repeated every 28 days) and daratumumab (16 mg/kg of actual body weight IV weekly on weeks 1 to 8 (8 doses), 16 mg/kg IV every other week on weeks 9 to 24 (8 doses), and then 16 mg/kg IV every 4 weeks starting on week 25) until disease progression was evaluated in a nonrandomized, phase Ib trial (n = 103; EQUULEUS trial). Administer standard pre-and post-infusion medications with daratumumab infusions. In patients receiving full dose dexamethasone, administer as 20 mg IV prior to the daratumumab infusion and then 20 mg PO the next day when these drugs are scheduled on the same week; patients receiving a 20 mg/week dexamethasone dose should receive the entire dose administered prior to the daratumumab infusion.

    Geriatric Adults over 75 years

    Daratumumab is FDA-approved in combination with pomalidomide and dexamethasone for this indication. Dexamethasone 20 mg IV/PO once weekly in combination with pomalidomide (4 mg PO daily on days 1 to 21 repeated every 28 days) and daratumumab (16 mg/kg of actual body weight IV weekly on weeks 1 to 8 (8 doses), 16 mg/kg IV every other week on weeks 9 to 24 (8 doses), and then 16 mg/kg IV every 4 weeks starting on week 25) until disease progression was evaluated in a nonrandomized, phase Ib trial (n = 103; EQUULEUS trial). Administer standard pre-and post-infusion medications with daratumumab infusions. Give dexamethasone prior to the daratumumab infusion when these drugs are scheduled on the same week.

    For the treatment of acute exacerbations of multiple sclerosis.
    Oral dosage
    Adults

    30 mg/day PO for 7 days, followed by doses of 4 to 12 mg PO every other day for 1 month have been shown to be effective. Controlled clinical trials have shown corticosteroids to be effective in speeding the resolution of acute exacerbations, they do not show that they affect the ultimate outcome or natural history of the disease.

    Infants, Children, and Adolescents

    0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.

    For the treatment of inflammatory bowel disease during critical periods of ulcerative colitis and regional enteritis (Crohn's disease).
    Oral dosage (dexamethasone)
    Adults

    Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. For many conditions, the dosing of corticosteroids is highly variable. Adjust according to patient response.

    Infants, Children, and Adolescents

    0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.

    Intravenous or Intramuscular dosage (dexamethasone sodium phosphate injection solution)
    Adults

    Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. For many conditions, the dosing of corticosteroids is highly variable. Adjust according to patient response.

    Infants, Children, and Adolescents

    0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.

    For the treatment of steroid-responsive inflammatory conditions of the palpebral and bulbar conjunctiva, cornea, and anterior segment inflammation of the globe, such as allergic conjunctivitis, eyelid acne rosacea, superficial punctate keratitis, herpes zoster ocular infection associated keratitis, iritis, cyclitis, vernal keratoconjunctivitis, selected infective viral conjunctivitis or postoperative ocular inflammation when the inherent hazard of steroid use is accepted to obtain an advisable diminution in edema and inflammation; corneal abrasion, corneal ulcer, or corneal injury from chemical or thermal burns, or penetration of foreign bodies; systemic treatment may be indicated for uveitis, sympathetic ophthalmia, and ocular inflammatory conditions unresponsive to topical corticosteroids.
    For the treatment of non-infectious uveitis affecting the posterior segment of the eye in adults.
    Intravitreal implant dosage (Ozurdex dexamethasone intravitreal implant only)
    Adults

    Inject the implant containing 0.7 mg dexamethasone in a solid polymer delivery system intravitreally. Monitor the patient for elevated intraocular pressure and endophthalmitis.

    Ophthalmic dosage (ophthalmic solution)
    Adults, Adolescents, and Children

    Instill 1 or 2 drops of 0.1% ophthalmic solution in the affected eye(s) every hour during the day and every 2 hours at night; reduce application to every 4 hours (while awake) once a favorable response occurs. Later, further reduction in dosage to 1 drop 3 or 4 times daily may suffice to control symptoms. The duration of treatment will vary with the type of lesion and may extend from a few days to several weeks, according to therapeutic response. Relapses, more common in chronic active lesions than in self-limited conditions, usually respond to treatment.

    Ophthalmic dosage (ophthalmic suspension)
    Adults

    Instill 1 or 2 drops of 0.1% ophthalmic suspension in the affected eye(s). In severe disease, drops may be used hourly, being tapered to discontinuation as the inflammation subsides. In mild disease, drops may be used up to 4 to 6 times daily.

    Oral dosage (dexamethasone)
    Adults

    Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response.

    Infants, Children and Adolescents

    0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.

    Intravenous or Intramuscular dosage (dexamethasone sodium phosphate)
    Adults

    Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust according to patient response.

    Infants, Children and Adolescents

    0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.

    For the treatment of diabetic macular edema.
    Intravitreal implant dosage (Orudex dexamethasone intravitreal implant only)
    Adults

    Inject the implant (containing 0.7 mg dexamethasone in a solid polymer delivery system) intravitreally. Monitor the patient for elevated intraocular pressure and endophthalmitis. According to the American Diabetes Association (ADA), intravitreous steroid injections are considered second-line alternative treatment options for central-involved diabetic macular edema (CIDME). These drugs are rarely used as first-line treatment options, because when compared against intravitreal injections of anti-vascular endothelial growth factor (anti-VEGF) agents, steroid therapies are associated with inferior visual acuity outcomes and increased rate of cataracts and glaucoma.

    For the treatment of macular edema following retinal vein occlusion, including branch retinal vein occlusion (BRVO) or central retinal vein occlusion (CRVO).
    Intravitreal implant dosage (Ozurdex dexamethasone intravitreal implant only)
    Adults

    Inject the implant (containing 0.7 mg dexamethasone in a solid polymer delivery system) intravitreally. Monitor the patient for elevated intraocular pressure and endophthalmitis.

    For the prevention of extubation failure in pediatric patients at increased risk for laryngeal edema (i.e., laryngeal edema prophylaxis†).
    Intravenous dosage (dexamethasone sodium phosphate)
    Infants, Children, and Adolescents

    0.5 mg/kg/dose IV (Maximum: 10 mg/dose IV) every 6 hours for 6 doses with the first dose given 6 to 12 hours prior to extubation has been studied with mixed results. One prospective, randomized study (n = 153) found no significant difference in the risk of postextubation stridor, the average number of racemic epinephrine treatments, or the number of patients requiring reintubation in patients receiving dexamethasone compared to those receiving placebo. Another prospective, randomized study (n = 66) found that dexamethasone-treated patients had a significantly lower rate of postextubation stridor at 10 minutes, 6 hours, and 12 hours but not 24 hours and fewer patients requiring epinephrine or reintubation compared to placebo-treated patients. A systematic review of clinical trials of dexamethasone for the prevention of postextubation stridor concluded that therapy may be beneficial in high-risk patients, such as those with underlying airway anomalies or multiple airway manipulations.

    Neonates

    Various regimens have been used. 0.25 mg/kg/dose IV every 8 hours for 3 doses with the first dose given approximately 4 hours prior to scheduled extubation was studied in a prospective, randomized trial in 50 premature neonates (mean gestational age, 27.7 to 28.7 weeks) who were at high risk for airway edema. The rate of postextubation stridor and reintubation was significantly lower in the dexamethasone group compared to the placebo group. A systematic review of clinical trials of dexamethasone for the prevention of extubation failure recommends therapy be reserved for use in high risk neonates, such as those with repeated or prolonged intubations, due to a lack of benefit in low risk neonates and the risk of adverse effects. Use preservative-free products for administration to neonates when possible.

    For use as an adjunct in the management of extradural malignant spinal cord compression† (MSCC†) associated with metastatic disease.
    Oral dosage (dexamethasone) or Intravenous dosage (dexamethasone sodium phosphate)
    Adults

    A bolus of 8 to 10 mg dexamethasone (or equivalent) PO or IV, followed by 16 mg/day PO (usually in twice-daily to four-times-daily doses for tolerance) is a typical dose; doses are adjusted to patient condition and are either maintained or tapered over a few weeks dependent on radiation therapy cycles and/or anticipated surgery. A broad dosage range of 16 to 100 mg/day has been used depending on the presence of paraparesis, etc. Higher quality data are needed to establish the benefits vs. risks and optimal dose and duration of therapy. Experts generally agree that patients who have neurologic deficits should receive dexamethasone; many patients with MSCC require corticosteroids to help preserve neurologic function, such as ambulation.

    For the adjunctive treatment of bacterial meningitis† (non-tuberculous).
    Oral dosage (dexamethasone) or Intravenous dosage (dexamethasone sodium phosphate)
    Adults

    For the treatment of proven or suspected pneumococcal meningitis due to S. pneumoniae, the Infectious Diseases Society of America (IDSA) recommends 0.15 mg/kg PO or IV every 6 hours for 2 to 4 days; the first dose should be given 10 to 20 minutes before or concomitantly with the first dose of antimicrobial agent. The IDSA suggests dexamethasone in these patients may reduce neuronal injury mediated by proinflammatory cytokine expression. Adjunctive dexamethasone should not be administered to patients who have already received antimicrobial therapy as this is unlikely to improve patient outcome. The IDSA does not routinely recommend dexamethasone as adjunctive therapy for meningitis caused by any other bacterial pathogens. NOTE: For the treatment of tuberculous meningitis, doses used for adjunctive treatment of TB.

    Infants, Children, and Adolescents

    For the treatment of meningitis due to H. influenzae type B, the IDSA recommends 0.15 mg/kg PO or IV every 6 hours for 2 to 4 days; the first dose should be given 10 to 20 minutes before or concomitantly with the first dose of antimicrobial agent. The IDSA suggests dexamethasone may reduce hearing impairment and neuronal injury mediated by proinflammatory cytokine expression. Adjunctive dexamethasone should not be administered to patients who have already received antimicrobial therapy as this is unlikely to improve patient outcome. The IDSA and the American Academy of Pediatrics (AAP) do not recommend routine dexamethasone as adjunctive therapy for meningitis caused by bacterial pathogens other than H. influenzae type B in pediatric patients. The use of dexamethasone in pneumococcal meningitis (S. pneumoniae) is controversial and may be considered in those greater than 6 weeks of age after weighing the possible benefits and risks. One study used dexamethasone 0.4 mg/kg IV twice daily for the first 2 days of antibiotic therapy in infants and children 2 months of age and older. NOTE: For the treatment of tuberculous meningitis, doses used for adjunctive treatment of TB.

    For the treatment of chemotherapy-induced nausea/vomiting† (CINV†) and for chemotherapy-induced nausea/vomiting prophylaxis†.
    Intravenous (dexamethasone sodium phosphate injection solution) or Oral dosage (dexamethasone)
    Adults


    American Society of Clinical Oncology (ASCO) guideline-based dosage regimens are stratified according to patient risk. HIGHLY EMETOGENIC CHEMOTHERAPY: 12 mg PO or IV prior to chemotherapy, then 8 mg PO or IV on days 2 to 3 or days 2 to 4. If aprepitant is not included in the anti-emetic regimen, increase to dexamethasone 20 mg PO or IV prior to chemotherapy, then 16 mg PO or IV on days 2 to 3 or days 2 to 4. MODERATELY EMETOGENIC CHEMOTHERAPY: 8 mg PO or IV prior to chemotherapy, then 8 mg PO or IV on days 2 and 3. LOW EMOTOGENIC RISK CHEMOTHERAPY: 8 mg PO or IV as a single dose prior to chemotherapy. (NOTE: Other regimens have been used historically during chemotherapy - e.g., 10 to 20 mg IV before administration of chemotherapy, with additional, lower doses given for 24 to 72 hours, as needed).

    Children and Adolescents

    10 to 14 mg/m2/dose IV is usually used prior to chemotherapy. A 5-HT3 antagonist is usually given along with dexamethasone for highly-emetogenic chemotherapy. An example regimen: dexamethasone 10 mg/m2/dose IV once daily, along with ondansetron. Some patients receive repeat dexamethasone every 12 hours, either IV or PO, but optimal regimens for repeat dosing are not established. For chemotherapy that is less emetogenic, doses as low as 6 mg/m2/dose PO have been given. The optimal dose of steroids for chemotherapy-induced nausea/vomiting (CINV) in children is not determined, and there are safety considerations.

    For the treatment of respiratory conditions including aspiration pneumonitis, berylliosis, chronic obstructive pulmonary disease (COPD), Loeffler's syndrome, or noncardiogenic pulmonary edema†.
    Oral dosage (dexamethasone)
    Adults

    Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Dosage of corticosteroids can be highly variable, depending on patient condition. Adjust according to patient response.

    Infants, Children and Adolescents

    0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response. Administer dexamethasone IV or IM initially for the treatment of severe respiratory conditions or those compromising the airway.

    Intravenous or Intramuscular dosage (dexamethasone sodium phosphate)
    Adults

    Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Dosage of corticosteroids can be highly variable, depending on patient condition. Adjust according to patient response.

    Infants, Children, and Adolescents

    0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response. Administer dexamethasone IV or IM initially for the treatment of severe respiratory conditions or those compromising the airway.

    For the treatment of acute respiratory distress syndrome (ARDS)†.
    Intravenous or Intramuscular dosage (dexamethasone sodium phosphate)
    Adults

    Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust according to patient response.

    Children and Adolescents

    0.06 to 0.3 mg/kg/day or 1.2 to 10 mg/m2/day IV or IM, in divided doses every 6 to 12 hours.

    For the treatment of laryngotracheobronchitis (croup)†.
    Oral, Intravenous, or Intramuscular dosage
    Infants, Children, and Adolescents

    0.6 mg/kg/dose PO, IV, or IM (Max: 8 to 20 mg/dose depending on study) as a single dose is the most commonly used regimen; however, lower doses of 0.15 mg/kg/dose PO, IV, or IM (Max: 3 mg/dose) have been shown to have similar efficacy.

    For hyaline membrane disease prophylaxis†, for the purpose of fetal lung maturation to prophylax against anticipated neonatal respiratory distress syndrome (RDS)† in premature infants.
    Intramuscular dosage (dexamethasone sodium phosphate)
    Pregnant females 24 to 34 weeks gestation

    Used to induce fetal lung maturation in preparation for premature delivery; the recommended maternal regimen is 6 mg IM every 12 hours for 4 doses in expectant mothers that are 24 to 34 weeks gestation at risk for premature delivery. Do not repeat the course of corticosteroids if delivery does not occur. Clinical consensus guidelines have clearly established a role for betamethasone and dexamethasone for this indication. Dexamethasone is comparable to betamethasone in preventing adverse outcomes and reducing neonatal intensive care unit (NICU) stays; more study is needed for optimal regimens, to determine if either drug has an advantage over the other, and long-term outcome studies are needed in the exposed children.

    For the prevention of chronic lung disease (CLD)† in mechanically ventilated neonates.
    Intravenous dosage (dexamethasone sodium phosphate)
    Preterm Neonates

    Numerous dosing schedules have been studied. Use is somewhat controversial, and most experts suggest using low doses and careful patient selection. The Dexamethasone: A Randomized Trial (DART) study (n = 70, median gestational age 25 weeks) used the following tapering dose schedule over 10 days: 0.075 mg/kg/dose IV twice daily for 3 days, 0.05 mg/kg/dose IV twice daily for 3 days, 0.025 mg/kg/dose IV twice daily for 2 days, and 0.01 mg/kg/dose IV twice daily for 2 days. This dosing regimen facilitated extubation by day 10 but did not significantly improve mortality or oxygen dependence at 36 weeks; follow-up at 2 years of age did not indicate any significant adverse neurodevelopmental outcomes in patients treated with dexamethasone. The American Academy of Pediatrics (AAP) recommends against the use of high-dose dexamethasone (greater than 0.5 mg/kg/day) due to the risk of short- and long-term adverse effects, including neurodevelopmental effects. Although the AAP states there is insufficient evidence to recommend low-dose dexamethasone (less than 0.2 mg/kg/day), other authors state that therapy may be considered after carefully weighing the risks versus benefits in patients at high-risk of developing chronic lung disease (e.g., those requiring mechanical ventilation after the first week of life). Use preservative-free products for administration to neonates when possible.

    For therapy in selected cases of acute rheumatic carditis, systemic dermatomyositis (polymyositis), systemic lupus erythematosus (SLE), temporal arteritis†, Churg-Strauss syndrome†, mixed connective tissue disease†, polyarteritis nodosa†, relapsing polychondritis†, polymyalgia rheumatica†, symptomatic sarcoidosis, vasculitis†, or Wegener's granulomatosis†; also for the treatment of neurologic or myocardial involvement associated with trichinosis.
    Oral dosage
    Adults

    Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Dosing can be quite variable, depending on the patient's condition. Adjust according to patient response.

    Children and Adolescents

    0.024 to 0.34 mg/kg/day PO or 0.66 to 10 mg/m2/day PO, given in 2 to 4 divided doses. Dosing can vary, depending on the patient's condition. Adjust according to patient response.

    Intramuscular or Intravenous dosage (dexamethasone sodium phosphate)
    Adults

    Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust according to patient response.

    Children and Adolescents

    0.06 to 0.3 mg/kg/day or 1.2 to 10 mg/m2/day IV or IM in divided doses every 6 to 12 hours. Adjust according to patient response.

    For the treatment of acute altitude sickness†, including the treatment of high altitude cerebral edema.
    Oral (dexamethasone) or Intravenous or Intramuscular dosage (dexamethasone sodium phosphate)
    Adults

    4 mg PO, IV, or IM every 6 hours for the treatment of acute altitude sickness without high altitude cerebral edema (HACE) or 8 mg PO, IV, or IM once followed by 4 mg PO, IV, or IM every 6 hours for the treatment of HACE is recommended by clinical practice guidelines. Descent is the preferred initial treatment. When descent is not possible or effective, symptomatic treatment (e.g., analgesics and antiemetics), oxygen, and other treatments, including dexamethasone, should be considered. Dexamethasone is more reliably effective than acetazolamide for acute altitude sickness of any degree, especially moderate to severe illness. Consideration can be given to adding acetazolamide for persons with HACE. Continue treatment until symptoms resolve. Of note, dexamethasone does not facilitate acclimatization.

    Infants, Children, and Adolescents

    0.15 mg/kg/dose PO, IV, or IM every 6 hours (Max: 4 mg/dose). Descent is the preferred initial treatment, particularly for younger children and infants. When descent is not effective or not possible, dexamethasone is the preferred pharmacologic therapy, especially for moderate to severe disease. Symptomatic treatment (e.g., analgesics and antiemetics), oxygen, and other treatments, including acetazolamide, should also be considered. Dexamethasone does not facilitate acclimatization; advise patients to delay further ascent until they are asymptomatic off medication. If the drug is discontinued at altitude before acclimatization, rebound can occur.

    For altitude sickness prophylaxis, including prevention of high altitude cerebral edema.
    Oral dosage
    Adults

    2 mg PO every 6 hours or 4 mg PO every 12 hours is recommended by clinical practice guidelines. 4 mg PO every 6 hours may be considered for very high risk situations necessitating immediate physical performance after being airlifted to high altitudes (e.g., military or search and rescue operations). Prophylactic medications should be considered in addition to slow ascent for moderate- to high-risk situations, and acetazolamide is preferred. Dexamethasone may be used in individuals with a history of intolerance or allergy to acetazolamide, or in emergency circumstances that require very rapid ascent, dexamethasone may be considered for concomitant use with acetazolamide. Start prophylaxis with dexamethasone the day of the ascent and continue prophylaxis for 2 to 3 days after reaching the target altitude or until descent is initiated. Duration of use should not exceed 10 days to prevent glucocorticoid toxicity or adrenal suppression.

    For the adjunctive treatment of infertility† in combination with clomiphene therapy.
    Oral dosage
    Adult females

    0.5 mg PO once daily at bedtime, administered on cycle days 3 to 12, days 5 to 9, or starting on day 5 and continuing through conception, in combination with clomiphene (doses ranging from 50 to 200 mg/day) has been studied. Alternatively, dexamethasone 2 mg PO once daily on cycle days 5 to 14 in combination with clomiphene 200 mg/day or dexamethasone 1 mg PO twice daily on cycle days 3 to 12 in combination with clomiphene 100 mg/day PO has also been studied; HCG was administered to augment ovulation. Optimal timing and dose of dexamethasone is not clear and has varied from study to study. Combination therapy has been shown to increase ovulation rates (range, 75% to 100%) and pregnancy rates (range, 38% to 74%) in women with both normal and elevated DHEA-S concentrations and in those women with or without polycystic ovary syndrome (PCOS). A Cochrane's review indicates that dexamethasone-clomiphene combination is one of the few adjunctive therapies for infertility that has been shown to improve pregnancy rates (fixed OR 11.3, 95% CI 5.3 to 24; NNT 2.7, 95% CI 2.1 to 3.6) ; the 2 studies in this review used differing doses of 0.5 mg PO at bedtime on days 5 to 9 or 2 mg PO/day on days 5 to 14. Several theories on the mechanism of dexamethasone in infertility exist. One theory is that dexamethasone enhances folliculogenesis by suppressing adrenal androgen hypersecretion, which should augment the actions of clomiphene. Dexamethasone may increase FSH concentrations thereby facilitating folliculogenesis. Finally, dexamethasone may decrease the elevated LH concentrations in patients with PCOS.

    For the treatment of post-operative nausea/vomiting (PONV)†.
    Intravenous dosage (dexamethasone sodium phosphate injection)
    Adults

    2 to 4 mg IV once for established post-operative nausea/vomiting (PONV), per treatment guidelines; readministration of longer-acting drugs, such as dexamethasone, is not recommended. If PONV prophylaxis was either inadequate or not initially given, dexamethasone is an appropriate rescue treatment option if not initially used for PONV prophylaxis. Of note, the 5-HT3 antagonists are the only class of drugs that have been adequately studied for the treatment of established PONV.

    For post-operative nausea/vomiting (PONV) prophylaxis†.
    Intravenous dosage (dexamethasone sodium phosphate injection solution)
    Adults

    4 to 5 mg IV at anesthesia induction is recommended by treatment guidelines for patients at an increased risk for post-operative nausea and vomiting (PONV); administration at induction rather than at the end of surgery is preferred. Some studies suggest that 8 mg IV is associated with a dose-dependent increase in quality of recovery, including reduced fatigue, postoperative pain, and need for opioid analgesia; however, further confirmation is necessary before larger doses are universally recommend. Safety data regarding the perioperative use of dexamethasone point to a possible increased risk of wound infection and/or increased blood glucose in some patients. A single dexamethasone dose (4 to 8 mg IV) is, however, considered safe for PONV prophylaxis. For patients with labile glucose control, dexamethasone use is relatively contraindicated.

    Children and Adolescents

    0.15 to 1 mg/kg/dose IV (Max: 8 to 25 mg/dose IV) given as a single intraoperative dose reduces the incidence of postoperative nausea/vomiting in the first 24 hours, improves postoperative pain control, and decreases the time to resumption of soft/solid diet without adverse effects and is recommended in patients undergoing tonsillectomy. A lower dose of 0.015 mg/kg/dose (Max: 5 mg/dose) in combination with ondansetron 0.1 mg/kg/dose (Max: 4 mg) is recommended first-line for postoperative vomiting prophylaxis in children by the Society for Ambulatory Anesthesiology.

    For the treatment of bronchiolitis†.
    Oral dosage
    Infants

    Due to the lack of consistent efficacy data and the high risk of adverse effects, the American Academy of Pediatrics does not recommend systemic corticosteroids for the management of bronchiolitis in any setting. However, other authors state corticosteroids may be beneficial in severely ill or mechanically ventilated patients. One randomized trial of 800 infants seen in the emergency department used 1 mg/kg PO once (Max: 10 mg/dose) followed by 0.6 mg/kg/dose PO once daily (Max: 10 mg/dose) for 5 days. Dexamethasone in combination with nebulized epinephrine was effective in reducing hospital admissions by day 7 of illness compared to treatment with dexamethasone alone, epinephrine alone, or placebo. In a study of 200 infants (median age 3.5 months) with an asthma risk, as determined by eczema or a family history of asthma in a first-degree relative, dexamethasone 1 mg/kg (single dose) PO then 0.6 mg/kg/dose PO once daily for 4 more days was administered with salbutamol. In infants receiving dexamethasone with salbutamol, the time to readiness for discharge was 18.6 hours vs. 27.1 hours in patients not receiving dexamethasone (p = 0.015). In contrast, 1 mg/kg/dose PO (Max: 12 mg/dose) given as a single dose did not reduce hospitalization rates, Respiratory Assessment Change Scores (RACS), length of hospitalization for those patients who required admission, or subsequent hospitalizations within 7 days compared to placebo in another large, randomized trial (n = 600).

    Intravenous dosage (dexamethasone sodium phosphate injection solution)
    Infants

    Due to the lack of consistent efficacy data and the high risk of adverse effects, the American Academy of Pediatrics does not recommend systemic corticosteroids for the management of bronchiolitis in any setting. However, other authors state corticosteroids may be beneficial in severely ill or mechanically ventilated patients. 0.15 mg/kg/dose IV every 6 hours for 48 hours with the first dose administered within 24 hours of mechanical ventilation was used in patients with respiratory syncytial virus. In a post hoc analysis of patients with bronchiolitis (n = 39), the mean duration of mechanical ventilation and of supplemental oxygen were significantly shorter in patients receiving dexamethasone compared to those receiving placebo (4.9 and 7.7 days vs. 9.2 and 11.3 days, respectively); no differences were seen in the length of intensive care unit or hospital stay.

    For the treatment of Waldenstrom macroglobulinemia†.
    For the treatment of newly diagnosed Waldenstrom macroglobulinemia, in combination with rituximab and cyclophosphamide†.
    Intravenous dosage (dexamethasone sodium phosphate)
    Adults

    20 mg IV on day 1 in combination with rituximab 375 mg/m2 IV on day 1 and cyclophosphamide 100 mg/m2 orally twice daily on days 1 to 5 (total dose of 1,000 mg/m2/cycle) repeated every 21 days for 6 cycles was evaluated in a single-arm, phase II trial.

