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  • CLASSES

    Systemic Corticosteroids, Plain

    DEA CLASS

    Rx

    DESCRIPTION

    Oral corticosteroid; metabolized in the liver to its active form, prednisolone; 4 times as potent as hydrocortisone; intermediate between hydrocortisone and dexamethasone in duration of action; has very little mineralocorticoid activity.

    COMMON BRAND NAMES

    Deltasone, Predone, RAYOS, Sterapred, Sterapred DS

    HOW SUPPLIED

    Deltasone/Prednisone/Predone/Sterapred/Sterapred DS Oral Tab: 1mg, 2.5mg, 5mg, 10mg, 20mg, 50mg
    Prednisone Oral Sol: 1mL, 5mg, 5mL
    RAYOS Oral Tab DR: 1mg, 2mg, 5mg

    DOSAGE & INDICATIONS

    For maintenance therapy (i.e., replacement therapy) of primary (Addison's disease) or secondary adrenocortical insufficiency.
    Oral dosage
    Adults

    5 mg PO in the morning and 2.5 mg PO in the evening. For acute conditions, parenteral steroid therapy is recommended initially. NOTE: Hydrocortisone and cortisone are the preferred agents; prednisone has little to no mineralocorticoid properties.

    Adolescents and Children

    4 mg/m2 to 5 mg/m2 PO given 1 to 4 times per day. For acute conditions, parenteral steroid therapy is recommended initially. NOTE: Hydrocortisone and cortisone are the preferred agents; prednisone has little to no mineralocorticoid properties.

    For the treatment of congenital adrenal hyperplasia.
    Oral dosage
    Adults

    2.5 mg to 5 mg PO once daily at bedtime.

    Children and Adolescents

    12 mg/m2 to 13 mg/m2 PO per day administered in 2 to 3 divided doses. NOTE: Hydrocortisone is the preferred glucocorticoid in infants.

    For kidney transplant rejection prophylaxis.
    Oral dosage
    Adults

    Titrate to response. The usual range is 5 mg to 30 mg PO once daily. Renal transplant guidelines recommend a calcineurin inhibitor (CNI) such as tacrolimus and an antiproliferative agent such as mycophenolate plus or minus corticosteroids for initial prophylaxis. In patients at low immunologic risk who receive induction therapy, corticosteroid discontinuation during first week after transplantation is suggested. Some evidence exists that steroids may be safely stopped in most patients after 3 to 12 months on combination therapy with a CNI and mycophenolate. Data suggest that the risk of steroid withdrawal depends on the use of concomitant immunosuppressives, immunological risk, ethnicity, and time after transplantation.

    For the treatment of chronic graft-versus-host disease (GVHD).
    Oral dosage
    Adults

    Prednisone alternating with cyclosporine has been recommended at doses of prednisone 1 mg/kg/day PO plus cyclosporine (10 mg/kg/day PO in 2 divided doses) based on actual or ideal body weight, whichever is lower. After 2 weeks if no disease progression is noted, the prednisone dose is tapered by 25% per week to 1 mg/kg of prednisone on alternate days. Once the prednisone taper is completed without a flare, the cyclosporine dose is tapered to alternate day dosing such that the patient is taking prednisone one day and cyclosporine the next day. Once patients reach their maximal response, therapy is continued for another 3 months and then tapered.

    For palliative management of acute lymphocytic leukemia (ALL).
    Oral dosage
    Adults

    40 mg/m2 to 50 mg/m2 PO once daily indefinitely.

    For the treatment of chronic lymphocytic leukemia (CLL).
    For the first-line treatment of CLL, in combination with cladribine†.
    Oral dosage
    Adults

    30 mg/m2 PO daily for 5 days in combination with cladribine 0.12 mg/kg/day IV over 2 hours for 5 days repeated every 28 days for up to 6 cycles has been studied in a randomized trial. NOTE: Prednisone is approved for the palliative treatment; however, all components of combination regimens may not have been evaluated by the FDA for the treatment of CLL.

    For the first-line treatment of CLL, in combination with chlorambucil†.
    Oral dosage
    Adults

    80 mg PO once daily on Day 1, Day 2, Day 3, Day 4, and Day 5 in combination with chlorambucil 30 mg/m2 PO on Day 1 repeated every 2 weeks for up to 18 months and maximum response was evaluated in a randomized study. Alternatively, prednisone 30 mg/m2 PO daily for 7 days plus chlorambucil 12 mg/m2 PO daily for 7 days repeated every 28 days for up to 6 courses was used in another randomized study. NOTE: Prednisone is approved for the palliative treatment of CLL; however, all components of combination regimens may not have been evaluated by the FDA for the treatment of CLL.

    For the palliative treatment of CLL.
    Oral dosage
    Adults

    Multiple dosage regimens have been studied. Initial dosage may vary from 5 mg/day to 60 mg/day PO. Dosage requirements are variable though and should be individualized based on the response of the patient and tolerance to treatment. NOTE: Prednisone is approved for the palliative treatment of CLL; however, all components of combination regimens may not have been evaluated by the FDA for the treatment of CLL.

    For the short-term treatment of hypercalcemia secondary to neoplastic disease.
    Oral dosage
    Adults

    50 mg/day to 100 mg/day PO for 3 to 5 days is usually effective for hypercalcemia due to hematologic cancers, lower doses may be effective for some tumors.

    For the treatment of inflammatory bowel disease, including Crohn's disease and ulcerative colitis.
    For short-term treatment of acute exacerbations of Crohn's disease.
    Oral dosage
    Adults

    Initially, 40 mg/day to 60 mg/day PO, adjusted to response. While evidence that maintenance therapy prevents recurrences is lacking, a substantial percentage of patients require chronic dosing (e.g., 5 mg/day to 15 mg/day PO). Corticosteroids for Crohn's disease are more effective for small-bowel involvement than for colonic involvement. Because of the potential complications of steroid use in this disease, steroids should be used selectively and in the lowest dose possible.

    For short-term treatment of acute exacerbations of ulcerative colitis.
    Oral dosage
    Adults

    Initially, 40 mg/day to 60 mg/day PO has been shown to be superior to 20 mg/day PO. Maximum dosage is 1 mg/kg/day PO. Improvement is usually noted after 7 to 10 days. Taper dose over the next 2 to 3 months and discontinue. Once clinical remission is achieved, discontinue prednisone since there is no evidence that maintenance therapy prevents recurrences.

    For the treatment of rheumatic conditions such as rheumatoid arthritis, juvenile rheumatoid arthritis (JRA)/juvenile idiopathic arthritis (JIA), psoriatic arthritis, ankylosing spondylitis, acute and subacute bursitis, acute non-specific tenosynovitis, acute gouty arthritis and gout, osteoarthritis, or epicondylitis.
    Oral dosage
    Adults

    Titrate to response. Usual dosage ranges from 5 to 30 mg PO once daily.

    Children and Adolescents

    0.05 mg/kg/day to 2 mg/kg/day PO given in 1 to 4 divided doses.

    For the treatment of systemic autoimmune conditions such as acquired hemolytic anemia, congenital hypoplastic anemia, mycosis fungoides, pemphigus, symptomatic sarcoidosis, or nonsuppurative thyroiditis.
    Oral dosage
    Adults

    Titrate to response. Usual dosage ranges from 5 mg to 30 mg PO once daily.

    For the treatment of asthma.
    For a moderate to severe asthma exacerbation in the emergency department or the hospital.
    Oral dosage
    Adults and Adolescents

    The National Asthma Education and Prevention Expert Panel (NAEPP) recommends 40 mg to 80 mg PO per day in 1 to 2 divided doses until the peak expiratory flow (PEF) reaches 70% of predicted or personal best. Total course of treatment may range from 3 to 10 days.

    Children

    The National Asthma Education and Prevention Expert Panel (NAEPP) recommends 1 mg/kg (up to 60 mg) PO per day in 2 divided doses until peak expiratory flow (PEF) reaches 70% of predicted or personal best. If a patient is given systemic corticosteroids, continue PO corticosteroids for a total course of 3 to 10 days. Tapering is not necessary for courses less than 1 week.

    For an acute asthma exacerbation on an outpatient basis in selected patients.
    Oral dosage
    Adults and Adolescents

    The National Asthma Education and Prevention Expert Panel (NAEPP) recommends 40 mg to 60 mg PO per day as a single dose or in 2 divided doses for 3 to 10 days.

    Children 5 to 12 years

    The National Asthma Education and Prevention Expert Panel (NAEPP) recommends 1 mg/kg to 2 mg/kg (up to 60 mg) PO per day in 2 divided doses for 3 to 10 days.