    For the treatment of newly diagnosed Waldenstrom macroglobulinemia, in combination with bortezomib and rituximab†.
    Intravenous dosage (dexamethasone sodium phosphate)
    Adults

    40 mg IV on days 1, 8, 15, and 22 in cycles 2 and 5 in combination with bortezomib and rituximab was evaluated in a nonrandomized phase II trial. Bortezomib was given as follows: 1.3 mg/m2 IV on days 1, 4, 8, and 11 for the first 21-day cycle (cycle 1) then 1.6 mg/m2 IV on days 1, 8, 15, and 22 repeated every 35 days for 4 additional cycles (cycles 2, 3, 4, and 5). Rituximab was given as 375 mg/m2 IV on days 1, 8, 15, and 22 in cycles 2 and 5 (for 8 total doses). All patients received premedication with acetaminophen 1,000 mg PO and diphenhydramine 50 mg IV prior to rituximab and herpes zoster prophylaxis with valacyclovir or acyclovir.

    For the treatment of amyloidosis†.
    For the treatment of systemic amyloid light-chain amyloidosis, in combination with lenalidomide and cyclophosphamide†.
    Oral dosage
    Adults

    Dexamethasone in combination with lenalidomide (15 mg PO daily on days 1 to 21) and cyclophosphamide repeated every 28 days has been evaluated in nonrandomized, phase II studies. Treatment duration, drug dosages of cyclophosphamide and dexamethasone, and thromboprophylaxis agents/recommendations varied in these studies. In one study, 12 cycles of dexamethasone (20 mg PO on days 1, 2, 3, 4, 9, 10, 11, and 12 for 6 cycles; then 20 mg PO on days 1, 2, 3, and 4 for an additional 6 cycles), lenalidomide, and cyclophosphamide (300 mg/m2 IV on days 1 and 8 for 6 cycles; then 300 mg/m2 IV on day 1 for an additional 6 cycles) were given and then maintenance therapy with lenalidomide and dexamethasone was administered for 3 additional years or until disease progression. Patients with cardiac stage III had an upfront dose modification of dexamethasone. In another study, dexamethasone (40 mg PO on days 1, 8, 15, and 22), lenalidomide, and cyclophosphamide (500 mg PO on days 1, 8, and 15) therapy was given for a maximum of 9 cycles; treatment was discontinued after cycle 6 if a complete response or partial response/very good partial response plus organ response was obtained. In this study, patients with fluid retention over 3% of body weight despite optimal diuretic use received a lower dose of dexamethasone (20 mg once weekly). In a third study, cycles of dexamethasone (40 mg PO on days 1, 8, 15, and 22), lenalidomide, and cyclophosphamide (300 mg/m2 PO on days 1, 8, and 15) were continued until disease progression, unacceptable toxicity, or up to 2 years; however, cyclophosphamide was given for up to a maximum of 12 cycles only.

    For the treatment of systemic amyloid light-chain amyloidosis, in combination with lenalidomide and melphalan†.
    Oral dosage
    Adults

    40 mg orally on days 1, 8, 15, and 22 in combination with lenalidomide (10 mg PO daily on days 1 to 21) and melphalan repeated every 28 days has been evaluated in nonrandomized studies. Treatment duration, the melphalan dosage, and thromboprophylaxis agents/recommendations varied in these studies. In one study, melphalan (0.18 mg/kg PO daily on days 1, 2, 3, and 4), lenalidomide, and dexamethasone therapy was given for a maximum of 9 cycles; single-agent lenalidomide was continued in responding patients. In another study, lenalidomide, melphalan (5 mg/m2 PO daily on days 1, 2, 3, and 4), and dexamethasone were continued until disease progression, unacceptable toxicity, or up to 12 cycles.

    †Indicates off-label use

    MAXIMUM DOSAGE

    Dosage must be individualized and is highly variable depending on the nature and severity of the disease, route of treatment, and on patient response.

    DOSING CONSIDERATIONS

    Hepatic Impairment

    Systemic dosage may need adjustment depending on the degree of hepatic insufficiency, but quantitative recommendations are not available.

    Renal Impairment

    Specific guidelines for dosage adjustments in renal impairment are not available; it appears that no dosage adjustments are needed.

    ADMINISTRATION

    Oral Administration

    Administer with food to minimize GI upset.
    If given once daily, give in the morning to coincide with the body's normal cortisol secretion.

    Injectable Administration

    Visually inspect parenteral products for particulate matter and discoloration prior to administration whenever solution and container permit.

    Intravenous Administration

    Direct IV injection:
    Dexamethasone sodium phosphate solution for injection 4 mg/mL or 10 mg/mL may be given directly from the vial.
     
    Intermittent or continuous IV infusion:
    Dexamethasone sodium phosphate solution for injection 4 mg/mL or 10 mg/mL may be added to 5% Dextrose injection or 0.9% Sodium Chloride injection and given by IV infusion. Use diluted solutions within 24 hours, as infusion solutions generally do not contain preservatives.

    Intramuscular Administration

    Dexamethasone sodium phosphate solution for injection 4 mg/mL or 10 mg/mL may be administered intramuscularly.

    Other Injectable Administration

    Intra-articular, Soft tissue, or Intralesional injection
    Dexamethasone sodium phosphate solution for injection 4 mg/mL may be administered into joints, soft tissues, or lesions, but administration of dexamethasone via these routes requires specialized techniques.
    Only clinicians familiar with these methods of administration and with management of potential complications should administer dexamethasone by these routes.
    Frequent intra-articular injections may result in damage to joint tissues.
    Dexamethasone sodium phosphate injection is particularly recommended for use in conjunction with one of the less soluble, longer-acting steroids for intra-articular and soft tissue injection.

    Ophthalmic Administration

    Apply ophthalmic solution topically to the eye.
    For ophthalmic suspensions, shake well prior to each administration.
    Instruct patient on appropriate instillation technique.
    Do not to touch the tip of the dropper or tube to the eye, fingertips, or other surface.
    To prevent contamination, each dropper is for one individual, do not share among patients.

    Otic Administration

    Otic Administration of Ophthalmic Solution:
    Clean the ear canal thoroughly and sponge dry prior to administration.
    Instill the solution directly into the ear canal.
    Alternatively, a gauze wick may be saturated with solution and packed into the ear canal. Keep the gauze wick moist with solution and remove from ear after 12 to 24 hours.

    Other Administration Route(s)

    Intravitreal Implant
    Intravitreal implantation should be performed only by surgeons who have observed or assisted in surgical implantation of the implant. Consult specialized instructions regarding insertion of the implant.
    Administer via intravitreal injection with the provided single-use plastic applicator.
    Use controlled aseptic conditions, which include the use of sterile gloves, a sterile drape, and a sterile eyelid speculum (or equivalent).
    Use each applicator for a single treatment only. If the contralateral eye requires treatment, a new applicator must be used and the sterile field should be changed.
    After the intravitreal injection, monitor patients for elevation in intraocular pressure and for endophthalmitis. Monitoring may consist of a check for reperfusion of the optic nerve head immediately after the injection, tonometry within 30 minutes after the injection, and biomicroscopy 2 to 7 days after the injection.
    Instruct patients to promptly report any symptoms suggestive of endophthalmitis.

    STORAGE

    Generic:
    - Store at controlled room temperature (between 68 and 77 degrees F)
    AK-Dex:
    - Store at room temperature (between 59 to 86 degrees F)
    Baycadron:
    - Protect from freezing
    - Store at controlled room temperature (between 68 and 77 degrees F)
    CUSHINGS SYNDROME DIAGNOSTIC :
    - Store at controlled room temperature (between 68 and 77 degrees F)
    Decadron:
    - Discard product if it contains particulate matter, is cloudy, or discolored
    - Do not autoclave
    - Protect from freezing
    - Protect from light
    - Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
    - Store in carton until time of use
    DexPak Jr TaperPak:
    - Protect from moisture
    - Store and dispense in original container
    - Store at controlled room temperature (between 68 and 77 degrees F)
    DexPak TaperPak:
    - Protect from moisture
    - Store and dispense in original container
    - Store at controlled room temperature (between 68 and 77 degrees F)
    DoubleDex:
    - Discard product if it contains particulate matter, is cloudy, or discolored
    - Discard unused portion. Do not store for later use.
    - Protect from extreme heat
    - Protect from freezing
    - Protect from light
    - Store at controlled room temperature (between 68 and 77 degrees F)
    - Store in carton until time of use
    - Use within 24 hours from time of preparation
    Maxidex:
    - Store between 46 to 77 degrees F
    - Store upright
    Ozurdex:
    - Store at room temperature (between 59 to 86 degrees F)
    Simplist Dexamethasone:
    - Discard product if it contains particulate matter, is cloudy, or discolored
    - Do not autoclave
    - Protect from freezing
    - Protect from light
    - Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
    - Store in carton until time of use
    Solurex:
    - Discard product if it contains particulate matter, is cloudy, or discolored
    - Do not autoclave
    - Protect from freezing
    - Protect from light
    - Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
    - Store in carton until time of use
    Zema-Pak:
    - Protect from moisture
    - Store and dispense in original container
    - Store at controlled room temperature (between 68 and 77 degrees F)
    ZoDex:
    - Protect from moisture
    - Store and dispense in original container
    - Store at controlled room temperature (between 68 and 77 degrees F)
    ZonaCort 11 Day:
    - Protect from moisture
    - Store and dispense in original container
    - Store at controlled room temperature (between 68 and 77 degrees F)
    ZonaCort 7 Day:
    - Protect from moisture
    - Store and dispense in original container
    - Store at controlled room temperature (between 68 and 77 degrees F)

    CONTRAINDICATIONS / PRECAUTIONS

    Epidural administration

    Epidural administration of corticosteroids should be used with great caution. Rare, but serious adverse reactions, including cortical blindness, stroke, spinal cord infarction, paralysis, seizures, nerve injury, brain edema, and death have been associated with epidural administration of injectable corticosteroids. These events have been reported with and without the use of fluoroscopy. Many cases were temporally associated with the corticosteroid injection; reactions occurred within minutes to 48 hours after injection. Some cases of neurologic events were confirmed through magnetic resonance imaging (MRI) or computed tomography (CT) scan. Many patients did not recover from the reported adverse effects. Discuss the benefits and risks of epidural corticosteroid injections with the patient before treatment. If a decision is made to proceed with corticosteroid epidural administration, counsel patients to seek emergency medical attention if they experience symptoms after injection such as vision changes, tingling in the arms or legs, dizziness, severe headache, seizures, or sudden weakness or numbness of face, arm, or leg.

    Abrupt discontinuation, corneal abrasion, Cushing's syndrome, hypothalamic-pituitary-adrenal (HPA) suppression, occlusive dressing, skin abrasion

    Systemic corticosteroids can aggravate Cushing's syndrome and should be avoided in patients with Cushing's syndrome. Pharmacological doses of systemic corticosteroids administered for prolonged periods or systemic absorption of topical preparations may result in hypothalamic-pituitary-adrenal (HPA) suppression and/or manifestations of Cushing's syndrome in some patients. However, the risk of developing HPA suppression while using topical dexamethasone only is low. Acute adrenal insufficiency and even death may occur following abrupt discontinuation of systemic therapy. In addition, a withdrawal syndrome unrelated to adrenocortical insufficiency may occur following sudden discontinuation of corticosteroid therapy. These effects are thought to be due to the sudden change in glucocorticoid concentration rather than to low corticosteroid levels. Withdrawal from prolonged systemic corticosteroid therapy should be gradual. HPA suppression can last for up to 12 months following cessation of systemic therapy. Recovery of HPA axis function is generally prompt and complete upon discontinuation of the topical corticosteroid. HPA-suppressed patients may need supplemental corticosteroid treatment during periods of physiologic stress, such as surgical procedures, acute blood loss, or infectious conditions, even after the corticosteroid has been discontinued. Conditions that increase systemic absorption of topical corticosteroids include use over large surface areas, prolonged use, use in areas where the epidermal barrier is disrupted (i.e., skin abrasion), and the use of an occlusive dressing. Ophthalmic dexamethasone should be used with caution in patients with corneal abrasion. Patients receiving large doses of dexamethasone applied to a large surface area should be evaluated periodically for evidence of HPA axis suppression and/or manifestations of Cushing's syndrome. If these effects are noted, an attempt should be made to withdraw the drug, to reduce the frequency of application, or to substitute a less potent corticosteroid.

    Children, growth inhibition, increased intracranial pressure

    Chronic systemic corticosteroid therapy in children may interfere with growth and development. The potential for growth inhibition should be monitored during prolonged therapy in children, and the potential for growth effects should be weighed against the clinical benefit obtained and the availability of other treatment alternatives. Administration of corticosteroids to pediatric patients should be limited to the least amount compatible with an effective therapeutic regimen. Children may absorb proportionally larger amounts of topical corticosteroids due to a larger skin surface area to body weight ratio, and therefore are more susceptible to developing systemic toxicity. Hypothalamic-pituitary-adrenal (HPA) axis suppression, Cushing's syndrome, and increased intracranial pressure have also been reported in children receiving topical corticosteroids. The safety and efficacy of the dexamethasone intravitreal implant has not been established in pediatric patients.

    Immunosuppression

    Patients receiving high-dose (e.g., equivalent to 1 mg/kg or more of prednisone daily) or systemic corticosteroid therapy like dexamethasone, for any period of time, particularly in conjunction with corticosteroid sparing drugs (e.g., troleandomycin) are at risk to develop immunosuppression; however, patients receiving moderate dosages of systemic corticosteroids for short periods or low dosages for prolonged periods also may be at risk. Treatment with topical corticosteroids lessens the risk of immunosuppression; although localized effects may be seen. When given in combination with other immunosuppressive agents, there is a risk of over-immunosuppression.

    Surgery

    If surgery is required, patients should advise their physician that they received systemic corticosteroid therapy, like dexamethasone, within the last 12 months and state the disease for which they were being treated. Identification cards that include disease state, type and dose of corticosteroid, and physician should always be carried with the patient.

    Acne rosacea, acne vulgaris, fungal infection, herpes infection, herpes simplex keratitis (dendritic keratitis), infection, measles, ocular infection, perioral dermatitis, peripheral vascular disease, tuberculosis, varicella, viral infection

    Systemic corticosteroid therapy can mask the symptoms of infection and should not be used in cases of viral infection, fungal infection, or bacterial infection that are not adequately controlled by antiinfective agents. Although the manufacturers state that systemic dexamethasone is contraindicated in patients with systemic fungal infections, most clinicians believe that systemic corticosteroids can be administered to these patients as long as appropriate antiinfective therapy is administered simultaneously. Systemic corticosteroids can reactivate tuberculosis and should not be used in patients with a history of active tuberculosis, except when chemoprophylaxis is instituted concomitantly. Patients receiving immunosuppressive doses of systemic corticosteroids should be advised to avoid exposure to viral infections (i.e., measles or varicella) because these diseases may be more serious or even fatal in immunosuppressed patients. Pediatric patients dependent on systemic corticosteroids should undergo anti-varicella zoster virus antibody testing. Ophthalmic dexamethasone is contraindicated in patients with an acute, untreated purulent bacterial, viral, or fungal ocular infection or periocular infection. As such, most viral diseases of the cornea and conjunctive are contraindications to use of ophthalmic preparations, including active epithelia herpes simplex keratitis (dendritic keratitis), vaccina, varicella, or mycobacterial infections, and fungal diseases. Application of topical corticosteroids to areas of infection, including tuberculosis of the skin, dermatologic fungal infection, and cutaneous or systemic viral infection (e.g., herpes infection, measles, varicella), should be initiated or continued only if the appropriate antiinfective treatment is instituted. If the infection does not respond to the antimicrobial therapy, the concurrent use of the topical corticosteroid should be discontinued until the infection is controlled. Topical corticosteroids should not be used to treat acne vulgaris, acne rosacea, or perioral dermatitis as they may exacerbate these conditions. Topical corticosteroids may delay the healing of non-infected wounds, such as venous stasis ulcers. Use topical dexamethasone preparations with caution in patients with markedly impaired circulation or peripheral vascular disease; skin ulceration has been reported in these patients following topical corticosteroid use.

    Myocardial infarction

    Systemic corticosteroid therapy, including dexamethasone, has been associated with left ventricular free-wall rupture in patients with recent myocardial infarction, so its use should be employed with extreme caution in these patients.

    Heart failure, hypertension

    Systemic corticosteroids, like dexamethasone, can cause edema and weight gain. Patients with congestive heart failure or hypertension can have an exacerbation of their condition. Systemic corticosteroids should be used with caution in these patients.

    Osteoporosis

    The risks and benefits of corticosteroid therapy should be considered for any individual patient. Prolonged systemic corticosteroid therapy can lead to osteoporosis, vertebral compression fractures, aseptic necrosis of femoral and humoral heads, and pathologic fractures of long bones secondary to protein catabolism. Elderly, debilitated, or postmenopausal patients because they are especially susceptible to these adverse effects. A high-protein diet may alleviate or prevent the adverse effects associated with protein catabolism. Detrimental effects on bone metabolism, such as osteoporosis are expected to be much lower with inhaled, rather than systemically-administered corticosteroids. Although not conclusive, some data suggest that high-dose inhaled steroids may also decrease bone formation and increased resorption.

    Diabetes mellitus

    Systemic corticosteroids may decrease glucose tolerance, produce hyperglycemia, and aggravate or precipitate diabetes mellitus. This may especially occur in patients predisposed to diabetes mellitus. When corticosteroid therapy is necessary in patients with diabetes mellitus, changes in insulin, oral antidiabetic agent dosage, and/or diet may be required. Ophthalmic dexamethasone therapy should be undertaken with caution in patients with diabetes mellitus because these patients have an increased risk of developing ocular hypertension during therapy. Topical corticosteroids should be used with caution in patients with diabetes mellitus. Exacerbation of diabetes may occur with systemic absorption of the topical corticosteroid. Use of topical corticosteroids may further delay healing of skin ulcers in diabetic patients.

    Diverticulitis, GI disease, GI perforation, inflammatory bowel disease, peptic ulcer disease, ulcerative colitis

    Use systemic corticosteroids with caution in patients with GI disease as use may inhibit gastroprotective prostaglandin production; further, oral corticosteroids can cause direct gastrointestinal irritation. As such, dexamethasone should be used with caution in patients with GI disease, diverticulitis, nonspecific ulcerative colitis, or intestinal anastomosis (because of the possibility of GI wall perforation). While used for the short-term treatment of acute exacerbations of chronic inflammatory bowel disease such as ulcerative colitis and Crohn's disease, corticosteroids should not be used in patients where there is a possibility of impending GI perforation, abscess, or pyogenic infection. Some patients may require long-term corticosteroid therapy to suppress disease activity, but generally this practice is not recommended. Corticosteroids should not be used in patients with peptic ulcer disease except under life-threatening circumstances.

    Hepatic disease, hypothyroidism, psychosis, renal disease, seizure disorder

    Systemic corticosteroids, like dexamethasone, should be used with extreme caution in patients with psychosis, emotional instability, renal disease, and seizure disorder because the drugs can exacerbate these conditions. Patients with hepatic disease, such as cirrhosis, or hypothyroidism can have an exaggerated response to systemic corticosteroids; use systemic corticosteroids with caution in these patients.

    Myasthenia gravis

    Systemic glucocorticoids, like dexamethasone, should be used with caution in patients with myasthenia gravis who are being treated with anticholinesterase agents. Muscle weakness can be increased transiently during the initiation of glucocorticoid therapy in patients with myasthenia gravis, necessitating respiratory support.

    Coagulopathy, thromboembolic disease

    Systemic corticosteroids, like dexamethasone, rarely may increase blood coagulability, causing intravascular thrombosis, thrombophlebitis, and thromboembolism. Systemic corticosteroids should, therefore, be used with caution in patients with preexisting coagulopathy (e.g., hemophilia) or thromboembolic disease.

    Cataracts, glaucoma, increased intraocular pressure, myopia, ocular exposure, open-angle glaucoma, rupture of posterior ocular lens capsule, visual disturbance

    Corticosteroids may exacerbate glaucoma. Systemic corticosteroids should be used cautiously in patients with glaucoma or other types of visual disturbance. Ophthalmic dexamethasone is more likely than other ophthalmic agents to cause increased intraocular pressure, so intraocular pressure should be measured every 2—4 weeks for the first 2 months of therapy, and every 1—2 months thereafter. Ophthalmic dexamethasone therapy should be undertaken with caution in patients with a history of open-angle glaucoma, myopia, or Krukenberg's spindle because these patients have an increased risk of developing ocular hypertension during therapy. Patients receiving corticosteroids chronically should be periodically assessed for cataract formation, since corticosteroid use is associated with cataract formation. There is also an increase in the propensity for secondary ocular infection caused by fungal or viral infections. Care should be taken to avoid ocular exposure to non-ophthalmic preparations, as visual impairment, ocular hypertension and worsened cataracts have been reported with ocular exposure to topical corticosteroids. The dexamethasone intravitreal implant is contraindicated in patients with glaucoma who have cup to disc ratio > 0.8. Dexamethasone intravitreal implant is also contraindicated in patients who have a tear or a rupture of posterior ocular lens capsule; these patients with an absent or torn posterior capsule of the lens are at increased risk of migration of the intravitreal implant into the anterior chamber. Laser posterior capsulotomy in pseudophakic patients is not a contraindication for the dexamethasone intravitreal implant.

    Pregnancy

    Dexamethasone is classified FDA pregnancy risk category C. Complications, including cleft palate, still birth, and premature abortion, have been reported when systemic corticosteroids were administered during pregnancy. In addition, dexamethasone has been shown to be teratogenic in mice and rabbits following topical ophthalmic application in multiples of the therapeutic dose. There are no adequate, well-controlled studies for the use of dexamethasone in pregnant women; therefore, the manufacturers recommend that the drug be used only if the potential benefit to the mother outweighs the potential risk to the fetus. Dexamethasone injections have been used medically later in pregnancy to induce fetal lung maturation in patients at risk for pre-term delivery; use is for select circumstances and for a limited duration of time. If dexamethasone must be used chronically during pregnancy, the potential risks should be discussed with the patient. Children born to women receiving large doses of systemic corticosteroids during pregnancy should be monitored for signs of adrenal insufficiency, and appropriate therapy should be initiated, if necessary.Topical corticosteroids should not be used in large amounts, on large areas, or for prolonged periods of time in pregnant women.

    Neonates, premature neonates

    The routine use of high-dose (greater than 0.5 mg/kg/day) dexamethasone for either the prevention or treatment of chronic lung disease in premature neonates is not recommended by the American Academy of Pediatrics (AAP) due to a lack of survival benefit and concern about long-term adverse outcomes, particularly increased rates of cerebral palsy. Studies utilizing lower doses of dexamethasone (less than 0.2 mg/kg/day) have not reported increased rates of adverse neurodevelopmental effects; however, due to the small number of patients included in these studies, the AAP states that there is insufficient evidence to recommend the use of low-dose dexamethasone and further study is warranted. In a geographical cohort study of 148 extremely premature pediatric patients (born < 28 weeks gestation), 55 (27%) received postnatal dexamethasone (mean cumulative dose 7.7 mg/kg) during the neonatal period. Patients receiving dexamethasone had smaller total brain tissue volume (mean difference -3.6%, p value = 0.04) and smaller white matter, thalami, and basal ganglia volumes (p < 0.05 for all) when compared with participants who did not receive postnatal dexamethasone. There was also a trend of smaller total brain and white matter volumes with increased dose of postnatal dexamethasone. Avoid use of dexamethasone injectable formulations containing benzyl alcohol in premature neonates and neonates. Administration of benzyl alcohol to neonates can result in 'gasping syndrome,' which is a potentially fatal condition characterized by metabolic acidosis and CNS, respiratory, circulatory, and renal dysfunction; it is also characterized by high concentrations of benzyl alcohol and its metabolites in the blood and urine. While the minimum amount of benzyl alcohol at which toxicity may occur is not known, 'gasping syndrome' has been associated with daily benzyl alcohol exposure above 99 mg/kg/day in neonates and low-birth-weight neonates. Additional symptoms may include gradual neurological deterioration, seizures, intracranial hemorrhage, hematologic abnormalities, skin breakdown, hepatic failure, renal failure, hypotension, bradycardia, and cardiovascular collapse. Rare cases of death, primarily in premature neonates, have been reported. Further, an increased incidence of kernicterus, especially in small, premature neonates has been reported. Practitioners administering this and other medications containing benzyl alcohol should consider the combined daily metabolic load of benzyl alcohol from all sources. Premature neonates, neonates with a low birth weight, and patients who receive a high dose may be more likely to develop toxicity.

    Breast-feeding

    Corticosteroids distribute into breast milk in low concentrations; the manufacturer recommends that women receiving pharmacological doses of systemic corticosteroids not breast-feed. It is not known if ocular administration of corticosteroids could result in detectable quantities in human milk. Dexamethasone has not been studied during breast-feeding. It may be prudent to consider using an alternate for chronic therapy if indicated; the American Academy of Pediatrics (AAP) considers prednisone and prednisolone usually compatible with breast-feeding. Alternative ophthalmic agents to dexamethasone include prednisolone ophthalmic products. Alternatives for injectable dexamethasone may be dependent on indication for the drug's use, as suitable alternatives may not be available for all scenarios. For asthma, inhaled budesonide or oral prednisone may be amenable choices. Low-dose inhaled corticosteroids are considered first line therapy for control of mild persistent asthma during pregnancy and lactation according to the 2004 guidelines of the National Asthma Education and Prevention Program (NAEPP) Asthma and Pregnancy Working Group. Due to greater availability of data in pregnancy, budesonide is the preferred agent in this population. However, there are no data to indicate safety concerns with other inhaled corticosteroids and maintaining a previously established treatment regimen may be more beneficial to the patient. While not measured, the amount of dexamethasone absorbed into the maternal bloodstream and excreted into breast-milk after inhalation is expected to be low; reviewers and an expert panel consider inhaled corticosteroids acceptable to use during breast-feeding. Consider the benefits of breast-feeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition. If a breast-feeding infant experiences an adverse effect related to a maternally ingested or administered drug, healthcare providers are encouraged to report the adverse effect to the FDA.