    Infants and Children 4 years and younger

    The National Asthma Education and Prevention Expert Panel (NAEPP) recommends 1 mg/kg to 2 mg/kg (up to 30 mg) PO per day in 2 divided doses for 3 to 10 days.

    For long-term prevention of symptoms in severe persistent asthma.
    Oral dosage
    Adults, Adolescents, and Children 12 years and older

    The National Asthma Education and Prevention Expert Panel (NAEPP) recommends 7.5 mg to 60 mg PO administered once daily in the morning or every other day. Taper to the lowest effective dose. One study indicates that administering the dose in the afternoon at 3 P.M. may increase efficacy, with no increase in adrenal suppression.

    Infants and Children 11 years and younger

    The National Asthma Education and Prevention Expert Panel (NAEPP) recommends 0.25 mg/kg to 2 mg/kg PO as a single dose each morning or every other day. Doses of 1 mg/kg/day or less may cause fewer behavioral adverse effects. Alternate day therapy may produce less adrenal suppression. Once stable, taper to the lowest effective dose.

    For the treatment of thrombocytopenia or idiopathic thrombocytopenic purpura (ITP).
    In patients with chronic immune thrombocytopenia/idiopathic thrombocytopenic purpura (ITP).
    Oral dosage
    Adults

    Initially, 1 mg/kg PO once daily; however, lower doses of 5 mg/day to 10 mg/day PO are preferable for long-term treatment.

    For autoimmune thrombocytopenia associated with SLE.
    Oral dosage
    Adults, Adolescents, and Children

    0.25 mg/kg/day PO was as effective as higher doses of 1 mg/kg/day.

    For the treatment of acute, severe urticaria or the treatment of late-phase angioedema, such as ACE-inhibitor induced angioedema once acute symptoms are controlled.
    Oral dosage
    Adults

    Short courses of 30 mg/day to 50 mg/day PO can be given during the late phase of an acute reaction, once oral therapy is appropriate.

    For the treatment of myasthenia gravis in patients who are poorly controlled with cholinesterase inhibitor therapy.
    Oral dosage
    Adults

    Initially, 15 mg/day to 20 mg/day PO. Increase by 5 mg every 2 to 3 days as needed. Maximum: 60 mg/day PO. For chronic use, may change to every other day therapy.

    For the treatment of nephrotic syndrome or to treat lupus nephritis.
    For the treatment of lupus nephritis.
    Oral dosage
    Adults

    0.5 mg/kg/day to 1 mg/kg/day PO (1 mg/kg/day recommended if crescents seen) after methylprednisolone 500 mg/day to 1000 mg/day IV for 3 doses in combination with either cyclophosphamide or mycophenolate for induction therapy of class III/IV disease. Insufficient data exist to recommend a specific steroid taper because nephritis and extrarenal manifestations vary from patient to patient; however, taper the dose after a few weeks to lowest effective dose. If improved after induction, a recommended option for maintenance is azathioprine or mycophenolate plus or minus low-dose daily glucocorticoid up to 10 mg/day PO prednisone. For class V disease without proliferative changes and with proteinuria greater than 3 grams/24 hours, use 0.5 mg/kg/day PO plus mycophenolate mofetil. For patients who do NOT improve, a dose of 0.5 mg/kg/day to 1 mg/kg/day PO is recommended after a glucocorticoid pulse along with cyclophosphamide. Doses required to suppress activity potentially with azathioprine are recommended for clinically active class III, IV, or V disease that is moderate to severe in pregnant patients.

    Oral dosage
    Adults

    40 mg/day to 80 mg/day PO until urine is protein-free; slowly taper as indicated. Some patients may require long-term therapy.

    Children and Adolescents

    2 mg/kg/day or 60 mg/m2/day (Maximum: 80 mg) PO once daily until urine is protein-free for 3 consecutive days. Then 1 mg/kg to 1.5 mg/kg or 40 mg/m2 PO every other day for 4 weeks. If needed, the long-term maintenance dose is 0.5 mg/kg to 1 mg/kg PO every other day for 3 to 6 months.

    For the treatment of severe erythema multiforme or Stevens-Johnson syndrome.
    Oral dosage
    Adults

    In patients with severe skin reactions, higher initial doses (e.g., 60 mg/day PO) are usually required. Adjust until a satisfactory response is noted. High-dose corticosteroids are controversial; administration has been associated with decreased survival. Prednisone doses of 60 mg/day to 250 mg/day PO are equivalent to the recommended hydrocortisone doses of 240 mg/day to 1000 mg/day.

    For the treatment of the acute respiratory distress syndrome (ARDS).
    Oral dosage
    Adults

    Corticosteroid use in ARDS is controversial. If there are no signs of improvement 7 to 14 days after ARDS onset, 2 mg/kg/day to 4 mg/kg/day PO for 7 to 14 days has been recommended.

    For the treatment of Hodgkin's disease in combination with antineoplastic agents.
    In combination with mechlorethamine, vincristine, vinblastine, and procarbazine (MVVPP regimen).
    Oral dosage
    Adults

    40 mg/m2/day PO on Day 1 through Day 22, then taper. Chemotherapy cycle is repeated every 57 days.

    In combination with mechlorethamine, vincristine, procarbazine, doxorubicin, bleomycin, and vinblastine (MOPP/APB regimen).
    Oral dosage
    Adults

    40 mg/m2/day PO on Day 1 through Day 14; cycle is repeated every 28 days.

    For the treatment of corticosteroid-responsive dermatitis and dermatologic disorders such as atopic dermatitis or eczema, bullous dermatitis herpetiformis, contact dermatitis, exfoliative dermatitis, or severe seborrheic dermatitis.
    Oral dosage
    Adults

    5 mg/day to 60 mg/day PO, administered in 1 to 4 divided doses, depending upon disease being treated. Depending on the indication, the initial dose may be gradually tapered after 1 to 2 weeks and discontinued by 4 to 6 weeks, as guided by symptoms. Oral corticosteroids are usually reserved for cases not responding to standard topical treatments.

    Children and Adolescents

    0.14 mg/kg/day to 2 mg/kg/day PO or 4 to 60 mg/m2/day PO, given in 1 to 4 divided doses. Depending on indication, gradually taper the initial dose after 1 to 2 weeks and discontinue by 4 to 6 weeks, guided by symptoms. Oral corticosteroids are usually reserved for cases not responding to standard topical treatments.

    For the treatment of Loeffler's syndrome, berylliosis, erythroblastopenia, or trichinosis.
    Oral dosage
    Adults

    5 mg to 60 mg PO per day, administered in 1 to 4 divided doses, depending upon disease being treated. Depending on the indication, the initial dose may be gradually tapered after 1 to 2 weeks and discontinued by 4 to 6 weeks, as guided by symptoms.

    Adolescents and Children

    0.14 to 2 mg/kg/day PO or 4 to 60 mg/m2/day PO, given in 4 divided doses. Depending on indication, gradually taper the initial dose after 1 to 2 weeks and discontinue by 4 to 6 weeks, guided by symptoms.

    For the treatment of pulmonary fibrosis due to known underlying causative conditions or for idiopathic pulmonary fibrosis†.
    Oral dosage
    Adults

    0.5 mg/kg/day PO for 4 weeks, then 0.25 mg/kg/day PO for 8 weeks. Taper to 0.125 mg/kg/day or 0.25 mg/kg/day PO on alternate days. Guidelines for idiopathic pulmonary fibrosis suggest treatment should be in combination with cyclophosphamide or azathioprine and continued for a minimum of 6 months. Objective responses may not be noted until the patient has received at least 3 months of therapy. Exact duration of treatment and need for long-term maintenance should be individualized based on clinical response and tolerance to therapy. Chronic doses of prednisone (15 mg to 20 mg PO once daily) may be adequate as maintenance therapy.

    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
    Adults

    The FDA-labeled dose is 5 mg/day to 60 mg/day PO, depending upon the disease being treated. 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 pericardial disease, an initial dose of 60 mg PO daily has been recommended by guidelines. Tapering strategies include a 10 mg per day weekly taper for a total duration of 6 weeks OR reducing the dose after 4 weeks to 30 mg PO daily for 4 weeks, then 15 mg PO daily for 2 weeks, then 5 mg PO daily for 1 week. Initial doses in clinical trials for tuberculosis in general have ranged from 0.75 mg/kg PO daily to 60 mg PO daily with durations from 9 to 17 weeks; many trials were prior to the use of rifampin, which may decrease bioavailability and increase plasma clearance of prednisone. For HIV patients co-infected with TB experiencing immune reconstitution inflammatory syndrome (IRIS), consider prednisone and taper over at least 4 weeks. For patients receiving rifampin, give prednisone 1.5 mg/kg/day PO for 2 weeks, then 0.75 mg/kg/day PO for 2 weeks. For patients receiving rifabutin, give prednisone 1 mg/kg/day PO for 2 weeks, then 0.5 mg/kg/day PO for 2 weeks. 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.