    Vaccination

    Corticosteroid therapy usually does not contraindicate vaccination with live-virus vaccines when such therapy is of short-term (< 2 weeks); low to moderate dose; long-term alternate day treatment with short-acting preparations; maintenance physiologic doses (replacement therapy); or administration topically (skin or eye), by aerosol, or by intra-articular, bursal or tendon injection. The immunosuppressive effects of steroid treatment differ, but many clinicians consider a dose equivalent to either 2 mg/kg/day or 20 mg/day of prednisone as sufficiently immunosuppressive to raise concern about the safety of immunization with live-virus vaccines. In general, patients with severe immunosuppression due to large doses of corticosteroids should not receive vaccination with live-virus vaccines. When cancer chemotherapy or immunosuppressive therapy is being considered (e.g., for patients with Hodgkin's disease or organ transplantation), vaccination should precede the initiation of chemotherapy or immunotherapy by >= 2 weeks. Patients vaccinated while on immunosuppressive therapy or in the 2 weeks prior to starting therapy should be considered unimmunized and should be revaccinated at least 3 months after discontinuation of therapy. In patients who have received high-dose, systemic corticosteroids for >= 2 weeks, it is recommended to wait at least 3 months after discontinuation of therapy before administering a live-virus vaccine.

    Asthma, benzyl alcohol hypersensitivity, sulfite hypersensitivity

    Some commercially available formulations of dexamethasone may contain sulfites; some parenteral products contain benzyl alcohol. Sulfites and benzyl alcohol may cause allergic reactions in some people. They should be used with caution in patients with known sulfite hypersensitivity or benzyl alcohol hypersensitivity. Patients who have asthma are more likely to experience a sulfite sensitivity reaction than non-asthmatic patients.

    Corticosteroid hypersensitivity

    Although true corticosteroid hypersensitivity is rare, patients who have demonstrated a prior hypersensitivity reaction to dexamethasone should not receive any form of dexamethasone. It is possible, though also rare, that such patients will display cross-hypersensitivity to other corticosteroids. It is advisable that patients who have a hypersensitivity reaction to any corticosteroid undergo skin testing, which, although not a conclusive predictor, may help to determine if hypersensitivity to another corticosteroid exists. Such patients should be carefully monitored during and following the administration of any corticosteroid.

    Geriatric

    Use systemic corticosteroids with caution in the geriatric patient; the risks and benefits of therapy should be considered for any individual patient. Geriatric and debilitated patients are especially susceptible to corticosteroid-induced decreases in bone mineral density and resultant fractures. Detrimental effects on bone metabolism, such as osteoporosis, are a risk with chronic, systemically-administered corticosteroids. According to the Beers Criteria, systemic corticosteroids are considered potentially inappropriate medications (PIMs) for use in geriatric patients with delirium or at high risk for delirium and should be avoided in these patient populations due to the possibility of new-onset delirium or exacerbation of the current condition. The Beers expert panel notes that oral and parenteral corticosteroids may be required for conditions such as exacerbation of chronic obstructive pulmonary disease (COPD) but should be prescribed in the lowest effective dose and for the shortest possible duration. The federal Omnibus Budget Reconciliation Act (OBRA) regulates medication use in residents of long-term care facilities (LTCFs). The OBRA guidelines caution that orally inhaled corticosteroids, such as dexamethasone, can cause throat irritation and oral candidiasis, particularly if the mouth is not rinsed after administration. The need for continued use of a glucocorticoid, with the exception of topical or inhaled formulations, should be documented, along with monitoring for and management of adverse consequences. Intermediate or longer-term use may cause hyperglycemia, psychosis, edema, insomnia, hypertension, osteoporosis, mood lability, or depression.

    ADVERSE REACTIONS

    Severe

    ocular hemorrhage / Delayed / 22.0-23.0
    increased intracranial pressure / Early / Incidence not known
    papilledema / Delayed / Incidence not known
    exfoliative dermatitis / Delayed / Incidence not known
    bone fractures / Delayed / Incidence not known
    avascular necrosis / Delayed / Incidence not known
    tendon rupture / Delayed / Incidence not known
    GI perforation / Delayed / Incidence not known
    esophageal ulceration / Delayed / Incidence not known
    peptic ulcer / Delayed / Incidence not known
    pancreatitis / Delayed / Incidence not known
    GI bleeding / Delayed / Incidence not known
    angioedema / Rapid / Incidence not known
    lupus-like symptoms / Delayed / Incidence not known
    skin atrophy / Delayed / Incidence not known
    anaphylactoid reactions / Rapid / Incidence not known
    tumor lysis syndrome (TLS) / Delayed / Incidence not known
    heart failure / Delayed / Incidence not known
    seizures / Delayed / Incidence not known
    keratoconjunctivitis / Early / Incidence not known
    endophthalmitis / Delayed / Incidence not known
    retinopathy / Delayed / Incidence not known
    keratitis / Delayed / Incidence not known
    optic neuritis / Delayed / Incidence not known
    visual impairment / Early / Incidence not known
    retinal detachment / Delayed / Incidence not known
    ocular hypertension / Delayed / Incidence not known
    vasculitis / Delayed / Incidence not known
    stroke / Early / Incidence not known
    thrombosis / Delayed / Incidence not known
    pulmonary edema / Early / Incidence not known
    cardiomyopathy / Delayed / Incidence not known
    myocardial infarction / Delayed / Incidence not known
    cardiac arrest / Early / Incidence not known
    bradycardia / Rapid / Incidence not known
    thromboembolism / Delayed / Incidence not known
    arrhythmia exacerbation / Early / Incidence not known

    Moderate

    glossitis / Early / Incidence not known
    anemia / Delayed / Incidence not known
    withdrawal / Early / Incidence not known
    adrenocortical insufficiency / Delayed / Incidence not known
    physiological dependence / Delayed / Incidence not known
    pseudotumor cerebri / Delayed / Incidence not known
    hypotension / Rapid / Incidence not known
    hypothalamic-pituitary-adrenal (HPA) suppression / Delayed / Incidence not known
    Cushing's syndrome / Delayed / Incidence not known
    hyperthyroidism / Delayed / Incidence not known
    postmenopausal bleeding / Delayed / Incidence not known
    diabetes mellitus / Delayed / Incidence not known
    glycosuria / Early / Incidence not known
    hyperglycemia / Delayed / Incidence not known
    hypothyroidism / Delayed / Incidence not known
    growth inhibition / Delayed / Incidence not known
    myopathy / Delayed / Incidence not known
    osteopenia / Delayed / Incidence not known
    osteoporosis / Delayed / Incidence not known
    impaired wound healing / Delayed / Incidence not known
    constipation / Delayed / Incidence not known
    gastritis / Delayed / Incidence not known
    erythema / Early / Incidence not known
    immunosuppression / Delayed / Incidence not known
    candidiasis / Delayed / Incidence not known
    neutropenia / Delayed / Incidence not known
    sodium retention / Delayed / Incidence not known
    edema / Delayed / Incidence not known
    fluid retention / Delayed / Incidence not known
    hypernatremia / Delayed / Incidence not known
    hypertension / Early / Incidence not known
    hypocalcemia / Delayed / Incidence not known
    metabolic alkalosis / Delayed / Incidence not known
    hypokalemia / Delayed / Incidence not known
    memory impairment / Delayed / Incidence not known
    mania / Early / Incidence not known
    euphoria / Early / Incidence not known
    impaired cognition / Early / Incidence not known
    peripheral neuropathy / Delayed / Incidence not known
    amnesia / Delayed / Incidence not known
    hallucinations / Early / Incidence not known
    psychosis / Early / Incidence not known
    EEG changes / Delayed / Incidence not known
    delirium / Early / Incidence not known
    neuritis / Delayed / Incidence not known
    depression / Delayed / Incidence not known
    ocular infection / Delayed / Incidence not known
    corneal edema / Early / Incidence not known
    blurred vision / Early / Incidence not known
    conjunctival hyperemia / Early / Incidence not known
    cataracts / Delayed / Incidence not known
    ocular inflammation / Early / Incidence not known
    exophthalmos / Delayed / Incidence not known
    conjunctivitis / Delayed / Incidence not known
    elevated hepatic enzymes / Delayed / Incidence not known
    hepatomegaly / Delayed / Incidence not known
    phlebitis / Rapid / Incidence not known
    hypercholesterolemia / Delayed / Incidence not known
    palpitations / Early / Incidence not known
    sinus tachycardia / Rapid / Incidence not known
    angina / Early / Incidence not known

    Mild

    xerophthalmia / Early / 5.0-5.0
    headache / Early / 0-4.0
    ptosis / Delayed / 2.0-2.0
    dizziness / Early / Incidence not known
    fever / Early / Incidence not known
    lethargy / Early / Incidence not known
    amenorrhea / Delayed / Incidence not known
    menstrual irregularity / Delayed / Incidence not known
    dysmenorrhea / Delayed / Incidence not known
    arthralgia / Delayed / Incidence not known
    weakness / Early / Incidence not known
    arthropathy / Delayed / Incidence not known
    myalgia / Early / Incidence not known
    abdominal pain / Early / Incidence not known
    weight loss / Delayed / Incidence not known
    weight gain / Delayed / Incidence not known
    diarrhea / Early / Incidence not known
    vomiting / Early / Incidence not known
    hiccups / Early / Incidence not known
    anorexia / Delayed / Incidence not known
    nausea / Early / Incidence not known
    appetite stimulation / Delayed / Incidence not known
    acne vulgaris / Delayed / Incidence not known
    skin hypopigmentation / Delayed / Incidence not known
    xerosis / Delayed / Incidence not known
    rash (unspecified) / Early / Incidence not known
    ecchymosis / Delayed / Incidence not known
    acneiform rash / Delayed / Incidence not known
    alopecia / Delayed / Incidence not known
    injection site reaction / Rapid / Incidence not known
    hirsutism / Delayed / Incidence not known
    petechiae / Delayed / Incidence not known
    urticaria / Rapid / Incidence not known
    telangiectasia / Delayed / Incidence not known
    striae / Delayed / Incidence not known
    diaphoresis / Early / Incidence not known
    purpura / Delayed / Incidence not known
    skin hyperpigmentation / Delayed / Incidence not known
    perineal pain / Early / Incidence not known
    pruritus / Rapid / Incidence not known
    infection / Delayed / Incidence not known
    restlessness / Early / Incidence not known
    insomnia / Early / Incidence not known
    malaise / Early / Incidence not known
    emotional lability / Early / Incidence not known
    irritability / Delayed / Incidence not known
    anxiety / Delayed / Incidence not known
    vertigo / Early / Incidence not known
    paresthesias / Delayed / Incidence not known
    foreign body sensation / Rapid / Incidence not known
    ocular hypotonia / Delayed / Incidence not known
    ocular pain / Early / Incidence not known
    ocular pruritus / Rapid / Incidence not known
    ocular irritation / Rapid / Incidence not known
    syncope / Early / Incidence not known

    DRUG INTERACTIONS

    Abatacept: (Moderate) Concomitant use of immunosuppressives, as well as long-term corticosteroids, may potentially increase the risk of serious infection in abatacept treated patients. Advise patients taking abatacept to seek immediate medical advice if they develop signs and symptoms suggestive of infection.
    Acetaminophen; Aspirin, ASA; Caffeine: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
    Acetaminophen; Butalbital: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Butalbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use.
    Acetaminophen; Butalbital; Caffeine: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Butalbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use.
    Acetaminophen; Butalbital; Caffeine; Codeine: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Butalbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use.
    Acetaminophen; Caffeine; Magnesium Salicylate; Phenyltoloxamine: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
    Acetaminophen; Caffeine; Phenyltoloxamine; Salicylamide: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
    Acetaminophen; Chlorpheniramine; Dextromethorphan; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Acetaminophen; Chlorpheniramine; Phenylephrine; Phenyltoloxamine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Acetaminophen; Dextromethorphan; Guaifenesin; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Acetaminophen; Dextromethorphan; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Acetaminophen; Guaifenesin; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Acetaminophen; Hydrocodone: (Moderate) Hydrocodone is metabolized by CYP3A4. Dexamethasone, an inducer of CYP3A4, may cause increased clearance of hydrocodone, which could result in lack of efficacy or the development of an abstinence syndrome in a patient who had developed physical dependence to hydrocodone. Monitor the patient for reduced efficacy of hydrocodone. A higher hydrocodone dose may be needed if used with dexamethasone.
    Acetazolamide: (Moderate) Corticosteroids may increase the risk of hypokalemia if used concurrently with acetazolamide. Hypokalemia may be especially severe with prolonged use of corticotropin, ACTH. Monitor serum potassium levels to determine the need for potassium supplementation and/or alteration in drug therapy.
    Acetohexamide: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Adalimumab: (Moderate) Closely monitor for the development of signs and symptoms of infection if coadministration of a corticosteroid with adalimumab is necessary. Adalimumab treatment increases the risk for serious infections that may lead to hospitalization or death. Patients taking concomitant immunosuppressants including corticosteroids may be at greater risk of infection.
    Albendazole: (Minor) Concomitant administration of albendazole with dexamethasone increases the plasma concentration of albendazole sulfoxide, presumably via reduction in albendazole sulfoxide clearance.
    Albiglutide: (Moderate) When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia and cause blood glucose concentrations to rise. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Aldesleukin, IL-2: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Alefacept: (Severe) Patients receiving other immunosuppressives should not receive concurrent therapy with alefacept; there is the possibility of excessive immunosuppression and subsequent risks of infection and other serious side effects.
    Alemtuzumab: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Aliskiren; Amlodipine: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased.
    Aliskiren; Amlodipine; Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased.
    Aliskiren; Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Alogliptin: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Alogliptin; Metformin: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. In addition, blood lactate concentrations and the lactate to pyruvate ratio increase when metformin is coadministered with corticosteroids (e.g., hydrocortisone). Elevated lactic acid concentrations are associated with increased morbidity rates. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted. (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Alogliptin; Pioglitazone: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Alosetron: (Minor) Dexamethasone can induce the activity of CYP3A4 and increase the metabolism of alosetron by increasing the metabolism of the drug, thus potentially reducing the effect of alosetron.
    Alpha-glucosidase Inhibitors: (Moderate) Systemic corticosteroids increase blood glucose levels. Because of this action, a potential pharmacodynamic interaction exists between corticosteroids and acarbose. Patients who are administered systemic corticosteroid therapy may require an adjustment in the dosing of acarbose.
    Altretamine: (Minor) Concurrent use of altretamine with other agents which cause bone marrow or immune suppression such as corticosteroids may result in additive effects.
    Ambenonium Chloride: (Minor) Corticosteroids may interact with cholinesterase inhibitors including ambenonium, neostigmine, and pyridostigmine, occasionally causing severe muscle weakness in patients with myasthenia gravis. Glucocorticoids are occasionally used therapeutically, however, in the treatment of some patients with myasthenia gravis. In such patients, it is recommended that corticosteroid therapy be initiated at low dosages and with close clinical monitoring. The dosage should be increased gradually as tolerated, with continued careful monitoring of the patient's clinical status.
    Amiloride; Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Aminosalicylate sodium, Aminosalicylic acid: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
    Amiodarone: (Major) Use caution when coadministering amiodarone with drugs which may induce hypokalemia and, or hypomagnesemia, including corticosteroids. Since antiarrhythmic drugs may be ineffective or may be arrhythmogenic in patients with hypokalemia, any potassium or magnesium deficiency should be corrected before instituting and during amiodarone therapy.
    Amlodipine: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased.
    Amlodipine; Atorvastatin: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased.
    Amlodipine; Benazepril: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased.
    Amlodipine; Hydrochlorothiazide, HCTZ; Olmesartan: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased.
    Amlodipine; Hydrochlorothiazide, HCTZ; Valsartan: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased.
    Amlodipine; Olmesartan: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased.
    Amlodipine; Telmisartan: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased.
    Amlodipine; Valsartan: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased.
    Amoxicillin; Clarithromycin; Lansoprazole: (Major) Coadministration of dexamethasone and clarithromycin may decrease clarithromycin serum concentrations due to CYP3A4 enzyme induction. While the 14-OH-clarithromycin active metabolite concentrations are increased, this metabolite has different antimicrobial activity compared to clarithromycin. The intended therapeutic effect of clarithromycin could be decreased. It is not clear if clarithromycin activity against other organisms would be reduced, but reduced efficacy is possible. Alternatives to clarithromycin should be considered in patients who are taking CYP3A4 inducers. Additionally, clarithromycin inhibits CYP3A4 and has the potential to result in increased plasma concentrations of dexamethasone. Increased blood concentrations and physiologic activity may necessitate a decrease in corticosteroid dosage. (Minor) Monitor for decreased efficacy of lansoprazole if coadministration with dexamethasone is necessary. Lansoprazole is metabolized by CYP2C19 and CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. Drugs known to induce CYP3A4 may lead to decreased lansoprazole plasma concentrations.
    Amoxicillin; Clarithromycin; Omeprazole: (Major) Coadministration of dexamethasone and clarithromycin may decrease clarithromycin serum concentrations due to CYP3A4 enzyme induction. While the 14-OH-clarithromycin active metabolite concentrations are increased, this metabolite has different antimicrobial activity compared to clarithromycin. The intended therapeutic effect of clarithromycin could be decreased. It is not clear if clarithromycin activity against other organisms would be reduced, but reduced efficacy is possible. Alternatives to clarithromycin should be considered in patients who are taking CYP3A4 inducers. Additionally, clarithromycin inhibits CYP3A4 and has the potential to result in increased plasma concentrations of dexamethasone. Increased blood concentrations and physiologic activity may necessitate a decrease in corticosteroid dosage. (Moderate) Monitor for decreased efficacy of omeprazole if coadministration with dexamethasone is necessary. Omeprazole is metabolized by CYP2C19 and CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. The manufacturer of omeprazole recommends avoidance with strong inducers because decreased exposure of omeprazole can occur. Recommendations are not available for concomitant use with moderate inducers of CYP3A4.
    Amphotericin B cholesteryl sulfate complex (ABCD): (Moderate) The potassium-wasting effects of corticosteroid therapy can be exacerbated by concomitant administration of other potassium-depleting drugs including amphotericin B. Serum potassium levels should be monitored in patients receiving these drugs concomitantly.
    Amphotericin B lipid complex (ABLC): (Moderate) The potassium-wasting effects of corticosteroid therapy can be exacerbated by concomitant administration of other potassium-depleting drugs including amphotericin B. Serum potassium levels should be monitored in patients receiving these drugs concomitantly.
    Amphotericin B liposomal (LAmB): (Moderate) The potassium-wasting effects of corticosteroid therapy can be exacerbated by concomitant administration of other potassium-depleting drugs including amphotericin B. Serum potassium levels should be monitored in patients receiving these drugs concomitantly.
    Amphotericin B: (Moderate) The potassium-wasting effects of corticosteroid therapy can be exacerbated by concomitant administration of other potassium-depleting drugs including amphotericin B. Serum potassium levels should be monitored in patients receiving these drugs concomitantly.
    Amprenavir: (Moderate) Exercise caution when administering dexamethasone and amprenavir concurrently. Dexamethasone decreases amprenavir serum concentrations. Amprenavir may be less effective in patients taking these agents together.
    Anthracyclines: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. Also, dexamethasone is a CYP3A4 inducer and doxorubicin is a major substrate of CYP3A4. However, these drugs are commonly used together in treatment
    Antithymocyte Globulin: (Moderate) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Antitumor antibiotics: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Aprepitant, Fosaprepitant: (Minor) Aprepitant, fosaprepitant is indicated for the treatment of chemotherapy-induced nausea/vomiting (CINV) in combination with dexamethasone and a 5HT3 antagonist; the pharmacokinetic interactions discussed here are accounted for in the recommended dosing for this indication. No dosage adjustment is needed when dexamethasone is used in combination with a single 40-mg dose of oral aprepitant. Dexamethasone is a CYP3A4 substrate. Aprepitant, when administered as a 3-day oral regimen (125 mg/80 mg/80 mg), is a moderate CYP3A4 inhibitor and inducer. The AUC of dexamethasone (8 mg PO on days 1, 2, and 3) was increased by approximately 2-fold on days 1 and 2 when given with a single 150-mg dose of IV fosaprepitant. After a 5-day regimen of oral aprepitant (125 mg/80 mg/80 mg/80 mg/80 mg), the AUC of dexamethasone increased 2.2-fold on days 1 and 5. A single dose of aprepitant 40 mg increased the AUC of dexamethasone by 1.45-fold, which was not considered clinically significant.
    Argatroban: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together.
    Aripiprazole: (Moderate) Because aripiprazole is metabolized by CYP3A4, concurrent use of CYP3A4 inducers such as dexamethasone may result in decreased plasma concentrations of aripiprazole. If these agents are used in combination, the patient should be carefully monitored for a decrease in aripiprazole efficacy. An increase in aripiprazole dosage may be clinically warranted in some patients. Avoid concurrent use of Abilify Maintena with a CYP3A4 inducer when the combined treatment period exceeds 14 days because aripiprazole blood concentrations decline and may become suboptimal.
    Armodafinil: (Minor) Armodafinil is partially metabolized via CYP3A4/5 isoenzymes. CYP3A4 inducers, such as dexamethasone, may potentially increase the metabolism of armodafinil. Decreased serum levels of armodafinil could potentially result in decreased efficacy of the drug.
    Arsenic Trioxide: (Major) Because electrolyte abnormalities increase the risk of QT interval prolongation and serious arrhythmias, avoid the concomitant use of arsenic trioxide with drugs that may cause electrolyte abnormalities, particularly hypokalemia and hypomagnesemia. Examples of drugs that may cause electrolyte abnormalities include corticosteroids. If concomitant drug use is unavoidable, frequently monitor serum electrolytes (and replace as necessary) and electrocardiograms.
    Artemether; Lumefantrine: (Major) Dexamethasone is a substrate/inducer and both components of artemether; lumefantrine are substrates of the CYP3A4 isoenzyme; therefore, coadministration may lead to decreased artemether; lumefantrine concentrations. Concomitant use warrants caution due to a possible reduction in antimalarial activity.
    Asparaginase Erwinia chrysanthemi: (Moderate) Concomitant use of L-asparaginase with corticosteroids can result in additive hyperglycemia. L-Asparaginase transiently inhibits insulin production contributing to hyperglycemia seen during concurrent corticosteroid therapy. Insulin therapy may be required in some cases. Administration of L-asparaginase after rather than before corticosteroids reportedly has produced fewer hypersensitivity reactions.
    Aspirin, ASA: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
    Aspirin, ASA; Butalbital; Caffeine: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Butalbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use. (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
    Aspirin, ASA; Butalbital; Caffeine; Codeine: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Butalbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use. (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
    Aspirin, ASA; Caffeine; Dihydrocodeine: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
    Aspirin, ASA; Carisoprodol: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
    Aspirin, ASA; Carisoprodol; Codeine: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
    Aspirin, ASA; Dipyridamole: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
    Aspirin, ASA; Omeprazole: (Moderate) Monitor for decreased efficacy of omeprazole if coadministration with dexamethasone is necessary. Omeprazole is metabolized by CYP2C19 and CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. The manufacturer of omeprazole recommends avoidance with strong inducers because decreased exposure of omeprazole can occur. Recommendations are not available for concomitant use with moderate inducers of CYP3A4. (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
    Aspirin, ASA; Oxycodone: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
    Aspirin, ASA; Pravastatin: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
    Atazanavir: (Major) Avoid concurrent use of dexamethasone with atazanavir. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance to atazanavir; consider use of an alternative corticosteroid. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; atazanavir is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone) whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use.
    Atazanavir; Cobicistat: (Major) Avoid concurrent use of dexamethasone with atazanavir. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance to atazanavir; consider use of an alternative corticosteroid. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; atazanavir is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone) whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. (Major) Avoid concurrent use of dexamethasone with cobicistat containing regimens. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; cobicistat is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use.
    Atenolol; Chlorthalidone: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Atracurium: (Moderate) Caution and close monitoring are advised if corticosteroids and neuromuscular blockers are used together, particularly for long periods, due to enhanced neuromuscular blocking effects. In such patients, a peripheral nerve stimulator may be of value in monitoring the response. Concurrent use may increase the risk of acute myopathy. This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis. Elevation of creatine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years.
    Atropine; Benzoic Acid; Hyoscyamine; Methenamine; Methylene Blue; Phenyl Salicylate: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
    Atropine; Hyoscyamine; Phenobarbital; Scopolamine: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Phenobarbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use.
    Avanafil: (Minor) Avanafil is primarily metabolized by CYP3A4, and although no studies have been performed, concomitant administration of CYP3A4 inducers, such as dexamethasone, may decrease avanafil plasma levels. Concomitant use is not recommended.
    Axitinib: (Major) Avoid coadministration of axitinib with dexamethasone, due to the risk of decreased efficacy of axitinib. Selection of a concomitant medication with no or minimal CYP3A4 induction potential is recommended. Axitinib is a CYP3A4 substrate and dexamethasone is a strong CYP3A4 inducer. Coadministration with another strong CYP3A4/5 inducer, rifampin, significantly decreased the plasma exposure of axitinib in healthy volunteers.
    Azacitidine: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Azathioprine: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Azilsartan; Chlorthalidone: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Azithromycin: (Moderate) Dexamethasone is a substrate of P-glycoprotein (PGP) and azithromycin is a PGP inhibitor; therefore, dexamethasone concentrations could be increased with coadministration. Monitor patients for increased side effects if these drugs are given together.
    Bacillus Calmette-Guerin Vaccine, BCG: (Severe) Live virus vaccines should generally not be administered to an immunosuppressed patient. Live virus vaccines may induce the illness they are intended to prevent and are generally contraindicated for use during immunosuppressive treatment. The immune response of the immunocompromised patient to vaccines may be decreased, even despite alternate vaccination schedules or more frequent booster doses. If immunization is necessary, choose an alternative to live vaccination, or, consider a delay or change in the immunization schedule. Practitioners should refer to the most recent CDC guidelines regarding vaccination of patients who are receiving drugs that adversely affect the immune system. Children who are receiving high doses of systemic corticosteroids (i.e., greater than or equal to 2 mg/kg prednisone orally per day) for 2 weeks or more may be vaccinated after steroid therapy has been discontinued for at least 3 months in accordance with general recommendations for the use of live-virus vaccines. The CDC has stated that discontinuation of steroids for 1 month prior to varicella virus vaccine live administration may be sufficient. Budesonide may affect the immunogenicity of live vaccines. An open-label study examined the immune responsiveness to varicella vaccine in 243 pediatric asthma patients who were treated with budesonide inhalation suspension 0.251 mg daily (n = 151) or non-corticosteroid asthma therapy (n = 92). The percentage of patients developing a seroprotective antibody titer of at least 5 (gpELISA value) in response to the vaccination was slightly lower in patients treated with budesonide compared to patients treated with non-corticosteroid asthma therapy (85% vs. 90%). Even though no patient treated with budesonide inhalation suspension developed chicken pox because of vaccination, live-virus vaccines should not be given to individuals who are considered to be immunocompromised until more information is available.
    Basiliximab: (Minor) Because systemically administered corticosteroids have immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives.
    Bedaquiline: (Major) Avoid concurrent use of dexamethasone with bedaquiline. Dexamethasone is a CYP3A4 inducer, which may result in decreased bedaquiline systemic exposure (AUC) and possibly reduced therapeutic effect.
    Belladonna Alkaloids; Ergotamine; Phenobarbital: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Phenobarbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use.
    Benazepril; Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Bendroflumethiazide; Nadolol: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Benzoic Acid; Hyoscyamine; Methenamine; Methylene Blue; Phenyl Salicylate: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
    Bepridil: (Moderate) Hypokalemia-producing agents, including corticosteroids, may increase the risk of bepridil-induced arrhythmias and should therefore be administered cautiously in patients receiving bepridil therapy.
    Bevacizumab: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Bexarotene: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents, such as bexarotene.
    Bicalutamide: (Major) Bicalutamide is metabolized by cytochrome P450 3A4. Drugs that are potent inducers of CYP3A4 activity, such as dexamethasone, will decrease the plasma concentrations of bicalutamide.It is not known if bicalutamide dosing adjustments are necessary.
    Bismuth Subsalicylate: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
    Bismuth Subsalicylate; Metronidazole; Tetracycline: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
    Bisoprolol; Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Boceprevir: (Moderate) Coadministration of dexamethasone and boceprevir is not recommended. If coadministered, close clinical monitoring for increased dexamethasone-related adverse events and for decreased boceprevir efficacy is advised. If dexamethasone dose adjustments are made, re-adjust the dose upon completion of boceprevir treatment. Predictions about the interaction can be made based on the metabolic pathways of dexamethasone and boceprevir. Dexamethasone is an inducer and substrate of the hepatic isoenzyme CYP3A4; boceprevir is an inhibitor and substrate of this isoenzyme. Additionally, both dexamethasone and boceprevir are substrates for the drug efflux transporter P-glycoprotein (PGP). When used in combination, the plasma concentrations of dexamethasone may be elevated and the plasma concentration of boceprevir may be deceased, resulting in an increased potential for dexamethasone-related adverse events and boceprevir treatment failure.
    Bortezomib: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Bosentan: (Minor) A dose adjustment of systemic dexamethasone may be necessary if bosentan is initiated or withdrawn during therapy. Bosentan may increase the metabolism of dexamethasone resulting in decreased exposure. Bosentan is an inducer of CYP3A4; dexamethasone is a CYP3A4 substrate.
    Brentuximab vedotin: (Moderate) Concomitant administration of brentuximab vedotin and dexamethasone may decrease the exposure of monomethyl auristatin E (MMAE), one of the 3 components released from brentuximab vedotin. MMAE is a CYP3A4 substrate and dexamethasone is a potent CYP3A4 inducer; therefore, the efficacy of brentuximab may be reduced.
    Brexpiprazole: (Moderate) Because brexpiprazole is partially metabolized by CYP3A4, concurrent use of CYP3A4 inducers such as dexamethasone may result in decreased plasma concentrations of brexpiprazole. If these agents are used in combination, the patient should be carefully monitored for a decrease in brexpiprazole efficacy. An increase in brexpiprazole dosage may be clinically warranted in some patients.
    Brigatinib: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration is necessary. Plasma concentrations of dexamethasone may decrease. Dexamethasone is a CYP3A4 substrate; brigatinib may induce CYP3A4.
    Bromocriptine: (Moderate) Caution and close monitoring are advised if bromocriptine and dexamethasone are used together. Concurrent use may decrease the plasma concentrations of bromocriptine resulting in loss of efficacy. Bromocriptine is extensively metabolized by the liver via CYP3A4; dexamethasone is a moderate inducer of CYP3A4.
    Brompheniramine; Carbetapentane; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Brompheniramine; Guaifenesin; Hydrocodone: (Moderate) Hydrocodone is metabolized by CYP3A4. Dexamethasone, an inducer of CYP3A4, may cause increased clearance of hydrocodone, which could result in lack of efficacy or the development of an abstinence syndrome in a patient who had developed physical dependence to hydrocodone. Monitor the patient for reduced efficacy of hydrocodone. A higher hydrocodone dose may be needed if used with dexamethasone.
    Brompheniramine; Hydrocodone; Pseudoephedrine: (Moderate) Hydrocodone is metabolized by CYP3A4. Dexamethasone, an inducer of CYP3A4, may cause increased clearance of hydrocodone, which could result in lack of efficacy or the development of an abstinence syndrome in a patient who had developed physical dependence to hydrocodone. Monitor the patient for reduced efficacy of hydrocodone. A higher hydrocodone dose may be needed if used with dexamethasone.
    Budesonide: (Moderate) Theoretically, induction of the cytochrome P450 (CYP) 3A4 isoenzyme may result in a lowering of budesonide plasma concentrations, reducing the clinical effect. Drugs known to induce the 3A4 isoenzyme include dexamethasone.
    Budesonide; Formoterol: (Moderate) Theoretically, induction of the cytochrome P450 (CYP) 3A4 isoenzyme may result in a lowering of budesonide plasma concentrations, reducing the clinical effect. Drugs known to induce the 3A4 isoenzyme include dexamethasone.
    Bupivacaine; Lidocaine: (Moderate) Concomitant use of systemic lidocaine and dexamethasone may decrease lidocaine plasma concentrations. Higher lidocaine doses may be required; titrate to effect. Lidocaine is a CYP3A4 and CYP1A2 substrate; dexamethasone induces CYP3A4.
    Bupropion: (Major) Bupropion is associated with a dose-related risk of seizures. Extreme caution is recommended during concurrent use of other drugs that may lower the seizure threshold such as systemic corticosteroids. The manufacturer recommends low initial dosing and slow dosage titration if these combinations must be used; the patient should be closely monitored.
    Bupropion; Naltrexone: (Major) Bupropion is associated with a dose-related risk of seizures. Extreme caution is recommended during concurrent use of other drugs that may lower the seizure threshold such as systemic corticosteroids. The manufacturer recommends low initial dosing and slow dosage titration if these combinations must be used; the patient should be closely monitored.
    Buspirone: (Moderate) Potent inducers of hepatic cytochrome P450 3A4, such as dexamethasone, may increase the rate of buspirone metabolism.
    Butabarbital: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Butabarbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use.
    Cabozantinib: (Moderate) Monitor for decreased efficacy of cabozantinib if concomitant use of cabozantinib and dexamethasone is necessary. Cabozantinib is primarily metabolized by CYP3A4 and dexamethasone is a CYP3A4 inducer. Coadministration with a strong CYP3A4 inducer, rifampin (600 mg daily for 31 days), decreased cabozantinib (single dose) exposure by 77%. The manufacturer of cabozantinib recommends a dose increase when used with strong CYP3A4 inducers; however, recommendations are not available for concomitant use with a moderate inducer of CYP3A4. Cabozantinib is also a P-glycoprotein (P-gp) inhibitor and dexamethasone is a substrate of P-gp; plasma concentrations of dexamethasone may be increased. However, the clinical relevance of this finding is unknown.
    Calcium Carbonate: (Moderate) Calcium absorption is reduced when calcium carbonate is taken concomitantly with systemic corticosteroids. Systemic corticosteroids induce a negative calcium balance by inhibiting intestinal calcium absorption as well as by increasing renal calcium losses. The mechanism by which these drugs inhibit calcium absorption in the intestine is likely to involve a direct inhibition of absorptive cell function.
    Calcium Carbonate; Magnesium Hydroxide: (Moderate) Calcium absorption is reduced when calcium carbonate is taken concomitantly with systemic corticosteroids. Systemic corticosteroids induce a negative calcium balance by inhibiting intestinal calcium absorption as well as by increasing renal calcium losses. The mechanism by which these drugs inhibit calcium absorption in the intestine is likely to involve a direct inhibition of absorptive cell function.
    Calcium Carbonate; Risedronate: (Moderate) Calcium absorption is reduced when calcium carbonate is taken concomitantly with systemic corticosteroids. Systemic corticosteroids induce a negative calcium balance by inhibiting intestinal calcium absorption as well as by increasing renal calcium losses. The mechanism by which these drugs inhibit calcium absorption in the intestine is likely to involve a direct inhibition of absorptive cell function.
    Calcium; Vitamin D: (Moderate) Calcium absorption is reduced when calcium carbonate is taken concomitantly with systemic corticosteroids. Systemic corticosteroids induce a negative calcium balance by inhibiting intestinal calcium absorption as well as by increasing renal calcium losses. The mechanism by which these drugs inhibit calcium absorption in the intestine is likely to involve a direct inhibition of absorptive cell function.
    Canagliflozin: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Canagliflozin; Metformin: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. In addition, blood lactate concentrations and the lactate to pyruvate ratio increase when metformin is coadministered with corticosteroids (e.g., hydrocortisone). Elevated lactic acid concentrations are associated with increased morbidity rates. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted. (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Candesartan; Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Capecitabine: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Captopril; Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Carbamazepine: (Moderate) Hepatic microsomal enzyme inducers, including carbamazepine, can increase the metabolism of dexamethasone. Dosage adjustments may be necessary, and closer monitoring of clinical and/or adverse effects is warranted when carbamazepine is used with dexamethasone.
    Carbetapentane; Chlorpheniramine; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Carbetapentane; Diphenhydramine; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Carbetapentane; Guaifenesin; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Carbetapentane; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Carbetapentane; Phenylephrine; Pyrilamine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Carbinoxamine; Hydrocodone; Phenylephrine: (Moderate) Hydrocodone is metabolized by CYP3A4. Dexamethasone, an inducer of CYP3A4, may cause increased clearance of hydrocodone, which could result in lack of efficacy or the development of an abstinence syndrome in a patient who had developed physical dependence to hydrocodone. Monitor the patient for reduced efficacy of hydrocodone. A higher hydrocodone dose may be needed if used with dexamethasone. (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Carbinoxamine; Hydrocodone; Pseudoephedrine: (Moderate) Hydrocodone is metabolized by CYP3A4. Dexamethasone, an inducer of CYP3A4, may cause increased clearance of hydrocodone, which could result in lack of efficacy or the development of an abstinence syndrome in a patient who had developed physical dependence to hydrocodone. Monitor the patient for reduced efficacy of hydrocodone. A higher hydrocodone dose may be needed if used with dexamethasone.
    Carbinoxamine; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Cariprazine: (Major) Cariprazine and its active metabolites are extensively metabolized by CYP3A4. Concurrent use of cariprazine with CYP3A4 inducers, such as dexamethasone, has not been evaluated and is not recommended because the net effect on active drug and metabolites is unclear.
    Carmustine, BCNU: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Carvedilol: (Minor) Increased concentrations of dexamethasone may occur if it is coadministered with carvedilol; exercise caution. Carvedilol is a P-glycoprotein (P-gp) inhibitor and dexamethasone is a P-gp substrate.
    Caspofungin: (Major) Data suggest that coadministration of inducers or mixed inducers/inhibitors of hepatic drug clearance along with caspofungin may result in reduced caspofungin blood concentrations. The reductions may be clinically significant. It is not known how caspofungin drug clearance is induced. Drugs that may lead to reductions in caspofungin concentrations include dexamethasone. For adult patients receiving dexamethasone, an increase in the caspofungin dose to 70 mg/day should be considered. For pediatric patients receiving dexamethasone, a daily dosage of 70 mg/m2, not to exceed 70 mg, should be considered.
    Ceritinib: (Moderate) Monitor for steroid-related adverse reactions if coadministration of ceritinib with dexamethasone is necessary, due to increased dexamethasone exposure. Ceritinib is a CYP3A4 inhibitor and dexamethasone is primarily metabolized by CYP3A4. A strong CYP3A4 inhibitor has been reported to decrease the metabolism of certain corticosteroids by up to 60%, leading to increased risk of corticosteroid side effects. The degree of inhibition of CYP3A4 by ceritinib is unknown.
    Certolizumab pegol: (Moderate) The safety and efficacy of certolizumab in patients with immunosuppression have not been evaluated. Patients receiving immunosuppressives along with certolizumab may be at a greater risk of developing an infection. Many of the serious infections occurred in patients on immunosuppressive therapy who received certolizumab.
    Chlophedianol; Guaifenesin; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Chlorambucil: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Chlorothiazide: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Chlorpheniramine; Dextromethorphan; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Chlorpheniramine; Dihydrocodeine; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Chlorpheniramine; Guaifenesin; Hydrocodone; Pseudoephedrine: (Moderate) Hydrocodone is metabolized by CYP3A4. Dexamethasone, an inducer of CYP3A4, may cause increased clearance of hydrocodone, which could result in lack of efficacy or the development of an abstinence syndrome in a patient who had developed physical dependence to hydrocodone. Monitor the patient for reduced efficacy of hydrocodone. A higher hydrocodone dose may be needed if used with dexamethasone.
    Chlorpheniramine; Hydrocodone: (Moderate) Hydrocodone is metabolized by CYP3A4. Dexamethasone, an inducer of CYP3A4, may cause increased clearance of hydrocodone, which could result in lack of efficacy or the development of an abstinence syndrome in a patient who had developed physical dependence to hydrocodone. Monitor the patient for reduced efficacy of hydrocodone. A higher hydrocodone dose may be needed if used with dexamethasone.
    Chlorpheniramine; Hydrocodone; Phenylephrine: (Moderate) Hydrocodone is metabolized by CYP3A4. Dexamethasone, an inducer of CYP3A4, may cause increased clearance of hydrocodone, which could result in lack of efficacy or the development of an abstinence syndrome in a patient who had developed physical dependence to hydrocodone. Monitor the patient for reduced efficacy of hydrocodone. A higher hydrocodone dose may be needed if used with dexamethasone. (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Chlorpheniramine; Hydrocodone; Pseudoephedrine: (Moderate) Hydrocodone is metabolized by CYP3A4. Dexamethasone, an inducer of CYP3A4, may cause increased clearance of hydrocodone, which could result in lack of efficacy or the development of an abstinence syndrome in a patient who had developed physical dependence to hydrocodone. Monitor the patient for reduced efficacy of hydrocodone. A higher hydrocodone dose may be needed if used with dexamethasone.
    Chlorpheniramine; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Chlorpropamide: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Chlorthalidone: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Chlorthalidone; Clonidine: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Cholestyramine: (Moderate) Cholestyramine may increase the clearance of corticosteroids.
    Choline Salicylate; Magnesium Salicylate: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
    Cimetidine: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together.
    Cisapride: (Moderate) Cisapride is metabolized by the hepatic cytochrome P450 enzyme system, specifically the CYP3A4 isoenzyme. Inducers of CYP3A4, such as dexamethasone, may increase the clearance of cisapride.
    Cisatracurium: (Moderate) Caution and close monitoring are advised if corticosteroids and neuromuscular blockers are used together, particularly for long periods, due to enhanced neuromuscular blocking effects. In such patients, a peripheral nerve stimulator may be of value in monitoring the response. Concurrent use may increase the risk of acute myopathy. This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis. Elevation of creatine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years.
    Citalopram: (Major) Citalopram causes dose-dependent QT interval prolongation. Concurrent use of citalopram and medications known to cause electrolyte imbalance may increase the risk of developing QT prolongation. Therefore, caution is advisable during concurrent use of citalopram and corticosteroids. It should be noted that CYP3A4 is one of the isoenzymes involved in the metabolism of citalopram, and dexamethasone is an inducer of this isoenzyme. In theory, decreased efficacy of citalopram is possible during combined use with dexamethasone; however, because citalopram is metabolized by multiple enzyme systems, induction of one pathway may not appreciably increase citalopram clearance.
    Clarithromycin: (Major) Coadministration of dexamethasone and clarithromycin may decrease clarithromycin serum concentrations due to CYP3A4 enzyme induction. While the 14-OH-clarithromycin active metabolite concentrations are increased, this metabolite has different antimicrobial activity compared to clarithromycin. The intended therapeutic effect of clarithromycin could be decreased. It is not clear if clarithromycin activity against other organisms would be reduced, but reduced efficacy is possible. Alternatives to clarithromycin should be considered in patients who are taking CYP3A4 inducers. Additionally, clarithromycin inhibits CYP3A4 and has the potential to result in increased plasma concentrations of dexamethasone. Increased blood concentrations and physiologic activity may necessitate a decrease in corticosteroid dosage.
    Clindamycin: (Moderate) Concomitant use of clindamycin and dexamethasone may increase clindamycin clearance and result in loss of efficacy of clindamycin. Clindamycin is a CYP3A4 substrate; dexamethasone is a moderate inducer of CYP3A4. Caution and close monitoring are advised if these drugs are used together. (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together.
    Clofarabine: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Clozapine: (Moderate) Caution is advisable during concurrent use of dexamethasone and clozapine. Dexamethasone is an inducer of CYP3A4, one of the isoenzymes responsible for the metabolism of clozapine. According to the manufacturer, patients receiving clozapine in combination with a weak to moderate CYP3A4 inducer should be monitored for loss of effectiveness. Consideration should be given to increasing the clozapine dose if necessary. Concurrent use with strong CYP3A4 inducers is not recommended. Topical corticosteroids are not likely to interact.
    Cobicistat: (Major) Avoid concurrent use of dexamethasone with cobicistat containing regimens. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; cobicistat is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use.
    Cobicistat; Elvitegravir; Emtricitabine; Tenofovir Alafenamide: (Major) Avoid concurrent use of dexamethasone with cobicistat containing regimens. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; cobicistat is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. (Major) Avoid concurrent use of dexamethasone with elvitegravir. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance to elvitegravir; consider use of an alternative corticosteroid, such as beclomethasone and prednisolone. Dexamethasone induces CYP3A4, and elvitegravir is a substrate of this enzyme.
    Cobicistat; Elvitegravir; Emtricitabine; Tenofovir Disoproxil Fumarate: (Major) Avoid concurrent use of dexamethasone with cobicistat containing regimens. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; cobicistat is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. (Major) Avoid concurrent use of dexamethasone with elvitegravir. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance to elvitegravir; consider use of an alternative corticosteroid, such as beclomethasone and prednisolone. Dexamethasone induces CYP3A4, and elvitegravir is a substrate of this enzyme.
    Cobimetinib: (Major) Avoid the concurrent use of cobimetinib with dexamethasone due to decreased cobimetinib efficacy. Cobimetinib is a CYP3A substrate in vitro, and dexamethasone is a moderate inducer of CYP3A. Based on simulations, cobimetinib exposure would decrease by 73% when coadministered with a moderate CYP3A inducer.
    Cod Liver Oil: (Minor) A relationship of functional antagonism exists between vitamin D analogs, which promote calcium absorption, and corticosteroids, which inhibit calcium absorption. Therapeutic effect of cod liver oil should be monitored when used concomitantly with corticosteroids.
    Codeine; Phenylephrine; Promethazine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Conivaptan: (Major) Coadministration of conivaptan, a CYP3A4/P-glycoprotein (P-gp) inhibitor and CYP3A4 substrate, and dexamethasone, a CYP3A4/P-gp substrate and CYP3A4 inducer, may result in elevated dexamethasone concentrations and decreased conivaptan concentrations. According to the manufacturer of conivaptan, concomitant use of conivaptan and CYP3A substrates should be avoided. Treatment with dexamethasone may be initiated no sooner than 1 week after completion of conivaptan therapy. In addition, conivaptan has been associated with hypokalemia (9.8%). Although not studied, consider the potential for additive hypokalemic effects if conivaptan is coadministered with drugs known to induce hypokalemia, such as corticosteroids.
    Corticorelin, Ovine: (Major) Patients pretreated with dexamethasone have demonstrated an inhibited or blunted response to corticotropin, ovine. Patients receiving corticotropin, ovine should not be pretreated with dexamethasone; no specific guidelines are available.
    Crizotinib: (Moderate) Monitor for steroid-related adverse reactions if coadministration of crizotinib with dexamethasone is necessary due to increased dexamethasone exposure. Dexamethasone is a CYP3A4 substrate and crizotinib is a moderate CYP3A4 inhibitor. A strong CYP3A4 inhibitor has been reported to decrease the metabolism of certain corticosteroids by up to 60%, increasing the risk of corticosteroid-related side effects.
    Cytarabine, ARA-C: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Dabrafenib: (Major) Use dabrafenib and dexamethasone together with caution; concentrations of either agent may be decreased. Use an alternate agent in place of dexamethasone if possible. If concomitant use cannot be avoided, monitor patients for loss of dexamethasone efficacy. Dexamethasone and dabrafenib are both CYP3A4 substrates and moderate CYP3A4 inducers.
    Daclatasvir: (Major) The dose of daclatasvir, a CYP3A4 substrate, must be increased to 90 mg PO once daily when administered in combination with moderate CYP3A4 inducers, such as dexamethasone. Taking these drugs together may decrease daclatasvir serum concentrations, potentially resulting in reduced antiviral efficacy and antimicrobial resistance. Conversely, the therapeutic effects of dexamethasone, a P-glycoprotein (P-gp) substrate, may be increased by daclatasvir, a P-gp inhibitor.
    Dapagliflozin: (Moderate) Systemic corticosteroids increase blood glucose levels; a potential pharmacodynamic interaction exists between corticosteroids and all antidiabetic agents. Diabetic patients who are administered systemic corticosteroid therapy may require an adjustment in the dosing of the antidiabetic agent. Blood lactate concentrations and the lactate to pyruvate ratio increased when metformin was coadministered with corticosteroids (e.g., hydrocortisone). Elevated lactic acid concentrations are associated with an increased risk of lactic acidosis, so patients on metformin concurrently with systemic steroids should be monitored closely.
    Dapagliflozin; Metformin: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. In addition, blood lactate concentrations and the lactate to pyruvate ratio increase when metformin is coadministered with corticosteroids (e.g., hydrocortisone). Elevated lactic acid concentrations are associated with increased morbidity rates. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted. (Moderate) Systemic corticosteroids increase blood glucose levels; a potential pharmacodynamic interaction exists between corticosteroids and all antidiabetic agents. Diabetic patients who are administered systemic corticosteroid therapy may require an adjustment in the dosing of the antidiabetic agent. Blood lactate concentrations and the lactate to pyruvate ratio increased when metformin was coadministered with corticosteroids (e.g., hydrocortisone). Elevated lactic acid concentrations are associated with an increased risk of lactic acidosis, so patients on metformin concurrently with systemic steroids should be monitored closely.
    Dapagliflozin; Saxagliptin: (Moderate) Systemic corticosteroids increase blood glucose levels. Diabetic patients who are administered systemic corticosteroid therapy may require an adjustment in the dosing of the antidiabetic agent. (Moderate) Systemic corticosteroids increase blood glucose levels; a potential pharmacodynamic interaction exists between corticosteroids and all antidiabetic agents. Diabetic patients who are administered systemic corticosteroid therapy may require an adjustment in the dosing of the antidiabetic agent. Blood lactate concentrations and the lactate to pyruvate ratio increased when metformin was coadministered with corticosteroids (e.g., hydrocortisone). Elevated lactic acid concentrations are associated with an increased risk of lactic acidosis, so patients on metformin concurrently with systemic steroids should be monitored closely.
    Dapsone: (Moderate) The metabolism of dapsone may be accelerated when administered concurrently with dexamethasone, a known inducer of CYP3A4. Coadministration is expected to decrease the plasma concentration of dapsone and increase the formation of dapsone hydroxylamine (a metabolite associated with hemolysis). If these drugs must be administered together, closely monitor for a reduction in dapsone efficacy and signs of hemolytic anemia.
    Darunavir: (Major) Avoid concurrent use of darunavir with dexamethasone. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance to darunavir; consider use of an alternative corticosteroid. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; darunavir is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use.
    Darunavir; Cobicistat: (Major) Avoid concurrent use of darunavir with dexamethasone. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance to darunavir; consider use of an alternative corticosteroid. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; darunavir is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. (Major) Avoid concurrent use of dexamethasone with cobicistat containing regimens. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; cobicistat is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use.
    Dasabuvir; Ombitasvir; Paritaprevir; Ritonavir: (Severe) Concurrent administration of dexamethasone with dasabuvir; ombitasvir; paritaprevir; ritonavir is contraindicated. Taking these drugs together could result in elevated dexamethasone plasma concentrations and decreased concentrations of dasabuvir, paritaprevir, and ritonavir. Antiviral efficacy could be affected. Dexamethasone is a P-glycoprotein (P-gp) substrate and a CYP3A4 substrate/inducer. Ritonavir is a P-gp inhibitor and a CYP3A4 substrate/potent inhibitor. Both paritaprevir and dasabuvir (minor) are CYP3A4 substrates. (Severe) Concurrent administration of dexamethasone with dasabuvir; ombitasvir; paritaprevir; ritonavir or ombitasvir; paritaprevir; ritonavir is contraindicated. Taking these drugs together could result in elevated dexamethasone plasma concentrations and decreased concentrations of dasabuvir, paritaprevir, and ritonavir. Antiviral efficacy could be affected. Dexamethasone is a P-glycoprotein (P-gp) substrate and a CYP3A4 substrate/inducer. Ritonavir is a P-gp inhibitor and a CYP3A4 substrate/potent inhibitor. Both paritaprevir and dasabuvir (minor) are CYP3A4 substrates. (Moderate) Close monitoring of therapeutic and adverse effects is required when dexamethasone is coadministered with ritonavir. Ritonavir inhibits CYP3A4 and dexamethasone is a CYP3A4 substrate.
    Decitabine: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Deferasirox: (Moderate) Because gastric ulceration and GI bleeding have been reported in patients taking deferasirox, use caution when coadministering with other drugs known to increase the risk of peptic ulcers or gastric hemorrhage including corticosteroids.
    Deflazacort: (Major) Avoid concomitant use of deflazacort and dexamethasone. Concurrent use may significantly decrease concentrations of 21-desDFZ, the active metabolite of deflazacort, resulting in loss of efficacy. Deflazacort is a CYP3A4 substrate; dexamethasone is a moderate inducer of CYP3A4. Administration of deflazacort with multiple doses of rifampin (a strong CYP3A4 inducer) resulted in geometric mean exposures that were approximately 95% lower compared to administration alone.
    Delavirdine: (Minor) Since dexamethasone may induce metabolism of delavirdine, concomitant use of these agents should be done with caution. Delavirdine therapy may be less effective due to decreased plasma levels in patients taking these drugs concomitantly.
    Denileukin Diftitox: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Denosumab: (Moderate) The safety and efficacy of denosumab use in patients with immunosuppression have not been evaluated. Patients receiving immunosuppressives along with denosumab may be at a greater risk of developing an infection.
    Desmopressin: (Major) Desmopressin, when used in the treatment of nocturia is contraindicated with corticosteroids because of the risk of severe hyponatremia. Desmopressin can be started or resumed 3 days or 5 half-lives after the corticosteroid is discontinued, whichever is longer.
    Dexlansoprazole: (Moderate) Monitor for decreased efficacy of dexlansoprazole if coadministration of dexamethasone is necessary. Dexlansoprazole is metabolized by CYP2C19 and CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. The manufacturer of dexlansoprazole recommends avoidance with strong inducers because decreased exposure of dexlansoprazole can occur. Recommendations are not available for concomitant use with moderate inducers of CYP3A4.
    Dextran: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together.
    Dextromethorphan; Diphenhydramine; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Dextromethorphan; Guaifenesin; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Dextromethorphan; Quinidine: (Moderate) Quinidine is a substrate of the CYP3A4 isoenzyme. Inducers of CYP3A4 such as dexamethasone may increase hepatic elimination of quinidine with the potential for reduced efficacy of quinidine.
    Digoxin: (Moderate) Hypokalemia, hypomagnesemia, or hypercalcemia increase digoxin's effect. Corticosteroids can precipitate digoxin toxicity via their effect on electrolyte balance. It is recommended that serum potassium, magnesium, and calcium be monitored regularly in patients receiving digoxin.
    Diphenhydramine; Hydrocodone; Phenylephrine: (Moderate) Hydrocodone is metabolized by CYP3A4. Dexamethasone, an inducer of CYP3A4, may cause increased clearance of hydrocodone, which could result in lack of efficacy or the development of an abstinence syndrome in a patient who had developed physical dependence to hydrocodone. Monitor the patient for reduced efficacy of hydrocodone. A higher hydrocodone dose may be needed if used with dexamethasone. (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Diphenhydramine; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Dofetilide: (Major) Corticosteroids can cause increases in blood pressure, sodium and water retention, and hypokalemia, predisposing patients to interactions with certain other medications. Corticosteroid-induced hypokalemia could also enhance the proarrhythmic effects of dofetilide.
    Dolutegravir; Rilpivirine: (Severe) Concurrent use of dexamethasone and rilpivirine is contraindicated. When these drugs are coadministered, there is a potential for treatment failure and/or the development of rilpivirine or NNRTI resistance. Dexamethasone is an inducer of CYP3A4, which is primarily responsible for the metabolism of rilpivirine. Coadministration may result in decreased rilpivirine serum concentrations, which could cause impaired virologic response to rilpivirine.
    Donepezil: (Minor) The elimination of donepezil may be increased by concurrent administration of inducers of the hepatic isoenzymes CYP2D6 and CYP3A4, such as dexamethasone.
    Donepezil; Memantine: (Minor) The elimination of donepezil may be increased by concurrent administration of inducers of the hepatic isoenzymes CYP2D6 and CYP3A4, such as dexamethasone.
    Doxacurium: (Moderate) Caution and close monitoring are advised if corticosteroids and neuromuscular blockers are used together, particularly for long periods, due to enhanced neuromuscular blocking effects. In such patients, a peripheral nerve stimulator may be of value in monitoring the response. Concurrent use may increase the risk of acute myopathy. This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis. Elevation of creatine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years.
    Dronabinol, THC: (Moderate) Use caution if coadministration of dronabinol with dexamethasone is necessary, and monitor for a decrease in the efficacy of dronabinol. Dronabinol is a CYP2C9 and 3A4 substrate; dexamethasone is a moderate inducer of CYP3A4. Concomitant use may result in decreased plasma concentrations of dronabinol.
    Dronedarone: (Major) The concomitant use of dronedarone and CYP3A4 inducers should be avoided. Dronedarone is metabolized by CYP3A and is an inhibitor of CYP3A and P-gp. Dexamethasone induces CYP3A4 and is a substrate for CYP3A4 and P-gp. Coadministration of CYP3A4 inducers, such as dexamethasone, with dronedarone may result in reduced plasma concentration and subsequent reduced effectiveness of dronedarone therapy; the plasma concentrations of dexamethasone may also be increased.
    Droperidol: (Moderate) Caution is advised when using droperidol in combination with corticosteroids which may lead to electrolyte abnormalities, especially hypokalemia or hypomagnesemia, as such abnormalities may increase the risk for QT prolongation or cardiac arrhythmias.
    Dulaglutide: (Moderate) When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia and cause blood glucose concentrations to rise. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Echinacea: (Moderate) Echinacea possesses immunostimulatory activity and may theoretically reduce the response to immunosuppressant drugs like corticosteroids. For some patients who are using corticosteroids for serious illness, such as cancer or organ transplant, this potential interaction may result in the preferable avoidance of Echinacea. Although documentation is lacking, coadministration of echinacea with immunosuppressants is not recommended by some resources.
    Econazole: (Minor) In vitro studies indicate that corticosteroids inhibit the antifungal activity of econazole against C. albicans in a concentration-dependent manner. When the concentration of the corticosteroid was equal to or greater than that of econazole on a weight basis, the antifungal activity of econazole was substantially inhibited. When the corticosteroid concentration was one-tenth that of econazole, no inhibition of antifungal activity was observed.
    Efalizumab: (Major) Patients receiving immunosuppressives should not receive concurrent therapy with efalizumab because of the possibility of increased infections and malignancies.
    Elbasvir; Grazoprevir: (Major) If possible, avoid concurrent administration of elbasvir with dexamethasone. Dexamethasone is a moderate CYP3A inducer, while elbasvir is a substrate of CYP3A. Use of these drugs together is expected to decrease the plasma concentrations of elbasvir, and may result in decreased virologic response. (Major) If possible, avoid concurrent administration of grazoprevir with dexamethasone. Dexamethasone is a moderate CYP3A inducer, while grazoprevir is a substrate of CYP3A. Use of these drugs together is expected to decrease the plasma concentrations of grazoprevir, and may result in decreased virologic response. Conversely, concentrations of dexamethasone (also a CYP3A substrate) may be increased when given with grazoprevir (a weak CYP3A inhibitor).
    Eliglustat: (Moderate) Coadministration of dexamethasone and eliglustat may result in increased plasma concentrations of dexamethasone. Monitor patients closely for corticosteroid-related adverse effects; if appropriate, consider reducing the dexamethasone dosage and titrating to clinical effect. Dexamethasone is a P-glycoprotein (P-gp) substrate; eliglustat is a P-gp inhibitor.
    Elvitegravir: (Major) Avoid concurrent use of dexamethasone with elvitegravir. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance to elvitegravir; consider use of an alternative corticosteroid, such as beclomethasone and prednisolone. Dexamethasone induces CYP3A4, and elvitegravir is a substrate of this enzyme.
    Empagliflozin: (Moderate) Systemic corticosteroids increase blood glucose levels. Because of this action, a potential pharmacodynamic interaction exists between corticosteroids and all antidiabetic agents. Diabetic patients who are administered systemic corticosteroid therapy may require an adjustment in the dosing of the antidiabetic agent.
    Empagliflozin; Linagliptin: (Major) Concomitant use of linagliptin with dexamethasone may result in decreased efficacy of linagliptin. When corticosteroids are administered exogenously, increases in blood glucose concentrations are expected, thereby decreasing the hypoglycemic effect of antidiabetic agents. In addition, linagliptin is a substrate of hepatic isoenzyme CYP3A4 and dexamethasone is a moderate inducer of CYP3A4. Coadministration may result in decreased concentrations of linagliptin and decreased efficacy. Patients receiving antidiabetic agents, such as linagliptin, should be closely monitored for signs indicating loss of diabetic control when dexamethasone is coadministered. (Moderate) Systemic corticosteroids increase blood glucose levels. Because of this action, a potential pharmacodynamic interaction exists between corticosteroids and all antidiabetic agents. Diabetic patients who are administered systemic corticosteroid therapy may require an adjustment in the dosing of the antidiabetic agent.
    Empagliflozin; Metformin: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. In addition, blood lactate concentrations and the lactate to pyruvate ratio increase when metformin is coadministered with corticosteroids (e.g., hydrocortisone). Elevated lactic acid concentrations are associated with increased morbidity rates. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted. (Moderate) Systemic corticosteroids increase blood glucose levels. Because of this action, a potential pharmacodynamic interaction exists between corticosteroids and all antidiabetic agents. Diabetic patients who are administered systemic corticosteroid therapy may require an adjustment in the dosing of the antidiabetic agent.
    Emtricitabine; Rilpivirine; Tenofovir alafenamide: (Severe) Concurrent use of dexamethasone and rilpivirine is contraindicated. When these drugs are coadministered, there is a potential for treatment failure and/or the development of rilpivirine or NNRTI resistance. Dexamethasone is an inducer of CYP3A4, which is primarily responsible for the metabolism of rilpivirine. Coadministration may result in decreased rilpivirine serum concentrations, which could cause impaired virologic response to rilpivirine.
    Emtricitabine; Rilpivirine; Tenofovir disoproxil fumarate: (Severe) Concurrent use of dexamethasone and rilpivirine is contraindicated. When these drugs are coadministered, there is a potential for treatment failure and/or the development of rilpivirine or NNRTI resistance. Dexamethasone is an inducer of CYP3A4, which is primarily responsible for the metabolism of rilpivirine. Coadministration may result in decreased rilpivirine serum concentrations, which could cause impaired virologic response to rilpivirine.
    Enalapril; Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Enzalutamide: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with enzalutamide is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A4 substrate and enzalutamide is a strong CYP3A4 inducer.
    Ephedrine: (Moderate) Ephedrine may enhance the metabolic clearance of corticosteroids. Decreased blood concentrations and lessened physiologic activity may necessitate an increase in corticosteroid dosage.
    Eprosartan; Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Erlotinib: (Major) Avoid the coadministration of erlotinib with dexamethasone if possible due to the risk of decreased erlotinib efficacy; if concomitant use is unavoidable, increase the dose of erlotinib by 50 mg increments at 2-week intervals, to a maximum of 450 mg. Erlotinib is primarily metabolized by CYP3A4, and to a lesser extent by CYP1A2. Dexamethasone is a CYP3A4 inducer. The erlotinib AUC was decreased by 58% to 80% when preceded by administration of rifampicin, a strong CYP3A4 inducer, for 7 to 11 days; coadministration with dexamethasone may also decrease erlotinib exposure.
    Erythromycin: (Moderate) Erythromycin inhibits CYP3A4 and has the potential to result in increased plasma concentrations of corticosteroids such as dexamethasone. Also, dexamethasone is a moderate inducer of CYP3A4, and may increase the clearance of erythromycin, resulting in decreased plasma concentration.
    Erythromycin; Sulfisoxazole: (Moderate) Erythromycin inhibits CYP3A4 and has the potential to result in increased plasma concentrations of corticosteroids such as dexamethasone. Also, dexamethasone is a moderate inducer of CYP3A4, and may increase the clearance of erythromycin, resulting in decreased plasma concentration.
    Escitalopram: (Minor) Escitalopram is metabolized by CYP2C19 and CYP3A4. Dexamethasone can induce the metabolism of various CYP 450 isoenzymes, including those involved in escitalopram metabolism. Although no clinical data are available to support a clinically significant interaction, escitalopram may need to be administered in higher doses in patients chronically taking dexamethasone.
    Esomeprazole: (Moderate) Monitor for decreased efficacy of esomeprazole if coadministration with dexamethasone is necessary. Esomeprazole is extensively metabolized in the liver by CYP2C19 and CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. Drugs known to induce CYP3A4 may lead to decreased esomeprazole plasma concentrations. The manufacturer of esomeprazole recommends avoidance with strong inducers because decreased exposure of esomeprazole can occur. Recommendations are not available for concomitant use with moderate inducers of CYP3A4.
    Esomeprazole; Naproxen: (Moderate) Monitor for decreased efficacy of esomeprazole if coadministration with dexamethasone is necessary. Esomeprazole is extensively metabolized in the liver by CYP2C19 and CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. Drugs known to induce CYP3A4 may lead to decreased esomeprazole plasma concentrations. The manufacturer of esomeprazole recommends avoidance with strong inducers because decreased exposure of esomeprazole can occur. Recommendations are not available for concomitant use with moderate inducers of CYP3A4.
    Estramustine: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Estrogens: (Moderate) Estrogens have been associated with elevated serum concentrations of corticosteroid binding globulin (CBG), leading to increased total circulating corticosteroids, although the free concentrations of these hormones may be lower; the clinical significance is not known. Estrogens are CYP3A4 substrates and dexamethasone is a CYP3A4 inducer; concomitant use may decrease the clinical efficacy of estrogens. Patients should be monitored for signs of decreased clinical effects of estrogens (e.g., breakthrough bleeding), oral contraceptives, or non-oral combination contraceptives if these drugs are used together.
    Eszopiclone: (Moderate) Potent inducers of CYP3A4, such as dexmethasone, may cause a reduction in the plasma concentration of eszopiclone.
    Etoposide, VP-16: (Major) Monitor for clinical efficacy of etoposide if used concomitantly with dexamethasone. Dexamethasone is an inducer of CYP3A4; etoposide, VP-16 is a CYP3A4 substrate. Coadministration of etoposide with a strong CYP3A4 inducer (phenytoin) resulted in increased etoposide clearance and reduced efficacy, as did coadministration with a weak inducer of CYP3A4 and P-glycoprotein (P-gp) (valproic acid).
    Etravirine: (Major) Dexamethasone can induce the activity of CYP3A4 and increase the metabolism of etravirine; decreased antiviral efficacy may be seen. While concomitant administration has not been evaluated, a potentially significant interaction may occur. Use these drugs concomitantly with caution, or consider alternative corticosteroids, particularly for long-term use.
    Exemestane: (Moderate) Use caution if coadministration of exemestane with dexamethasone is necessary, and monitor for a possible decrease in the efficacy of exemestane. Exemestane is a CYP3A4 substrate; dexamethasone is a moderate CYP3A4 inducer. In a pharmacokinetic interaction study (n = 10) with a strong CYP3A4 inducer, rifampicin (600 mg daily for 14 days), the mean Cmax and AUC of exemestane (single dose) decreased by 41% and 54%, respectively. The manufacturer of exemestane recommends a dose increase when concomitant use with a strong CYP3A4 inducer is necessary; recommendations are not available for moderate CYP3A4 inducers.
    Exenatide: (Moderate) When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia and cause blood glucose concentrations to rise. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Flibanserin: (Major) The concomitant use of flibanserin with CYP3A4 inducers significantly decreases flibanserin exposure compared to the use of flibanserin alone. Therefore, concurrent use of flibanserin and CYP3A4 inducers, such as dexamethasone, is not recommended.
    Floxuridine: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Fluconazole: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together.
    Fluorouracil, 5-FU: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Fluoxymesterone: (Moderate) Coadministration of corticosteroids and fluoxymesterone may increase the risk of edema, especially in patients with underlying cardiac or hepatic disease. Corticosteroids with greater mineralocorticoid activity, such as fludrocortisone, may be more likely to cause edema. Administer these drugs in combination with caution.
    Food: (Moderate) The incidence of marijuana associated adverse effects may change following coadministration with dexamethasone. Dexamethasone is an inducer of CYP3A4, an isoenzyme partially responsible for the metabolism of marijuana's most psychoactive compound, delta-9-tetrahydrocannabinol (Delta-9-THC). When given concurrently with dexamethasone, the amount of Delta-9-THC converted to the active metabolite 11-hydroxy-delta-9-tetrahydrocannabinol (11-OH-THC) may be increased. These changes in Delta-9-THC and 11-OH-THC plasma concentrations may result in an altered marijuana adverse event profile.
    Fosamprenavir: (Moderate) Dexamethasone decreases amprenavir serum concentrations. Therefore, use caution when administering dexamethasone and fosamprenavir concurrently. Fosamprenavir may be less effective in patients taking these agents together.
    Fosinopril; Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Gallium Ga 68 Dotatate: (Moderate) Corticosteroids may accentuate the electrolyte loss associated with diuretic therapy resulting in hypokalemia. Also, corticotropin may cause calcium loss and sodium and fluid retention. Mannitol itself can cause hypernatremia. Close monitoring of electrolytes should occur in patients receiving these drugs concomitantly.
    Gefitinib: (Moderate) Monitor for clinical response of gefitinib if used concomitantly with dexamethasone. Gefitinib is metabolized significantly by CYP3A4 and dexamethasone is a CYP3A4 inducer; coadministration may increase gefitinib metabolism and decrease gefitinib concentrations. While the manufacturer has provided no guidance regarding the use of gefitinib with mild or moderate CYP3A4 inducers, administration of a single 500 mg gefitinib dose with a concurrent strong CYP3A4 inducer (rifampin) resulted in reduced mean AUC of gefitinib by 83%.
    Gemcitabine: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Gentamicin: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together.
    Glecaprevir; Pibrentasvir: (Moderate) Caution is advised with the coadministration of glecaprevir and dexamethasone as coadministration may increase serum concentrations of dexamethasone and increase the risk of adverse effects. Dexamethasone is a substrate of P-glycoprotein (P-gp); glecaprevir is a P-gp inhibitor. (Moderate) Caution is advised with the coadministration of pibrentasvir and dexamethasone as coadministration may increase serum concentrations of dexamethasone and increase the risk of adverse effects. Dexamethasone is a substrate of P-glycoprotein (P-gp); pibrentasvir is a P-gp inhibitor.
    Glimepiride: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Glimepiride; Pioglitazone: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Glimepiride; Rosiglitazone: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Glipizide: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Glipizide; Metformin: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. In addition, blood lactate concentrations and the lactate to pyruvate ratio increase when metformin is coadministered with corticosteroids (e.g., hydrocortisone). Elevated lactic acid concentrations are associated with increased morbidity rates. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted. (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Glyburide: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Glyburide; Metformin: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. In addition, blood lactate concentrations and the lactate to pyruvate ratio increase when metformin is coadministered with corticosteroids (e.g., hydrocortisone). Elevated lactic acid concentrations are associated with increased morbidity rates. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted. (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Glycerol Phenylbutyrate: (Moderate) Corticosteroids may induce elevated blood ammonia concentrations. Corticosteroids should be used with caution in patients receiving glycerol phenylbutyrate. Monitor ammonia concentrations closely.
    Golimumab: (Moderate) The safety and efficacy of golimumab in patients with immunosuppression have not been evaluated. Patients receiving immunosuppressives along with golimumab may be at a greater risk of developing an infection.
    Guaifenesin; Hydrocodone: (Moderate) Hydrocodone is metabolized by CYP3A4. Dexamethasone, an inducer of CYP3A4, may cause increased clearance of hydrocodone, which could result in lack of efficacy or the development of an abstinence syndrome in a patient who had developed physical dependence to hydrocodone. Monitor the patient for reduced efficacy of hydrocodone. A higher hydrocodone dose may be needed if used with dexamethasone.
    Guaifenesin; Hydrocodone; Pseudoephedrine: (Moderate) Hydrocodone is metabolized by CYP3A4. Dexamethasone, an inducer of CYP3A4, may cause increased clearance of hydrocodone, which could result in lack of efficacy or the development of an abstinence syndrome in a patient who had developed physical dependence to hydrocodone. Monitor the patient for reduced efficacy of hydrocodone. A higher hydrocodone dose may be needed if used with dexamethasone.
    Guaifenesin; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Guanfacine: (Major) Dexamethasone may significantly decrease guanfacine plasma concentrations. FDA-approved labeling for extended-release (ER) guanfacine recommends that, if these agents are taken together, doubling the recommended dose of guanfacine should be considered; if dexamethasone is added in a patient already receiving guanfacine, this escalation should occur over 1 to 2 weeks. If dexamethasone is discontinued, decrease the guanfacine ER dosage back to the recommended dose over 1 to 2 weeks. Specific recommendations for immediate-release (IR) guanfacine are not available. Guanfacine is primarily metabolized by CYP3A4, and dexamethasone is a moderate CYP3A4 inducer.
    Halofantrine: (Major) Due to the risks of cardiac toxicity of halofantrine in patients with hypokalemia and/or hypomagnesemia, the use of halofantrine should be avoided in combination with agents that may lead to electrolyte losses, such as corticosteroids.
    Haloperidol: (Major) QT prolongation has been observed during haloperidol treatment. Use of haloperidol and medications known to cause electrolyte imbalance may increase the risk of QT prolongation. Therefore, caution is advisable during concurrent use of haloperidol and corticosteroids. Topical corticosteroids are less likely to interact.
    Hemin: (Moderate) Hemin works by inhibiting aminolevulinic acid synthetase. Corticosteroids increase the activity of this enzyme should not be used with hemin.
    Heparin: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together.
    Hetastarch: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together.
    Homatropine; Hydrocodone: (Moderate) Hydrocodone is metabolized by CYP3A4. Dexamethasone, an inducer of CYP3A4, may cause increased clearance of hydrocodone, which could result in lack of efficacy or the development of an abstinence syndrome in a patient who had developed physical dependence to hydrocodone. Monitor the patient for reduced efficacy of hydrocodone. A higher hydrocodone dose may be needed if used with dexamethasone.
    Hydantoins: (Moderate) Hydantoin anticonvulsants induce hepatic microsomal enzymes and may increase the metabolism of dexamethasone, leading to reduced efficacy. Depending on the individual clinical situation and the indication for the interacting medication, enzyme-induction interactions may not always produce reductions in treatment efficacy.
    Hydralazine; Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Hydrochlorothiazide, HCTZ: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Hydrochlorothiazide, HCTZ; Irbesartan: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Hydrochlorothiazide, HCTZ; Lisinopril: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Hydrochlorothiazide, HCTZ; Losartan: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Hydrochlorothiazide, HCTZ; Methyldopa: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Hydrochlorothiazide, HCTZ; Metoprolol: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Hydrochlorothiazide, HCTZ; Moexipril: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Hydrochlorothiazide, HCTZ; Olmesartan: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Hydrochlorothiazide, HCTZ; Propranolol: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required. (Moderate) Patients receiving corticosteroids during propranolol therapy may be at increased risk of hypoglycemia due to the loss of counter-regulatory cortisol response. This effect may be more pronounced in infants and young children. If concurrent use is necessary, carefully monitor vital signs and blood glucose concentrations as clinically indicated.
    Hydrochlorothiazide, HCTZ; Quinapril: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Hydrochlorothiazide, HCTZ; Spironolactone: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Hydrochlorothiazide, HCTZ; Telmisartan: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Hydrochlorothiazide, HCTZ; Triamterene: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Hydrochlorothiazide, HCTZ; Valsartan: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Hydrocodone: (Moderate) Hydrocodone is metabolized by CYP3A4. Dexamethasone, an inducer of CYP3A4, may cause increased clearance of hydrocodone, which could result in lack of efficacy or the development of an abstinence syndrome in a patient who had developed physical dependence to hydrocodone. Monitor the patient for reduced efficacy of hydrocodone. A higher hydrocodone dose may be needed if used with dexamethasone.
    Hydrocodone; Ibuprofen: (Moderate) Hydrocodone is metabolized by CYP3A4. Dexamethasone, an inducer of CYP3A4, may cause increased clearance of hydrocodone, which could result in lack of efficacy or the development of an abstinence syndrome in a patient who had developed physical dependence to hydrocodone. Monitor the patient for reduced efficacy of hydrocodone. A higher hydrocodone dose may be needed if used with dexamethasone.
    Hydrocodone; Phenylephrine: (Moderate) Hydrocodone is metabolized by CYP3A4. Dexamethasone, an inducer of CYP3A4, may cause increased clearance of hydrocodone, which could result in lack of efficacy or the development of an abstinence syndrome in a patient who had developed physical dependence to hydrocodone. Monitor the patient for reduced efficacy of hydrocodone. A higher hydrocodone dose may be needed if used with dexamethasone. (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Hydrocodone; Potassium Guaiacolsulfonate: (Moderate) Hydrocodone is metabolized by CYP3A4. Dexamethasone, an inducer of CYP3A4, may cause increased clearance of hydrocodone, which could result in lack of efficacy or the development of an abstinence syndrome in a patient who had developed physical dependence to hydrocodone. Monitor the patient for reduced efficacy of hydrocodone. A higher hydrocodone dose may be needed if used with dexamethasone.
    Hydrocodone; Potassium Guaiacolsulfonate; Pseudoephedrine: (Moderate) Hydrocodone is metabolized by CYP3A4. Dexamethasone, an inducer of CYP3A4, may cause increased clearance of hydrocodone, which could result in lack of efficacy or the development of an abstinence syndrome in a patient who had developed physical dependence to hydrocodone. Monitor the patient for reduced efficacy of hydrocodone. A higher hydrocodone dose may be needed if used with dexamethasone.
    Hydrocodone; Pseudoephedrine: (Moderate) Hydrocodone is metabolized by CYP3A4. Dexamethasone, an inducer of CYP3A4, may cause increased clearance of hydrocodone, which could result in lack of efficacy or the development of an abstinence syndrome in a patient who had developed physical dependence to hydrocodone. Monitor the patient for reduced efficacy of hydrocodone. A higher hydrocodone dose may be needed if used with dexamethasone.
    Hydroxyurea: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Hylan G-F 20: (Major) The safety and efficacy of hylan G-F 20 given concomitantly with other intra-articular injectables have not been established. Other intra-articular injections may include intra-articular steroids (betamethasone, dexamethasone, hydrocortisone, prednisolone, methylprednisolone, and triamcinolone).
    Hyoscyamine; Methenamine; Methylene Blue; Phenyl Salicylate; Sodium Biphosphate: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided. (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia.
    Ibritumomab Tiuxetan: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together. (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia. (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Ibrutinib: (Moderate) Use ibrutinib and dexamethasone together with caution; decreased ibrutinib levels may occur resulting in reduced ibrutinib efficacy. Monitor patients for signs of decreased ibrutinib efficacy if these agents are used together. Ibrutinib is a CYP3A4 substrate; dexamethasone is a moderate CYP3A inducer. Simulations using physiologically-based pharmacokinetic (PBPK) models suggest that moderate CYP3A4 inducers may decrease ibrutinib exposure up to 3-fold.
    Idelalisib: (Major) Avoid concomitant use of idelalisib, a strong CYP3A inhibitor, with dexamethasone, a CYP3A substrate, as dexamethasone toxicities may be significantly increased. The AUC of a sensitive CYP3A substrate was increased 5.4-fold when coadministered with idelalisib.
    Ifosfamide: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Imatinib: (Minor) Any drug that induces cytochrome P450 3A4, such as dexamethasone, may increase the metabolism of imatinib and decrease imatinib concentrations and clinical effects.
    Incretin Mimetics: (Moderate) When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia and cause blood glucose concentrations to rise. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Indapamide: (Moderate) Additive hypokalemia may occur when indapamide is coadministered with other drugs with a significant risk of hypokalemia such as systemic corticosteroids. Coadminister with caution and careful monitoring.
    Indinavir: (Moderate) Dexamethasone is a moderate inducer of CYP3A4. Coadministration with other drugs that are metabolized by CYP3A4 (e.g., indinavir) may increase their clearance, resulting in decreased plasma concentration.
    Infliximab: (Moderate) Many serious infections during infliximab therapy have occurred in patients who received concurrent immunosuppressives that, in addition to their underlying Crohn's disease or rheumatoid arthritis, predisposed patients to infections. The impact of concurrent infliximab therapy and immunosuppression on the development of malignancies is unknown. In clinical trials, the use of concomitant immunosuppressant agents appeared to reduce the frequency of antibodies to infliximab and appeared to reduce infusion reactions.
    Insulin Degludec; Liraglutide: (Moderate) When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia and cause blood glucose concentrations to rise. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Insulin Glargine; Lixisenatide: (Moderate) When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia and cause blood glucose concentrations to rise. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Insulins: (Moderate) Monitor patients receiving insulin closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Endogenous counter-regulatory hormones are released in response to hypoglycemia. When released, blood glucose concentrations rise. When these hormones or their derivatives (e.g., corticosteroids) are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of insulin.
    Interferon Alfa-2a: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Interferon Alfa-2b: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Interferon Alfa-2b; Ribavirin: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Intranasal Influenza Vaccine: (Severe) Live virus vaccines should generally not be administered to an immunosuppressed patient. Live virus vaccines may induce the illness they are intended to prevent and are generally contraindicated for use during immunosuppressive treatment. The immune response of the immunocompromised patient to vaccines may be decreased, even despite alternate vaccination schedules or more frequent booster doses. If immunization is necessary, choose an alternative to live vaccination, or, consider a delay or change in the immunization schedule. Practitioners should refer to the most recent CDC guidelines regarding vaccination of patients who are receiving drugs that adversely affect the immune system. Children who are receiving high doses of systemic corticosteroids (i.e., greater than or equal to 2 mg/kg prednisone orally per day) for 2 weeks or more may be vaccinated after steroid therapy has been discontinued for at least 3 months in accordance with general recommendations for the use of live-virus vaccines. The CDC has stated that discontinuation of steroids for 1 month prior to varicella virus vaccine live administration may be sufficient. Budesonide may affect the immunogenicity of live vaccines. An open-label study examined the immune responsiveness to varicella vaccine in 243 pediatric asthma patients who were treated with budesonide inhalation suspension 0.251 mg daily (n = 151) or non-corticosteroid asthma therapy (n = 92). The percentage of patients developing a seroprotective antibody titer of at least 5 (gpELISA value) in response to the vaccination was slightly lower in patients treated with budesonide compared to patients treated with non-corticosteroid asthma therapy (85% vs. 90%). Even though no patient treated with budesonide inhalation suspension developed chicken pox because of vaccination, live-virus vaccines should not be given to individuals who are considered to be immunocompromised until more information is available.
    Iohexol: (Major) Serious adverse events, including death, have been observed during intrathecal administration of both corticosteroids (i.e., dexamethasone) and radiopaque contrast agents (i.e., iohexol); therefore, concurrent use of these medications via the intrathecal route is contraindicated. Cases of cortical blindness, stroke, spinal cord infarction, paralysis, seizures, nerve injury, brain edema, and death have been temporally associated (i.e., within minutes to 48 hours after injection) with epidural administration of injectable corticosteroids. In addition, patients inadvertently administered iohexol formulations not indicated for intrathecal use have experienced seizures, convulsions, cerebral hemorrhages, brain edema, and death. Administering these medications together via the intrathecal route may increase the risk for serious adverse events.
    Iopamidol: (Severe) Because both intrathecal corticosteroids (i.e., dexamethasone) and intrathecal radiopaque contrast agents (i.e., iopamidoll) can increase the risk of seizures, the intrathecal administration of corticosteroids with intrathecal radiopaque contrast agents is contraindicated.
    Isavuconazonium: (Major) Avoid concurrent use of dexamethasone with isavuconazonium. An alternative corticosteroid should be considered. Dexamethasone is a substrate and inducer of the hepatic isoenzyme CYP3A4 and a substrate of the drug transporter P-glycoprotein (P-gp); isavuconazole, the active moiety of isavuconazonium, is a sensitive substrate and moderate inhibitor of CYP3A4 and an inhibitor of P-gp. Concurrent use may result in significant decreases in the plasma concentrations of isavuconazole, leading to a reduction of antifungal efficacy and the potential for treatment failure. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression.
    Isoniazid, INH: (Minor) Serum concentrations of isoniazid, INH may be decreased when used concurrently with dexamethasone; this may be due to either changes in the metabolism or changes in the renal excretion of isoniazid. Despite the alterations in isoniazid plasma concentrations, patient response to treatment was excellent.
    Isoniazid, INH; Pyrazinamide, PZA; Rifampin: (Moderate) A dose adjustment of dexamethasone may be necessary when administered concurrently with rifamycins, due to the potential for decreased exposure of dexamethasone. Rifamycins are inducers of CYP3A4; dexamethasone is a CYP3A4 substrate (Minor) Serum concentrations of isoniazid, INH may be decreased when used concurrently with dexamethasone; this may be due to either changes in the metabolism or changes in the renal excretion of isoniazid. Despite the alterations in isoniazid plasma concentrations, patient response to treatment was excellent.
    Isoniazid, INH; Rifampin: (Moderate) A dose adjustment of dexamethasone may be necessary when administered concurrently with rifamycins, due to the potential for decreased exposure of dexamethasone. Rifamycins are inducers of CYP3A4; dexamethasone is a CYP3A4 substrate (Minor) Serum concentrations of isoniazid, INH may be decreased when used concurrently with dexamethasone; this may be due to either changes in the metabolism or changes in the renal excretion of isoniazid. Despite the alterations in isoniazid plasma concentrations, patient response to treatment was excellent.
    Isoproterenol: (Moderate) The risk of cardiac toxicity with isoproterenol in asthma patients appears to be increased with the coadministration of corticosteroids. Intravenous infusions of isoproterenol in refractory asthmatic children at rates of 0.05 to 2.7 mcg/kg/min have caused clinical deterioration, myocardial infarction (necrosis), congestive heart failure and death.
    Isotretinoin: (Minor) Both isotretinoin and corticosteroids can cause osteoporosis during chronic use. Patients receiving systemic corticosteroids should receive isotretinoin therapy with caution.
    Itraconazole: (Moderate) Monitor for corticosteroid-related adverse effects and altered response to itraconazole if coadminsitration is necessary. Itraconazole is a strong CYP3A4 inhibitor and substrate; dexamethasone is a moderate CYP3A4 inducer and substrate. Another strong CYP3A4 inhibitor has been reported to decrease the metabolism of certain corticosteroids by up to 60%, leading to increased risk of corticosteroid side effects. The clearance of itraconazole may also be increased, resulting in decreased plasma concentrations.
    Ivabradine: (Major) Avoid coadministration of ivabradine and dexamethasone. Ivabradine is primarily metabolized by CYP3A4; dexamethasone is an inducer of CYP3A4. Coadministration may decrease the plasma concentrations of ivabradine resulting in the potential for treatment failure.
    Ivacaftor: (Moderate) Use caution when administering ivacaftor and dexamethasone concurrently; the clinical impact of this interaction has not yet been determined. Administration of ivacaftor with strong CYP3A inducers is not recommended because sub-therapeutic ivacaftor exposure could result. Ivacaftor is a CYP3A substrate and dexamethasone is a CYP3A inducer. Co-administration with rifampin, a strong CYP3A inducer, decreased the ivacaftor exposure by approximately 9-fold. Ivacaftor is also an inhibitor of CYP3A and P-glycoprotein (Pgp); dexamethasone is metabolized by CYP3A and is a substrate of Pgp. Co-administration may increase dexamethasone exposure leading to increased or prolonged therapeutic effects and adverse events.
    Ixabepilone: (Major) Ixabepilone is a CYP3A4 substrate and concomitant use with strong CYP3A4 inducers such as dexamethasone may lead to reduced and subtherapeutic concentrations of ixabepilone. Caution should be utilized when CYP3A4 inducers are coadministered with ixabepilone, and alternative therapies with low enzyme induction potential should be considered.
    Ketoconazole: (Moderate) Coadministration may result in increased exposure to dexamethasone and increased corticosteroid-related adverse effects. Ketoconazole has been reported to decrease the metabolism of certain corticosteroids by up to 60%. In addition, ketoconazole alone can inhibit adrenal corticosteroid synthesis and may cause adrenal insufficiency during corticosteroid withdrawal.
    Lansoprazole: (Minor) Monitor for decreased efficacy of lansoprazole if coadministration with dexamethasone is necessary. Lansoprazole is metabolized by CYP2C19 and CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. Drugs known to induce CYP3A4 may lead to decreased lansoprazole plasma concentrations.
    Lansoprazole; Naproxen: (Minor) Monitor for decreased efficacy of lansoprazole if coadministration with dexamethasone is necessary. Lansoprazole is metabolized by CYP2C19 and CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. Drugs known to induce CYP3A4 may lead to decreased lansoprazole plasma concentrations.
    Lapatinib: (Major) Lapatinib is metabolized by CYP3A4 and CYP3A5 enzymes. Drugs that are inducers of CYP3A4 activity, such as dexamethasone, will decrease the plasma concentrations of lapatinib. The combination may also result in additive immunosuppression.
    L-Asparaginase Escherichia coli: (Moderate) Concomitant use of L-asparaginase with corticosteroids can result in additive hyperglycemia. L-Asparaginase transiently inhibits insulin production contributing to hyperglycemia seen during concurrent corticosteroid therapy. Insulin therapy may be required in some cases. Administration of L-asparaginase after rather than before corticosteroids reportedly has produced fewer hypersensitivity reactions.
    Ledipasvir; Sofosbuvir: (Moderate) Caution and close monitoring of dexamethasone-associated adverse reactions is advised with concomitant administration of ledipasvir. Dexamethasone is a substrate of the drug transporter P-glycoprotein (P-gp); ledipasvir is a P-gp inhibitor. Taking these drugs together may increase dexamethasone plasma concentrations.
    Levetiracetam: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together.
    Levomethadyl: (Major) Caution is advised when using levomethadyl in combination with other agents, such as corticosteroids, that may lead to electrolyte abnormalities, especially hypokalemia or hypomagnesemia.
    Lidocaine: (Moderate) Concomitant use of systemic lidocaine and dexamethasone may decrease lidocaine plasma concentrations. Higher lidocaine doses may be required; titrate to effect. Lidocaine is a CYP3A4 and CYP1A2 substrate; dexamethasone induces CYP3A4.
    Linagliptin: (Major) Concomitant use of linagliptin with dexamethasone may result in decreased efficacy of linagliptin. When corticosteroids are administered exogenously, increases in blood glucose concentrations are expected, thereby decreasing the hypoglycemic effect of antidiabetic agents. In addition, linagliptin is a substrate of hepatic isoenzyme CYP3A4 and dexamethasone is a moderate inducer of CYP3A4. Coadministration may result in decreased concentrations of linagliptin and decreased efficacy. Patients receiving antidiabetic agents, such as linagliptin, should be closely monitored for signs indicating loss of diabetic control when dexamethasone is coadministered.
    Linagliptin; Metformin: (Major) Concomitant use of linagliptin with dexamethasone may result in decreased efficacy of linagliptin. When corticosteroids are administered exogenously, increases in blood glucose concentrations are expected, thereby decreasing the hypoglycemic effect of antidiabetic agents. In addition, linagliptin is a substrate of hepatic isoenzyme CYP3A4 and dexamethasone is a moderate inducer of CYP3A4. Coadministration may result in decreased concentrations of linagliptin and decreased efficacy. Patients receiving antidiabetic agents, such as linagliptin, should be closely monitored for signs indicating loss of diabetic control when dexamethasone is coadministered. (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. In addition, blood lactate concentrations and the lactate to pyruvate ratio increase when metformin is coadministered with corticosteroids (e.g., hydrocortisone). Elevated lactic acid concentrations are associated with increased morbidity rates. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Liraglutide: (Moderate) When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia and cause blood glucose concentrations to rise. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Lisdexamfetamine: (Minor) The amphetamines may interfere with laboratory tests for the determination of corticosteroids. Plasma cortisol concentrations may be increased, especially during evening hours. Amphetamines may also interfere with urinary steroid determinations.
    Live Vaccines: (Severe) Live virus vaccines should generally not be administered to an immunosuppressed patient. Live virus vaccines may induce the illness they are intended to prevent and are generally contraindicated for use during immunosuppressive treatment. The immune response of the immunocompromised patient to vaccines may be decreased, even despite alternate vaccination schedules or more frequent booster doses. If immunization is necessary, choose an alternative to live vaccination, or, consider a delay or change in the immunization schedule. Practitioners should refer to the most recent CDC guidelines regarding vaccination of patients who are receiving drugs that adversely affect the immune system. Children who are receiving high doses of systemic corticosteroids (i.e., greater than or equal to 2 mg/kg prednisone orally per day) for 2 weeks or more may be vaccinated after steroid therapy has been discontinued for at least 3 months in accordance with general recommendations for the use of live-virus vaccines. The CDC has stated that discontinuation of steroids for 1 month prior to varicella virus vaccine live administration may be sufficient. Budesonide may affect the immunogenicity of live vaccines. An open-label study examined the immune responsiveness to varicella vaccine in 243 pediatric asthma patients who were treated with budesonide inhalation suspension 0.251 mg daily (n = 151) or non-corticosteroid asthma therapy (n = 92). The percentage of patients developing a seroprotective antibody titer of at least 5 (gpELISA value) in response to the vaccination was slightly lower in patients treated with budesonide compared to patients treated with non-corticosteroid asthma therapy (85% vs. 90%). Even though no patient treated with budesonide inhalation suspension developed chicken pox because of vaccination, live-virus vaccines should not be given to individuals who are considered to be immunocompromised until more information is available.
    Lixisenatide: (Moderate) When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia and cause blood glucose concentrations to rise. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Lomustine, CCNU: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Loop diuretics: (Moderate) Corticosteroids may accentuate the electrolyte loss associated with diuretic therapy resulting in hypokalemia and/or hypomagnesemia. While glucocorticoids with mineralocorticoid activity (e.g., cortisone, hydrocortisone) can cause sodium and fluid retention. Close monitoring of electrolytes should occur in patients receiving these drugs concomitantly.
    Loperamide: (Moderate) The plasma concentration and efficacy of loperamide may be reduced when administered concurrently with dexamethasone. Loperamide is metabolized by the hepatic enzyme CYP3A4; dexamethasone is an inducer of this enzyme.
    Loperamide; Simethicone: (Moderate) The plasma concentration and efficacy of loperamide may be reduced when administered concurrently with dexamethasone. Loperamide is metabolized by the hepatic enzyme CYP3A4; dexamethasone is an inducer of this enzyme.
    Lopinavir; Ritonavir: (Major) Decreased plasma levels of lopinavir are seen when dexamethasone and lopinavir; ritonavir (Kaletra) coadministered. Use this treatment combination with caution and carefully monitor HIV treatment status, as decreased clinical efficacy of lopinavir; ritonavir may be seen. (Moderate) Close monitoring of therapeutic and adverse effects is required when dexamethasone is coadministered with ritonavir. Ritonavir inhibits CYP3A4 and dexamethasone is a CYP3A4 substrate.
    Lumacaftor; Ivacaftor: (Moderate) Concomitant use of dexamethasone and lumacaftor; ivacaftor may alter dexamethasone exposure. If used together, dexamethasone dosages may need to be adjusted to achieve desired therapeutic effects. Dexamethasone is a substrate and moderate inducer of CYP3A and a substrate of the P-glycoprotein (P-gp) drug transporter. Ivacaftor is a sensitive CYP3A substrate and lumacaftor is a strong CYP3A inducer; in vitro data suggests lumacaftor; ivacaftor may also induce and/or inhibit P-gp. Although induction of dexamethasone through the CYP3A pathway may lead to decreased drug efficacy, the net effect of lumacaftor; ivacaftor on P-gp transport is not clear. Monitor the patient for decreased corticosteroid efficacy or increased or prolonged therapeutic effects and adverse events. Additionally, ivacaftor exposure could theoretically be further decreased when given with another CYP3A inducer; however, ivacaftor; lumacaftor dosage adjustments are not recommended with concomitant use of a moderate CYP3A inducer such as dexamethasone.
    Lumacaftor; Ivacaftor: (Moderate) Use caution when administering ivacaftor and dexamethasone concurrently; the clinical impact of this interaction has not yet been determined. Administration of ivacaftor with strong CYP3A inducers is not recommended because sub-therapeutic ivacaftor exposure could result. Ivacaftor is a CYP3A substrate and dexamethasone is a CYP3A inducer. Co-administration with rifampin, a strong CYP3A inducer, decreased the ivacaftor exposure by approximately 9-fold. Ivacaftor is also an inhibitor of CYP3A and P-glycoprotein (Pgp); dexamethasone is metabolized by CYP3A and is a substrate of Pgp. Co-administration may increase dexamethasone exposure leading to increased or prolonged therapeutic effects and adverse events.
    Lurasidone: (Moderate) Because lurasidone is primarily metabolized by CYP3A4, decreased plasma concentrations of lurasidone may occur when the drug is co-administered with inducers of CYP3A4. Decreased plasma concentrations of lurasidone may lead to a decrease in efficacy of lurasidone. If lurasidone is used with a moderate CYP3A4 inducer, it may be necessary to increase the lurasidone dose after chronic treatment (7 days or more).
    Magnesium Salicylate: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
    Mannitol: (Moderate) Corticosteroids may accentuate the electrolyte loss associated with diuretic therapy resulting in hypokalemia. Also, corticotropin may cause calcium loss and sodium and fluid retention. Mannitol itself can cause hypernatremia. Close monitoring of electrolytes should occur in patients receiving these drugs concomitantly.
    Maraviroc: (Moderate) Use caution if coadministration of maraviroc with dexamethasone is necessary, due to a possible decrease in maraviroc exposure. Maraviroc is a CYP3A substrate and dexamethasone is a CYP3A4 inducer. Monitor for a decrease in maraviroc efficacy with concomitant use.
    Measles Virus; Mumps Virus; Rubella Virus; Varicella Virus Vaccine, Live: (Severe) Live virus vaccines should generally not be administered to an immunosuppressed patient. Live virus vaccines may induce the illness they are intended to prevent and are generally contraindicated for use during immunosuppressive treatment. The immune response of the immunocompromised patient to vaccines may be decreased, even despite alternate vaccination schedules or more frequent booster doses. If immunization is necessary, choose an alternative to live vaccination, or, consider a delay or change in the immunization schedule. Practitioners should refer to the most recent CDC guidelines regarding vaccination of patients who are receiving drugs that adversely affect the immune system. Children who are receiving high doses of systemic corticosteroids (i.e., greater than or equal to 2 mg/kg prednisone orally per day) for 2 weeks or more may be vaccinated after steroid therapy has been discontinued for at least 3 months in accordance with general recommendations for the use of live-virus vaccines. The CDC has stated that discontinuation of steroids for 1 month prior to varicella virus vaccine live administration may be sufficient. Budesonide may affect the immunogenicity of live vaccines. An open-label study examined the immune responsiveness to varicella vaccine in 243 pediatric asthma patients who were treated with budesonide inhalation suspension 0.251 mg daily (n = 151) or non-corticosteroid asthma therapy (n = 92). The percentage of patients developing a seroprotective antibody titer of at least 5 (gpELISA value) in response to the vaccination was slightly lower in patients treated with budesonide compared to patients treated with non-corticosteroid asthma therapy (85% vs. 90%). Even though no patient treated with budesonide inhalation suspension developed chicken pox because of vaccination, live-virus vaccines should not be given to individuals who are considered to be immunocompromised until more information is available.
    Measles/Mumps/Rubella Vaccines, MMR: (Severe) Live virus vaccines should generally not be administered to an immunosuppressed patient. Live virus vaccines may induce the illness they are intended to prevent and are generally contraindicated for use during immunosuppressive treatment. The immune response of the immunocompromised patient to vaccines may be decreased, even despite alternate vaccination schedules or more frequent booster doses. If immunization is necessary, choose an alternative to live vaccination, or, consider a delay or change in the immunization schedule. Practitioners should refer to the most recent CDC guidelines regarding vaccination of patients who are receiving drugs that adversely affect the immune system. Children who are receiving high doses of systemic corticosteroids (i.e., greater than or equal to 2 mg/kg prednisone orally per day) for 2 weeks or more may be vaccinated after steroid therapy has been discontinued for at least 3 months in accordance with general recommendations for the use of live-virus vaccines. The CDC has stated that discontinuation of steroids for 1 month prior to varicella virus vaccine live administration may be sufficient. Budesonide may affect the immunogenicity of live vaccines. An open-label study examined the immune responsiveness to varicella vaccine in 243 pediatric asthma patients who were treated with budesonide inhalation suspension 0.251 mg daily (n = 151) or non-corticosteroid asthma therapy (n = 92). The percentage of patients developing a seroprotective antibody titer of at least 5 (gpELISA value) in response to the vaccination was slightly lower in patients treated with budesonide compared to patients treated with non-corticosteroid asthma therapy (85% vs. 90%). Even though no patient treated with budesonide inhalation suspension developed chicken pox because of vaccination, live-virus vaccines should not be given to individuals who are considered to be immunocompromised until more information is available.
    Mecasermin rinfabate: (Moderate) Additional monitoring may be required when coadministering systemic or inhaled corticosteroids and mecasermin, recombinant, rh-IGF-1. In animal studies, corticosteroids impair the growth-stimulating effects of growth hormone (GH) through interference with the physiological stimulation of epiphyseal chondrocyte proliferation exerted by GH and IGF-1. Dexamethasone administration on long bone tissue in vitro resulted in a decrease of local synthesis of IGF-1. Similar counteractive effects are expected in humans. If systemic or inhaled glucocorticoid therapy is required, the steroid dose should be carefully adjusted and growth rate monitored.
    Mecasermin, Recombinant, rh-IGF-1: (Moderate) Additional monitoring may be required when coadministering systemic or inhaled corticosteroids and mecasermin, recombinant, rh-IGF-1. In animal studies, corticosteroids impair the growth-stimulating effects of growth hormone (GH) through interference with the physiological stimulation of epiphyseal chondrocyte proliferation exerted by GH and IGF-1. Dexamethasone administration on long bone tissue in vitro resulted in a decrease of local synthesis of IGF-1. Similar counteractive effects are expected in humans. If systemic or inhaled glucocorticoid therapy is required, the steroid dose should be carefully adjusted and growth rate monitored.
    Mefloquine: (Moderate) Mefloquine is metabolized by CYP3A4. Dexamethasone is an inducer of CYP3A4, and may increase the metabolism of mefloquine and reduce mefloquine plasma concentrations if coadministered.
    Meglitinides: (Moderate) Drugs which may cause hyperglycemia, including corticosteroids, may cause temporary loss of glycemic control. Diabetic patients who are administered systemic corticosteroid therapy may require an adjustment in the dosing of the antidiabetic agent.
    Melphalan: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Mepenzolate: (Minor) Anticholinergics, such as mepenzolate, antagonize the effects of antiglaucoma agents. Mepenzolate is contraindicated in patients with glaucoma and therefore should not be coadministered with medications being prescribed for the treatment of glaucoma. In addition, anticholinergic drugs taken concurrently with corticosteroids in the presence of increased intraocular pressure may be hazardous.
    Mephobarbital: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Mephobarbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use.
    Metformin: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. In addition, blood lactate concentrations and the lactate to pyruvate ratio increase when metformin is coadministered with corticosteroids (e.g., hydrocortisone). Elevated lactic acid concentrations are associated with increased morbidity rates. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Metformin; Pioglitazone: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. In addition, blood lactate concentrations and the lactate to pyruvate ratio increase when metformin is coadministered with corticosteroids (e.g., hydrocortisone). Elevated lactic acid concentrations are associated with increased morbidity rates. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Metformin; Repaglinide: (Moderate) Drugs which may cause hyperglycemia, including corticosteroids, may cause temporary loss of glycemic control. Diabetic patients who are administered systemic corticosteroid therapy may require an adjustment in the dosing of the antidiabetic agent. (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. In addition, blood lactate concentrations and the lactate to pyruvate ratio increase when metformin is coadministered with corticosteroids (e.g., hydrocortisone). Elevated lactic acid concentrations are associated with increased morbidity rates. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Metformin; Rosiglitazone: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. In addition, blood lactate concentrations and the lactate to pyruvate ratio increase when metformin is coadministered with corticosteroids (e.g., hydrocortisone). Elevated lactic acid concentrations are associated with increased morbidity rates. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Metformin; Saxagliptin: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. In addition, blood lactate concentrations and the lactate to pyruvate ratio increase when metformin is coadministered with corticosteroids (e.g., hydrocortisone). Elevated lactic acid concentrations are associated with increased morbidity rates. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted. (Moderate) Systemic corticosteroids increase blood glucose levels. Diabetic patients who are administered systemic corticosteroid therapy may require an adjustment in the dosing of the antidiabetic agent.
    Metformin; Sitagliptin: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. In addition, blood lactate concentrations and the lactate to pyruvate ratio increase when metformin is coadministered with corticosteroids (e.g., hydrocortisone). Elevated lactic acid concentrations are associated with increased morbidity rates. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted. (Moderate) Systemic corticosteroids increase blood glucose levels. Diabetic patients who are administered systemic corticosteroid therapy may require an adjustment in the dosing of the antidiabetic agent.
    Methazolamide: (Moderate) Corticosteroids may increase the risk of hypokalemia if used concurrently with methazolamide. Hypokalemia may be especially severe with prolonged use of corticotropin, ACTH. Monitor serum potassium levels to determine the need for potassium supplementation and/or alteration in drug therapy. The chronic use of corticosteroids may augment calcium excretion with methazolamide leading to increased risk for hypocalcemia and/or osteoporosis.
    Methenamine; Sodium Acid Phosphate: (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia.
    Methenamine; Sodium Acid Phosphate; Methylene Blue; Hyoscyamine: (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia.
    Methoxsalen: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Methyclothiazide: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Metolazone: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Metyrapone: (Severe) Medications which affect pituitary or adrenocortical function, including all corticosteroid therapy, should be discontinued prior to and during testing with metyrapone. Patients taking inadvertent doses of corticosteroids on the test day may exhibit abnormally high basal plasma cortisol levels and a decreased response to the test. Although systemic absorption of ocular, inhaled and topical corticosteroids is minimal, temporary discontinuation of these products should be considered if possible to reduce the potential for interference with the test results.
    Micafungin: (Moderate) Leukopenia, neutropenia, anemia, and thrombocytopenia have been associated with micafungin. Patients who are taking immunosuppressives such as the corticosteroids with micafungin concomitantly may have additive risks for infection or other side effects. In a pharmacokinetic trial, micafungin had no effect on the pharmacokinetics of prednisolone. Acute intravascular hemolysis and hemoglobinuria was seen in a healthy volunteer during infusion of micafungin (200 mg) and oral prednisolone (20 mg). This reaction was transient, and the subject did not develop significant anemia.
    Mifepristone, RU-486: (Major) Mifepristone (Mifeprex) is contraindicated in patients on long-term corticosteroid therapy and Korlym is contraindicated in patients who require concomitant treatment with systemic corticosteroids for serious medical conditions or illnesses (e.g., immunosuppression after organ transplantation). Mifepristone, RU-486 (Mifeprex) and Mifepristone (Korlym) both exhibit antiglucocorticoid activity that may antagonize corticosteroids. In rats, the activity of dexamethasone was inhibited by oral mifepristone doses of 10 to 25 mg/kg. A mifepristone dose of 4.5 mg/kg in humans resulted in compensatory increases in ACTH and cortisol.
    Mitotane: (Major) Use caution if mitotane and dexamethasone are used concomitantly, and monitor for decreased efficacy of dexamethasone and a possible change in dosage requirements. Mitotane is a strong CYP3A4 inducer and dexamethasone is a CYP3A4 substrate; coadministration may result in decreased plasma concentrations of dexamethasone.
    Mitoxantrone: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Mivacurium: (Moderate) Caution and close monitoring are advised if corticosteroids and neuromuscular blockers are used together, particularly for long periods, due to enhanced neuromuscular blocking effects. In such patients, a peripheral nerve stimulator may be of value in monitoring the response. Concurrent use may increase the risk of acute myopathy. This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis. Elevation of creatine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years.
    Modafinil: (Minor) Drugs that exhibit significant induction of the hepatic microsomal CYP3A4 isoenzyme, such as dexamethasone, may potentially increase the metabolism of modafinil. Decreased serum levels of modafinil could potentially result in decreased efficacy of modafinil.
    Moxifloxacin: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together.
    Muromonab-CD3: (Major) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. While therapy is designed to take advantage of this effect, patients may be predisposed to over-immunosuppression resulting in an increased risk for the development of severe infections. Close clinical monitoring is advised with concurrent use; in the presence of serious infections, continuation of the corticosteroid or immunosuppressive agent may be necessary but should be accompanied by appropriate antimicrobial therapies as indicated.
    Natalizumab: (Major) Ordinarily, patients receiving chronic immunosuppressant therapy should not be treated with natalizumab. Treatment recommendations for combined corticosteroid therapy are dependent on the underlying indication for natalizumab therapy. Corticosteroids should be tapered in those patients with Crohn's disease who are on chronic corticosteroids when they start natalizumab therapy, as soon as a therapeutic benefit has occurred. If the patient cannot discontinue systemic corticosteroids within 6 months, discontinue natalizumab. The concomitant use of natalizumab and corticosteroids may further increase the risk of serious infections, including progressive multifocal leukoencephalopathy, over the risk observed with use of natalizumab alone. In multiple sclerosis (MS) clinical trials, an increase in infections was seen in patients concurrently receiving short courses of corticosteroids. However, the increase in infections in natalizumab-treated patients who received steroids was similar to the increase in placebo-treated patients who received steroids. Short courses of steroid use during natalizumab, such as when they are needed for MS relapse treatment, appear to be acceptable for use concurrently.
    Nateglinide: (Moderate) Drugs which may cause hyperglycemia, including corticosteroids, may cause temporary loss of glycemic control. Diabetic patients who are administered systemic corticosteroid therapy may require an adjustment in the dosing of the antidiabetic agent.
    Nelarabine: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Neostigmine: (Minor) Corticosteroids may interact with cholinesterase inhibitors including ambenonium, neostigmine, and pyridostigmine, occasionally causing severe muscle weakness in patients with myasthenia gravis. Glucocorticoids are occasionally used therapeutically, however, in the treatment of some patients with myasthenia gravis. In such patients, it is recommended that corticosteroid therapy be initiated at low dosages and with close clinical monitoring. The dosage should be increased gradually as tolerated, with continued careful monitoring of the patient's clinical status.
    Neratinib: (Major) Avoid concomitant use of dexamethasone with neratinib due to decreased efficacy of neratinib. Neratinib is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. The effect of moderate CYP3A4 induction on neratinib concentrations has not been studied; however, coadministration with a strong CYP3A4 inducer decreased neratinib exposure by 87% and decreased exposure to active metabolites M6 and M7 by 37% to 49%. Because of the significant impact on neratinib exposure from strong CYP3A4 induction, the potential impact on neratinib efficacy from concomitant use with moderate CYP3A4 inducers should be considered as they may also significantly decrease neratinib exposure.
    Netupitant; Palonosetron: (Moderate) Netupitant is a moderate inhibitor of CYP3A4 and should be used with caution in patients receiving concomitant medications that are primarily metabolized through CYP3A4, such as dexamethasone. The plasma concentrations of CYP3A4 substrates can increase when co-administered with netupitant. The inhibitory effect on CYP3A4 can last for multiple days. A two-fold increase in the systemic exposure of dexamethasone was observed 4 days after single dose of netupitant. The duration of the effect was not studied beyond 4 days. If coadministration is necessary, decrease the dose of dexamethasone.
    Neuromuscular blockers: (Moderate) Caution and close monitoring are advised if corticosteroids and neuromuscular blockers are used together, particularly for long periods, due to enhanced neuromuscular blocking effects. In such patients, a peripheral nerve stimulator may be of value in monitoring the response. Concurrent use may increase the risk of acute myopathy. This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis. Elevation of creatine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years.
    Nilotinib: (Major) Avoid the concurrent use of nilotinib, a CYP3A4 substrate and moderate inhibitor and glycoprotein (P-gp) inhibitor, and dexamethasone, a CYP3A4 substrate and strong inducer and P-gp substrate. Decreased nilotinib concentrations are likely and increased dexamethasone levels may occur. Selecting an alternate agent with less potential for CYP3A4 induction is recommended. If use of both of these agents is required, increasing the nilotinib dosage will most likely not account for the loss of exposure based on the nonlinear pharmacokinetics of nilotinib.
    Nintedanib: (Major) Dexamethasone is a CYP3A4 inducer and nintedanib is a minor substrate of CYP3A4. Coadministration of nintedanib with CYP3A4 inducers such as dexamethasone should be avoided as these drugs may decrease exposure to nintedanib and compromise its efficacy. In addition, because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen.
    Nonsteroidal antiinflammatory drugs: (Moderate) Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged concomitant administration should be avoided. Concomitant use of corticosteroids appears to increase the risk of adverse GI events due to NSAIDs. Corticosteroids can have profound effects on sodium-potassium balance; NSAIDs also can affect sodium and fluid balance. Monitor serum potassium concentrations; potassium supplementation may be necessary. In addition, NSAIDs may mask fever, pain, swelling and other signs and symptoms of an infection; use NSAIDs with caution in patients receiving immunosuppressant dosages of corticosteroids. The Beers criteria recommends that this drug combination be avoided in older adults; if coadministration cannot be avoided, provide gastrointestinal protection.
    Ocrelizumab: (Moderate) Ocrelizumab has not been studied in combination with other immunosuppressive or immune modulating therapies used for the treatment of multiple sclerosis, including immunosuppressant doses of corticosteroids. Concomitant use of ocrelizumab with any of these therapies may increase the risk of immunosuppression. Monitor patients carefully for signs and symptoms of infection.
    Olaparib: (Major) Avoid the coadministration of olaparib with dexamethasone due to decreased olaparib exposure; if concomitant use is unavoidable, there is a potential for decreased efficacy of olaparib. Olaparib is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Coadministration with a moderate CYP3A inducer is predicted to decrease the AUC of olaparib by 60%.
    Ombitasvir; Paritaprevir; Ritonavir: (Severe) Concurrent administration of dexamethasone with dasabuvir; ombitasvir; paritaprevir; ritonavir or ombitasvir; paritaprevir; ritonavir is contraindicated. Taking these drugs together could result in elevated dexamethasone plasma concentrations and decreased concentrations of dasabuvir, paritaprevir, and ritonavir. Antiviral efficacy could be affected. Dexamethasone is a P-glycoprotein (P-gp) substrate and a CYP3A4 substrate/inducer. Ritonavir is a P-gp inhibitor and a CYP3A4 substrate/potent inhibitor. Both paritaprevir and dasabuvir (minor) are CYP3A4 substrates. (Moderate) Close monitoring of therapeutic and adverse effects is required when dexamethasone is coadministered with ritonavir. Ritonavir inhibits CYP3A4 and dexamethasone is a CYP3A4 substrate.
    Omeprazole: (Moderate) Monitor for decreased efficacy of omeprazole if coadministration with dexamethasone is necessary. Omeprazole is metabolized by CYP2C19 and CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. The manufacturer of omeprazole recommends avoidance with strong inducers because decreased exposure of omeprazole can occur. Recommendations are not available for concomitant use with moderate inducers of CYP3A4.
    Omeprazole; Sodium Bicarbonate: (Moderate) Monitor for decreased efficacy of omeprazole if coadministration with dexamethasone is necessary. Omeprazole is metabolized by CYP2C19 and CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. The manufacturer of omeprazole recommends avoidance with strong inducers because decreased exposure of omeprazole can occur. Recommendations are not available for concomitant use with moderate inducers of CYP3A4.
    Ondansetron: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together.
    Oritavancin: (Minor) Dexamethasone is metabolized by CYP3A4; oritavancin is a weak CYP3A4 inducer. Plasma concentrations and efficacy of dexamethasone may be reduced if these drugs are administered concurrently. Dosages of dexamethasone may require adjustment if oritavancin is initiated or withdrawn during dexamethasone therapy.
    Oxymetholone: (Moderate) Concomitant use of oxymetholone with corticosteroids or corticotropin, ACTH may cause increased edema. Manage edema with diuretic and/or digitalis therapy.
    Palbociclib: (Major) Use caution and monitor patients for decreased palbociclib efficacy if dexamethasone is used concomitantly with palbociclib. Palbociclib is a primary substrate of CYP3A and dexamethasone is a moderate CYP3A inducer. In a drug interaction study, coadministration of multiple daily doses of a moderate CYP3A inducer, modafinil, decreased the plasma exposure of a single dose of palbociclib in healthy patients by 32% and the Cmax by 11% (n = 14).
    Pancuronium: (Moderate) Caution and close monitoring are advised if corticosteroids and neuromuscular blockers are used together, particularly for long periods, due to enhanced neuromuscular blocking effects. In such patients, a peripheral nerve stimulator may be of value in monitoring the response. Concurrent use may increase the risk of acute myopathy. This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis. Elevation of creatine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years.
    Pazopanib: (Major) Avoid administering pazopanib in patients who require chronic treatment with a strong CYP3A4 inducer, such as dexamethasone. The concomitant use of pazopanib, a weak CYP3A4 inhibitor and a substrate for CYP3A4 and P-glycoprotein (P-gp), and dexamethasone, a strong CYP3A4 inducer and a CYP3A4and P-gp substrate, may result in altered pazopanib and/or dexamethasone concentrations. In addition, because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with antineoplastic agents. While therapy is designed to take advantage of this effect, patients may be predisposed to over-immunosuppression resulting in an increased risk for the development of severe infections. Close clinical monitoring is advised with concurrent use; in the presence of serious infections, continuation of the corticosteroid or immunosuppressive agent may be necessary but should be accompanied by appropriate antimicrobial therapies as indicated.
    Pegaspargase: (Moderate) Concomitant use of pegaspargase with corticosteroids can result in additive hyperglycemia. Insulin therapy may be required in some cases.
    Peginterferon Alfa-2a: (Moderate) Additive myelosuppressive effects may be seen when alpha interferons are given concurrently with other myelosuppressive agents, such as antineoplastic agents or immunosuppressives.
    Penicillamine: (Major) Agents such as immunosuppressives have adverse reactions similar to those of penicillamine. Concomitant use of penicillamine with these agents is contraindicated because of the increased risk of developing severe hematologic and renal toxicity.
    Perampanel: (Major) Start perampanel at a higher initial dose of 4 mg once daily at bedtime when using concurrently with dexamethasone due to a potential reduction in perampanel plasma concentration. If introduction or withdrawal of dexamethasone occurs during perampanel therapy, closely monitor patient response; a dosage adjustment may be necessary. Dexamethasone is a moderate CYP3A4 inducer, and perampanel is a CYP3A4 substrate.
    Perindopril; Amlodipine: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased.
    Phenobarbital: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Phenobarbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use.
    Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Phenylephrine; Promethazine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
    Phosphorus Salts: (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia.
    Photosensitizing agents: (Minor) Corticosteroids administered systemically prior to or concomitantly with photosensitizing agents may decrease the efficacy of photodynamic therapy.
    Physostigmine: (Minor) Corticosteroids may interact with cholinesterase inhibitors, occasionally causing severe muscle weakness in patients with myasthenia gravis. Glucocorticoids are occasionally used therapeutically, however, in the treatment of some patients with myasthenia gravis. In such patients, it is recommended that corticosteroid therapy be initiated at low dosages and with close clinical monitoring. The dosage should be increased gradually as tolerated, with continued careful monitoring of the patient's clinical status.
    Pimozide: (Moderate) Pimozide is associated with a well-established risk of QT prolongation and torsade de pointes (TdP). Use of pimozide and medications known to cause electrolyte imbalance may increase the risk of QT prolongation. Therefore, caution is advisable during concurrent use of pimozide and corticosteroids. Topical corticosteroids are less likely to interact. According to the manufacturer, potassium deficiencies should be correctly prior to treatment with pimozide and normalized potassium levels should be maintained during treatment.
    Posaconazole: (Moderate) Posaconazole and dexamethasone should be coadministered with caution due to an increased potential for adverse events. Posaconazole is a potent inhibitor of CYP3A4, an isoenzyme partially responsible for the metabolism of dexamethasone. Further, both dexamethasone and posaconazole are substrates of the drug efflux protein, P-glycoprotein, which when administered together may increase the absorption or decrease the clearance of the other drug. This complex interaction may cause alterations in the plasma concentrations of both posaconazole and dexamethasone, ultimately resulting in an increased risk of adverse events.
    Potassium Phosphate; Sodium Phosphate: (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia.
    Potassium Salts: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together.
    Potassium: (Moderate) Corticotropin can cause alterations in serum potassium levels. The use of potassium salts or supplements would be expected to alter the effects of corticotropin on serum potassium levels. Also, there have been reports of generalized tonic-clonic seizures and/or loss of consciousness associated with use of bowel preparation products in patients with no prior history of seizure disorder. Therefore, magnesium sulfate; potassium sulfate; sodium sulfate should be administered with caution during concurrent use of medications that lower the seizure threshold such as systemic corticosteroids.
    Potassium-sparing diuretics: (Minor) The manufacturer of spironolactone lists corticosteroids as a potential drug that interacts with spironolactone. Intensified electrolyte depletion, particularly hypokalemia, may occur. However, potassium-sparing diuretics such as spironolactone do not induce hypokalemia. In fact, hypokalemia is one of the indications for potassium-sparing diuretic therapy. Therefore, drugs that induce potassium loss, such as corticosteroids, could counter the hyperkalemic effects of potassium-sparing diuretics.
    Pramlintide: (Moderate) Systemic corticosteroids increase blood glucose levels. Because of this action, a potential pharmacodynamic interaction exists between corticosteroids and all antidiabetic agents. Diabetic patients who are administered systemic corticosteroid therapy may require an adjustment in the dosing of the antidiabetic agent.
    Prasterone, Dehydroepiandrosterone, DHEA (Dietary Supplements): (Moderate) Corticosteroids blunt the adrenal secretion of endogenous DHEA and DHEAS, resulting in reduced DHEA and DHEAS serum concentrations.
    Prasterone, Dehydroepiandrosterone, DHEA (FDA-approved): (Moderate) Corticosteroids blunt the adrenal secretion of endogenous DHEA and DHEAS, resulting in reduced DHEA and DHEAS serum concentrations.
    Praziquantel: (Moderate) Drugs that induce hepatic metabolism via the microsomal CYP450 enzyme system decrease the bioavailability of praziquantel. Plasma levels of praziquantel have been reported to be 50% lower when dexamethasone was given simultaneously, presumably due to CYP induction by dexamethasone.
    Primidone: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Primidone is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use.
    Propranolol: (Moderate) Patients receiving corticosteroids during propranolol therapy may be at increased risk of hypoglycemia due to the loss of counter-regulatory cortisol response. This effect may be more pronounced in infants and young children. If concurrent use is necessary, carefully monitor vital signs and blood glucose concentrations as clinically indicated.
    Purine analogs: (Minor) Concurrent use of purine analogs with other agents which cause bone marrow or immune suppression such as other antineoplastic agents or immunosuppressives may result in additive effects.
    Pyridostigmine: (Minor) Corticosteroids may interact with cholinesterase inhibitors including ambenonium, neostigmine, and pyridostigmine, occasionally causing severe muscle weakness in patients with myasthenia gravis. Glucocorticoids are occasionally used therapeutically, however, in the treatment of some patients with myasthenia gravis. In such patients, it is recommended that corticosteroid therapy be initiated at low dosages and with close clinical monitoring. The dosage should be increased gradually as tolerated, with continued careful monitoring of the patient's clinical status.
    Pyrimidine analogs: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Quetiapine: (Major) QT prolongation has occurred during concurrent use of quetiapine and medications known to cause electrolyte imbalance. Therefore, caution is advisable during concurrent use of quetiapine and corticosteroids.
    Quinidine: (Moderate) Quinidine is a substrate of the CYP3A4 isoenzyme. Inducers of CYP3A4 such as dexamethasone may increase hepatic elimination of quinidine with the potential for reduced efficacy of quinidine.
    Quinolones: (Moderate) Quinolones have been associated with an increased risk of tendon rupture requiring surgical repair or resulting in prolonged disability; this risk is further increased in those receiving concomitant corticosteroids. Discontinue quinolone therapy at the first sign of tendon inflammation or tendon pain, as these are symptoms that may precede rupture of the tendon.
    Rapacuronium: (Moderate) Caution and close monitoring are advised if corticosteroids and neuromuscular blockers are used together, particularly for long periods, due to enhanced neuromuscular blocking effects. In such patients, a peripheral nerve stimulator may be of value in monitoring the response. Concurrent use may increase the risk of acute myopathy. This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis. Elevation of creatine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years.
    Repaglinide: (Moderate) Drugs which may cause hyperglycemia, including corticosteroids, may cause temporary loss of glycemic control. Diabetic patients who are administered systemic corticosteroid therapy may require an adjustment in the dosing of the antidiabetic agent.
    Ribociclib: (Moderate) Use caution if coadministration of ribociclib with dexamethasone is necessary, as the systemic exposure of dexamethasone may be increased resulting in increase in treatment-related adverse reactions. Exposure to ribociclib may also decrease, resulting in decreased efficacy. Ribociclib is a moderate CYP3A4 inhibitor and CYP3A4 substrate; dexamethasone is a CYP3A4 substrate and inducer.
    Ribociclib; Letrozole: (Moderate) Use caution if coadministration of ribociclib with dexamethasone is necessary, as the systemic exposure of dexamethasone may be increased resulting in increase in treatment-related adverse reactions. Exposure to ribociclib may also decrease, resulting in decreased efficacy. Ribociclib is a moderate CYP3A4 inhibitor and CYP3A4 substrate; dexamethasone is a CYP3A4 substrate and inducer.
    Rifabutin: (Moderate) A dose adjustment of dexamethasone may be necessary when administered concurrently with rifamycins, due to the potential for decreased exposure of dexamethasone. Rifamycins are inducers of CYP3A4; dexamethasone is a CYP3A4 substrate
    Rifampin: (Moderate) A dose adjustment of dexamethasone may be necessary when administered concurrently with rifamycins, due to the potential for decreased exposure of dexamethasone. Rifamycins are inducers of CYP3A4; dexamethasone is a CYP3A4 substrate
    Rifamycins: (Moderate) A dose adjustment of dexamethasone may be necessary when administered concurrently with rifamycins, due to the potential for decreased exposure of dexamethasone. Rifamycins are inducers of CYP3A4; dexamethasone is a CYP3A4 substrate
    Rifapentine: (Moderate) A dose adjustment of dexamethasone may be necessary when administered concurrently with rifamycins, due to the potential for decreased exposure of dexamethasone. Rifamycins are inducers of CYP3A4; dexamethasone is a CYP3A4 substrate
    Rilonacept: (Moderate) Patients receiving immunosuppressives along with rilonacept may be at a greater risk of developing an infection.
    Rilpivirine: (Severe) Concurrent use of dexamethasone and rilpivirine is contraindicated. When these drugs are coadministered, there is a potential for treatment failure and/or the development of rilpivirine or NNRTI resistance. Dexamethasone is an inducer of CYP3A4, which is primarily responsible for the metabolism of rilpivirine. Coadministration may result in decreased rilpivirine serum concentrations, which could cause impaired virologic response to rilpivirine.
    Ritodrine: (Major) Ritodrine has caused maternal pulmonary edema, which appears more often in patients treated concomitantly with corticosteroids. Patients so treated should be closely monitored in the hospital.
    Ritonavir: (Moderate) Close monitoring of therapeutic and adverse effects is required when dexamethasone is coadministered with ritonavir. Ritonavir inhibits CYP3A4 and dexamethasone is a CYP3A4 substrate.
    Rituximab: (Moderate) Rituximab and corticosteroids are commonly used together; however, monitor the patient for immunosuppression and signs and symptoms of infection during combined chronic therapy.
    Rituximab; Hyaluronidase: (Moderate) Rituximab and corticosteroids are commonly used together; however, monitor the patient for immunosuppression and signs and symptoms of infection during combined chronic therapy.
    Rivaroxaban: (Minor) Coadministration of rivaroxaban and dexamethasone may result in decreased rivaroxaban exposure and may decrease the efficacy of rivaroxaban. Dexamethasone is an inducer of CYP3A4, and rivaroxaban is a substrate of CYP3A4. If these drugs are administered concurrently, monitor the patient for signs of lack of efficacy of rivaroxaban.
    Rocuronium: (Moderate) Caution and close monitoring are advised if corticosteroids and neuromuscular blockers are used together, particularly for long periods, due to enhanced neuromuscular blocking effects. In such patients, a peripheral nerve stimulator may be of value in monitoring the response. Concurrent use may increase the risk of acute myopathy. This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis. Elevation of creatine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years.
    Roflumilast: (Major) Coadminister dexamethasone and roflumilast cautiously as this may lead to reduced systemic exposure to roflumilast. Dexamethasone induces CYP3A4 and roflumilast is a CYP3A4 substrate. In pharmacokinetic study, administration of a single dose of roflumilast in patients receiving another CYP3A4 inducer, rifampin, resulted in decreased roflumilast Cmax and AUC, as well as increased Cmax and decreased AUC of the active metabolite roflumilast N-oxide.
    Romidepsin: (Major) The concomitant use of romidepsin, a CYP3A4 substrate, and dexamethasone, a strong CYP3A4 inducer, may result in significantly altered romidepsin plasma exposure. Therefore, avoid using romidepsin with potent CYP3A4 inducers if possible.
    Rotavirus Vaccine: (Severe) Live virus vaccines should generally not be administered to an immunosuppressed patient. Live virus vaccines may induce the illness they are intended to prevent and are generally contraindicated for use during immunosuppressive treatment. The immune response of the immunocompromised patient to vaccines may be decreased, even despite alternate vaccination schedules or more frequent booster doses. If immunization is necessary, choose an alternative to live vaccination, or, consider a delay or change in the immunization schedule. Practitioners should refer to the most recent CDC guidelines regarding vaccination of patients who are receiving drugs that adversely affect the immune system. Children who are receiving high doses of systemic corticosteroids (i.e., greater than or equal to 2 mg/kg prednisone orally per day) for 2 weeks or more may be vaccinated after steroid therapy has been discontinued for at least 3 months in accordance with general recommendations for the use of live-virus vaccines. The CDC has stated that discontinuation of steroids for 1 month prior to varicella virus vaccine live administration may be sufficient. Budesonide may affect the immunogenicity of live vaccines. An open-label study examined the immune responsiveness to varicella vaccine in 243 pediatric asthma patients who were treated with budesonide inhalation suspension 0.251 mg daily (n = 151) or non-corticosteroid asthma therapy (n = 92). The percentage of patients developing a seroprotective antibody titer of at least 5 (gpELISA value) in response to the vaccination was slightly lower in patients treated with budesonide compared to patients treated with non-corticosteroid asthma therapy (85% vs. 90%). Even though no patient treated with budesonide inhalation suspension developed chicken pox because of vaccination, live-virus vaccines should not be given to individuals who are considered to be immunocompromised until more information is available.
    Rubella Virus Vaccine Live: (Severe) Live virus vaccines should generally not be administered to an immunosuppressed patient. Live virus vaccines may induce the illness they are intended to prevent and are generally contraindicated for use during immunosuppressive treatment. The immune response of the immunocompromised patient to vaccines may be decreased, even despite alternate vaccination schedules or more frequent booster doses. If immunization is necessary, choose an alternative to live vaccination, or, consider a delay or change in the immunization schedule. Practitioners should refer to the most recent CDC guidelines regarding vaccination of patients who are receiving drugs that adversely affect the immune system. Children who are receiving high doses of systemic corticosteroids (i.e., greater than or equal to 2 mg/kg prednisone orally per day) for 2 weeks or more may be vaccinated after steroid therapy has been discontinued for at least 3 months in accordance with general recommendations for the use of live-virus vaccines. The CDC has stated that discontinuation of steroids for 1 month prior to varicella virus vaccine live administration may be sufficient. Budesonide may affect the immunogenicity of live vaccines. An open-label study examined the immune responsiveness to varicella vaccine in 243 pediatric asthma patients who were treated with budesonide inhalation suspension 0.251 mg daily (n = 151) or non-corticosteroid asthma therapy (n = 92). The percentage of patients developing a seroprotective antibody titer of at least 5 (gpELISA value) in response to the vaccination was slightly lower in patients treated with budesonide compared to patients treated with non-corticosteroid asthma therapy (85% vs. 90%). Even though no patient treated with budesonide inhalation suspension developed chicken pox because of vaccination, live-virus vaccines should not be given to individuals who are considered to be immunocompromised until more information is available.
    Ruxolitinib: (Moderate) Ruxolitinib is a CYP3A4 substrate. When used with drugs that are CYP3A4 inducers such as dexamethasone, a dose adjustment is not necessary, but closely monitor patients and titrate the ruxolitinib dose based on safety and efficacy. The Cmax and AUC of a single 50 mg dose of ruxolitinib was decreased by 32% and 61%, respectively, after rifampin 600 mg once daily was administered for 10 days. The relative exposure to ruxolitinib's active metabolites increased by about 100%, which may partially explain the reported disproportionate 10% reduction in the pharmacodynamic marker pSTAT3 inhibition.
    Salicylates: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
    Salsalate: (Moderate) Salicylates or NSAIDs should be used cautiously in patients receiving corticosteroids. While there is controversy regarding the ulcerogenic potential of corticosteroids alone, concomitant administration of corticosteroids with aspirin may increase the GI toxicity of aspirin and other non-acetylated salicylates. Withdrawal of corticosteroids can result in increased plasma concentrations of salicylate and possible toxicity. Concomitant use of corticosteroids may increase the risk of adverse GI events due to NSAIDs. Although some patients may need to be given corticosteroids and NSAIDs concomitantly, which can be done successfully for short periods of time without sequelae, prolonged coadministration should be avoided.
    Sapropterin: (Moderate) Caution is advised with the concomitant use of sapropterin and dexamethasone as coadministration may result in increased systemic exposure of dexamethasone. Dexamethasone is a substrate for the drug transporter P-glycoprotein (P-gp); in vitro data show that sapropterin may inhibit P-gp. If these drugs are used together, closely monitor for increased side effects of dexamethasone.
    Saquinavir: (Major) Avoid concurrent administration of dexamethasone and saquinavir boosted with ritonavir. Dexamethasone is may induce the CYP3A4 metabolism of saquinavir, resulting in reduced saquinavir plasma concentrations. Decreased saquinavir plasma concentrations could lead to HIV treatment failures or the development of viral-resistance. If used concomitantly, the patient should be observed for changes in the clinical efficacy and concentrations of the antiretroviral regimen.
    Saxagliptin: (Moderate) Systemic corticosteroids increase blood glucose levels. Diabetic patients who are administered systemic corticosteroid therapy may require an adjustment in the dosing of the antidiabetic agent.
    Sildenafil: (Minor) Sildenafil is metabolized principally by CYP3A4. It can be expected that concomitant administration of sildenafil with CYP3A4 enzyme inducers like dexamethasone will decrease plasma concentrations of sildenafil.
    Simeprevir: (Major) Avoid concurrent use of simeprevir and systemic dexamethasone. Induction of CYP3A4 by dexamethasone may reduce the plasma concentrations of simeprevir, resulting in treatment failure.
    Simvastatin; Sitagliptin: (Moderate) Systemic corticosteroids increase blood glucose levels. Diabetic patients who are administered systemic corticosteroid therapy may require an adjustment in the dosing of the antidiabetic agent.
    Sipuleucel-T: (Major) Concomitant use of sipuleucel-T and immunosuppressives should be avoided. Concurrent administration of immunosuppressives with the leukapheresis procedure that occurs prior to sipuleucel-T infusion has not been studied. Sipuleucel-T stimulates the immune system and patients receiving immunosuppressives may have a diminished response to sipuleucel-T. When appropriate, consider discontinuing or reducing the dose of immunosuppressives prior to initiating therapy with sipuleucel-T.
    Sirolimus: (Major) Dexamethasone is an inducer of CYP3A4. Sirolimus is extensively metabolized by CYP3A4 in the gut and liver. Concurrent use of sirolimus with dexamethasone may decrease patient exposure to sirolimus. Consider alternative steroid therapy. Use sirolimus and dexamethasone with caution, if at all, and monitor patients closely.
    Sitagliptin: (Moderate) Systemic corticosteroids increase blood glucose levels. Diabetic patients who are administered systemic corticosteroid therapy may require an adjustment in the dosing of the antidiabetic agent.
    Smallpox Vaccine, Vaccinia Vaccine: (Severe) Live virus vaccines should generally not be administered to an immunosuppressed patient. Live virus vaccines may induce the illness they are intended to prevent and are generally contraindicated for use during immunosuppressive treatment. The immune response of the immunocompromised patient to vaccines may be decreased, even despite alternate vaccination schedules or more frequent booster doses. If immunization is necessary, choose an alternative to live vaccination, or, consider a delay or change in the immunization schedule. Practitioners should refer to the most recent CDC guidelines regarding vaccination of patients who are receiving drugs that adversely affect the immune system. Children who are receiving high doses of systemic corticosteroids (i.e., greater than or equal to 2 mg/kg prednisone orally per day) for 2 weeks or more may be vaccinated after steroid therapy has been discontinued for at least 3 months in accordance with general recommendations for the use of live-virus vaccines. The CDC has stated that discontinuation of steroids for 1 month prior to varicella virus vaccine live administration may be sufficient. Budesonide may affect the immunogenicity of live vaccines. An open-label study examined the immune responsiveness to varicella vaccine in 243 pediatric asthma patients who were treated with budesonide inhalation suspension 0.251 mg daily (n = 151) or non-corticosteroid asthma therapy (n = 92). The percentage of patients developing a seroprotective antibody titer of at least 5 (gpELISA value) in response to the vaccination was slightly lower in patients treated with budesonide compared to patients treated with non-corticosteroid asthma therapy (85% vs. 90%). Even though no patient treated with budesonide inhalation suspension developed chicken pox because of vaccination, live-virus vaccines should not be given to individuals who are considered to be immunocompromised until more information is available.
    Sodium Benzoate; Sodium Phenylacetate: (Moderate) Corticosteroids may cause protein breakdown, which could lead to elevated blood ammonia concentrations, especially in patients with an impaired ability to form urea. Corticosteroids should be used with caution in patients receiving treatment for hyperammonemia.
    Sodium Chloride: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together.
    Sodium Phenylbutyrate: (Moderate) The concurrent use of corticosteroids with sodium phenylbutyrate may increase plasma ammonia levels (hyperammonemia) by causing the breakdown of body protein. Patients with urea cycle disorders being treated with sodium phenylbutyrate usually should not receive regular treatment with corticosteroids.
    Sofosbuvir; Velpatasvir: (Major) Avoid coadministration of velpatasvir with dexamethasone. Taking these drugs together may significantly decrease velpatasvir plasma concentrations, potentially resulting in loss of antiviral efficacy. Velpatasvir is a CYP3A4 substrate; dexamethasone a moderate inducer of CYP3A4. Additionally, velpatasvir is an inhibitor of the drug transporter P-glycoprotein (P-gp). Coadministration with substrates of this transporter, such as dexamethasone, may increase their exposure.
    Sofosbuvir; Velpatasvir; Voxilaprevir: (Major) Avoid coadministration of velpatasvir with dexamethasone. Taking these drugs together may significantly decrease velpatasvir plasma concentrations, potentially resulting in loss of antiviral efficacy. Velpatasvir is a CYP3A4 substrate; dexamethasone a moderate inducer of CYP3A4. Additionally, velpatasvir is an inhibitor of the drug transporter P-glycoprotein (P-gp). Coadministration with substrates of this transporter, such as dexamethasone, may increase their exposure. (Major) Avoid coadministration of voxilaprevir (a CYP3A4 substrate) with moderate to strong inducers of CYP3A4, such as dexamethasone. Taking these drugs together may significantly decrease voxilaprevir plasma concentrations, potentially resulting in loss of antiviral efficacy. In addition, voxilaprevir, a P-glycoprotein (P-gp) inhibitor, may alter concentrations of dexamethasone, a P-gp substrate.
    Somatropin, rh-GH: (Moderate) Corticosteroids can retard bone growth and therefore, can inhibit the growth-promoting effects of somatropin. If corticosteroid therapy is required, the corticosteroid dose should be carefully adjusted.
    Sonidegib: (Major) Avoid the concomitant use of sonidegib and dexamethasone; sonidegib levels may be significantly decreased and its efficacy reduced. Sonidegib is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Physiologic-based pharmacokinetics (PBPK) simulations indicate that the sonidegib geometric mean steady-state AUC (0-24 hours) would decrease by 56% in cancer patients who received 14 days of sonidegib 200 mg/day with a moderate CYP3A inducer. Additionally, the PBPK model predicts that the sonidegib geometric mean steady-state AUC (0-24 hours) would decrease by 69% in cancer patients who received sonidegib 200 mg/day with a moderate CYP3A inducer for 4 months.
    Sorafenib: (Major) Sorafenib is a CYP3A4 substrate, and concomitant use with a strong CYP3A4 inducer such as dexamethasone may lead to reduced sorafenib concentrations. For example, concurrent use of sorafenib and the CYP3A4 inducer rifampicin resulted in an average 37% reduction in the sorafenib AUC. Avoid the use of sorafenib with a strong CYP3A4 inducer. If a strong CYP3A4 inducer must be coadministered with sorafenib, consider a sorafenib dose increase
    Succinylcholine: (Moderate) Caution and close monitoring are advised if corticosteroids and neuromuscular blockers are used together, particularly for long periods, due to enhanced neuromuscular blocking effects. In such patients, a peripheral nerve stimulator may be of value in monitoring the response. Concurrent use may increase the risk of acute myopathy. This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis. Elevation of creatine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years.
    Sulfonylureas: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Sunitinib: (Major) Concurrent administration of sunitinib with strong inducers of CYP3A4 such as dexamethasone results in decreased concentrations of sunitinib and its primary active metabolite. Whenever possible selection of an alternative concomitant medication with no or minimal enzyme inhibition potential is recommended. A dosage increase should be considered when sunitinib must be administered concurrently with strong CYP3A4 inducers.
    Tadalafil: (Minor) Tadalafil is metabolized principally by cytochrome P450 3A4. Studies have shown that concomitant administration of CYP3A4 enzyme-inducers, such as dexamethasone, will decrease plasma levels of tadalafil.
    Tamoxifen: (Major) Concomitant use of dexamethasone and tamoxifen may result in decreased concentrations of tamoxifen and its active metabolites, which may compromise efficacy. Monitor patients for changes in therapeutic effect of tamoxifen. Dexamethasone is a moderate CYP3A4 inducer. Tamoxifen is metabolized by CYP3A4, CYP2D6, and to a lesser extent by both CYP2C9 and CYP2C19, to other potent, active metabolites including endoxifen, which have up to 33 times more affinity for the estrogen receptor than tamoxifen. These metabolites are then inactivated by sulfotransferase 1A1 (SULT1A1). Plasma concentrations of tamoxifen and its active metabolites have been reduced when coadministered with other CYP3A4 inducers.
    Tasimelteon: (Moderate) Caution is recommended during concurrent use of tasimelteon and dexamethasone. Because tasimelteon is partially metabolized via CYP3A4, use with CYP3A4 inducers, such as dexamethasone, may reduce the efficacy of tasimelteon.
    Taxanes: (Moderate) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. In addition, Cabazitaxel is a CYP3A4 substrate and concomitant use with strong CYP3A4 inducers such as dexamethasone may lead to reduced concentrations of cabazitaxel. Avoid concomitant use of cabazitaxel and strong CYP3A4 inducers. Consider alternative therapies with low enzyme induction potential.
    Telaprevir: (Moderate) Coadministration of dexamethasone and telaprevir is not recommended. If coadministered, close clinical monitoring for increased dexamethasone-related adverse events and for decreased telaprevir efficacy is advised. If dexamethasone dose adjustments are made, re-adjust the dose upon completion of telaprevir treatment. Predictions about the interaction can be made based on the metabolic pathways of dexamethasone and telaprevir. Dexamethasone is an inducer and substrate of the hepatic isoenzyme CYP3A4; telaprevir is an inhibitor and substrate of this isoenzyme. Additionally, both dexamethasone and telaprevir are substrates for the drug efflux transporter P-glycoprotein (PGP). When used in combination, the plasma concentrations of dexamethasone may be elevated and the plasma concentration of telaprevir may be deceased, resulting in an increased potential for dexamethasone-related adverse events and telaprevir treatment failure.
    Telbivudine: (Moderate) The risk of myopathy may be increased if corticosteroids are coadministered with telbivudine. Monitor patients for any signs or symptoms of unexplained muscle pain, tenderness, or weakness, particularly during periods of upward dosage titration.
    Telithromycin: (Major) Concentrations of dexamethasone may be increased and concentrations of telithromycin may be decreased with coadministration. Dexamethasone is a CYP3A4 and P-glycoprotein (PGP) substrate and telithromycin is a strong CYP3A4 inhibitor and potential PGP inhibitor. Additionally, dexamethasone is a CYP3A4 inducer, while telithromycin is CYP3A4 substrate.
    Telotristat Ethyl: (Moderate) Use caution if coadministration of telotristat ethyl and dexamethasone is necessary, as the systemic exposure of dexamethasone may be decreased resulting in reduced efficacy. If these drugs are used together, monitor patients for suboptimal efficacy of dexamethasone; consider increasing the dose of dexamethasone if necessary. Dexamethasone is a CYP3A4 substrate. The mean Cmax and AUC of another sensitive CYP3A4 substrate was decreased by 25% and 48%, respectively, when coadministered with telotristat ethyl; the mechanism of this interaction appears to be that telotristat ethyl increases the glucuronidation of the CYP3A4 substrate.
    Temsirolimus: (Major) Avoid coadministration of temsirolimus with dexamethasone due to the risk of decreased efficacy of temsirolimus. If concomitant use cannot be avoided, consider increasing the dose of temsirolimus from 25 mg per week up to 50 mg per week. If dexamethasone is discontinued, decrease the dose of temsirolimus to the dose used before initiation of dexamethasone. Temsirolimus is a CYP3A4 substrate and dexamethasone is a CYP3A4 inducer. Coadministration of temsirolimus with rifampin, a strong CYP3A4 inducer, had no significant effect on the AUC or Cmax of temsirolimus, but decreased the sirolimus AUC and Cmax by 56% and 65%, respectively.
    Terbinafine: (Moderate) Due to the risk for breakthrough fungal infections, caution is advised when administering terbinafine with dexamethasone. Although this interaction has not been studied by the manufacturer, and published literature suggests the potential for interactions to be low, taking these drugs together may decrease the systemic exposure of terbinafine. Predictions about the interaction can be made based on the metabolic pathways of both drugs. Terbinafine is metabolized by at least 7 CYP isoenyzmes, with major contributions coming from CYP3A4; dexamethasone induces this enzyme. Monitor patients for breakthrough fungal infections.
    Testosterone: (Moderate) Coadministration of corticosteroids and testosterone may increase the risk of edema, especially in patients with underlying cardiac or hepatic disease. Corticosteroids with greater mineralocorticoid activity, such as fludrocortisone, may be more likely to cause edema. Administer these drugs in combination with caution.
    Thalidomide: (Moderate) Coadministration of dexamethasone with thalidomide should be employed cautiously, as toxic epidermal necrolysis has been reported with concomitant use.
    Thiazide diuretics: (Moderate) Additive hypokalemia may occur when non-potassium sparing diuretics, including thiazide diuretics, are coadministered with other drugs with a significant risk of hypokalemia, such as corticosteroids. Monitoring serum potassium levels and cardiac function is advised, and potassium supplementation may be required.
    Thiazolidinediones: (Moderate) Drugs which may cause hyperglycemia, including corticosteroids, may cause temporary loss of glycemic control. Diabetic patients who are administered systemic corticosteroid therapy may require an adjustment in the dosing of the antidiabetic agent.
    Thyroid hormones: (Moderate) The metabolism of corticosteroids is increased in hyperthyroidism and decreased in hypothyroidism. Dosage adjustments may be necessary when initiating, changing or discontinuing thyroid hormones or antithyroid agents.
    Ticagrelor: (Moderate) Coadministration of ticagrelor with dexamethasone may result in decreased concentrations of ticagrelor. Use combination with caution and monitor for decreased efficacy of ticagrelor. Ticagrelor is a substrate of CYP3A4/5 and dexamethasone is a moderate CYP3A4 inducer.
    Tobramycin: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium chloride intake from all sources, including intake from sodium-containing intravenous fluids and antibiotic admixtures. Carefully monitor sodium concentrations and fluid status if sodium-containing drugs and corticosteroids must be used together.
    Tocilizumab: (Moderate) Closely observe patients for signs of infection if biologic agents are used concomitantly. Most patients taking tocilizumab who developed serious infections were taking concomitant immunosuppressives such as systemic corticosteroids.
    Tofacitinib: (Major) Dexamethasone is a CYP3A4 inducer, and tofacitinib exposure is decreased when coadministered with potent CYP3A4 inducers. A loss of response or reduced clinical response to tofacitinib may occur.
    Tolazamide: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Tolbutamide: (Moderate) Endogenous counter-regulatory hormones such as glucocorticoids are released in response to hypoglycemia. When released, blood glucose concentrations rise. When corticosteroids are administered exogenously, increases in blood glucose concentrations would be expected thereby decreasing the hypoglycemic effect of antidiabetic agents. Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Tolvaptan: (Major) Tolvaptan is metabolized by CYP3A4. Dexamethasone is an inducer of CYP3A4. Coadministration of CYP3A4 inducers, such as dexamethasone, with tolvaptan may result in reduced plasma concentration and subsequent reduced effectiveness of tolvaptan therapy and should be avoided. If coadministration is unavoidable, an increase in the tolvaptan dose may be necessary and patients should be monitored for decreased effectiveness of tolvaptan. Additionally, the potassium-wasting effects of corticosteroid therapy can be exacerbated by concomitant administration of other potassium-depleting drugs including diuretics. Serum potassium levels should be monitored in patients receiving these drugs concomitantly.
    Tositumomab: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Trabectedin: (Moderate) Use caution if coadministration of trabectedin and dexamethasone is necessary, due to the risk of decreased trabectedin exposure. Trabectedin is a CYP3A substrate and dexamethasone is a moderate CYP3A inducer. Coadministration with rifampin (600 mg daily for 6 days), a strong CYP3A inducer, decreased the systemic exposure of a single dose of trabectedin by 31% and the Cmax by 21% compared to a single dose of trabectedin given alone. The manufacturer of trabectedin recommends avoidance of coadministration with strong CYP3A inducers; there are no recommendations for concomitant use of moderate or weak CYP3A inducers.
    Trastuzumab: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Tretinoin, ATRA: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
    Tuberculin Purified Protein Derivative, PPD: (Moderate) Immunosuppressives may decrease the immunological response to tuberculin purified protein derivative, PPD. This suppressed reactivity can persist for up to 6 weeks after treatment discontinuation. Consider deferring the skin test until completion of the immunosuppressive therapy.
    Tubocurarine: (Moderate) Caution and close monitoring are advised if corticosteroids and neuromuscular blockers are used together, particularly for long periods, due to enhanced neuromuscular blocking effects. In such patients, a peripheral nerve stimulator may be of value in monitoring the response. Concurrent use may increase the risk of acute myopathy. This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis. Elevation of creatine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years.
    Typhoid Vaccine: (Severe) Live virus vaccines should generally not be administered to an immunosuppressed patient. Live virus vaccines may induce the illness they are intended to prevent and are generally contraindicated for use during immunosuppressive treatment. The immune response of the immunocompromised patient to vaccines may be decreased, even despite alternate vaccination schedules or more frequent booster doses. If immunization is necessary, choose an alternative to live vaccination, or, consider a delay or change in the immunization schedule. Practitioners should refer to the most recent CDC guidelines regarding vaccination of patients who are receiving drugs that adversely affect the immune system. Children who are receiving high doses of systemic corticosteroids (i.e., greater than or equal to 2 mg/kg prednisone orally per day) for 2 weeks or more may be vaccinated after steroid therapy has been discontinued for at least 3 months in accordance with general recommendations for the use of live-virus vaccines. The CDC has stated that discontinuation of steroids for 1 month prior to varicella virus vaccine live administration may be sufficient. Budesonide may affect the immunogenicity of live vaccines. An open-label study examined the immune responsiveness to varicella vaccine in 243 pediatric asthma patients who were treated with budesonide inhalation suspension 0.251 mg daily (n = 151) or non-corticosteroid asthma therapy (n = 92). The percentage of patients developing a seroprotective antibody titer of at least 5 (gpELISA value) in response to the vaccination was slightly lower in patients treated with budesonide compared to patients treated with non-corticosteroid asthma therapy (85% vs. 90%). Even though no patient treated with budesonide inhalation suspension developed chicken pox because of vaccination, live-virus vaccines should not be given to individuals who are considered to be immunocompromised until more information is available.
    Ulipristal: (Moderate) Ulipristal is a substrate of CYP3A4 and dexamethasone is a CYP3A4 inducer. Concomitant use may decrease the plasma concentration and effectiveness of ulipristal.
    Vancomycin: (Moderate) Concomitant use of systemic sodium chloride, especially at high doses, and corticosteroids may result in sodium and fluid retention. Assess sodium c