    Adolescents, Children, and Infants

    1 mg/kg/day to 2 mg/kg/day PO in 1 to 4 divided doses for 6 to 8 weeks. Higher initial doses (4 mg/kg/day for 7 days, followed by 2 mg/kg/day for 3 weeks and gradual taper) have also been reported in children. In a case series of 7 children, the 3 children who received higher doses had no tuberculoma on follow-up compared with the 4 children who received standard doses of 2 mg/kg/day PO, who all developed tuberculoma within 2 to 8 months of treatment. Doses of 4 mg/kg/day PO have also been used in children receiving rifampin as part of an anti-tuberculosis regimen due to the decreased bioavailability and increased plasma clearance of prednisone by rifampin. Full dose is usually given for a couple weeks, followed by a gradual tapering; a longer tapering over a few months may be necessary in some patients. Adjunctive corticosteroid therapy has been shown to improve survival for patients with tuberculosis involving the CNS and pericardium.

    For the treatment of multiple myeloma†.
    For the palliative treatment of multiple myeloma in combination with melphalan†.
    Oral dosage
    Adults

    2 mg/kg/day PO for 4 days plus 0.25 mg/kg/day PO for 4 days repeated every 6 weeks has been studied. Treatment cycles may be repeated when the granulocyte and platelet counts returned to normal. Response may be gradual over several months. NOTE: Melphalan is FDA approved for the palliative treatment of multiple myeloma and has been studied in combination with prednisone.

    For newly diagnosed multiple myeloma in geriatric adults or transplant ineligible patients, in combination with melphalan and thalidomide†.
    Oral dosage
    Geriatric Adults

    The optimal dosage of melphalan and prednisone plus thalidomide has not been clearly established and dosages have varied in randomized controlled trials. In one study, previously untreated patients between 65 and 75 years of age received melphalan (0.25 mg/kg PO daily) for 4 days and prednisone 2 mg/kg PO once daily for 4 days, cycles were repeated every 6 weeks for 12 cycles plus thalidomide (200 mg/day PO for 2 to 4 weeks escalated up to a maximum dose of 400 mg/day PO if no severe adverse events; most patients received thalidomide 200 mg/day or less). Thalidomide was stopped after day 4 of the last cycle. In another study, patients aged 75 years and older received melphalan (0.2 mg/kg PO daily) for 4 days and prednisone 2 mg/kg PO once daily for 4 days and repeated every 6 weeks for 12 cycles plus thalidomide 100 mg/day PO at bedtime.

    For previously untreated multiple myeloma, in combination with melphalan and bortezomib†.
    Oral dosage
    Adults

    Prednisone 60 mg/m2/day PO on Day 1, Day 2, Day 3, and Day 4 and melphalan 9 mg/m2/day PO on Day 1, Day 2, Day 3, and Day 4 plus bortezomib repeated every 6 weeks for 9 cycles. In cycles 1 through 4, bortezomib 1.3 mg/m2/dose IV/SC is given on Days 1, 4, 8, and 11 followed by a 10 day rest period (days 12 through 21) and again on Days 22, 25, 29, and 32 followed by a 10 day rest period (days 33 through 42); this 6-week cycle is considered one course. In cycles 5 to 9, bortezomib 1.3 mg/m2/dose IV/SC is given on Days 1, 8, 22, and 29; this 6-week cycle is considered one course. NOTE: Bortezomib is FDA approved in combination with melphalan and prednisone for use in previously untreated multiple myeloma.

    For the treatment of serious manifestations of Behcet's syndrome†.
    Oral dosage
    Adults

    1 mg/kg PO once daily is recommended.

    For the symptomatic treatment of Duchenne muscular dystrophy†.
    Oral dosage
    Children and Adolescents

    Current practice guidelines issued by the American Academy of Neurology and the Child Neurology Society recommend 0.75 mg/kg/day PO. If side effects (e.g., weight gain and Cushingoid facial appearance) outweigh benefits on muscle strength and function, gradual dose reduction to as low as 0.3 mg/kg/day PO can still be beneficial.

    For the adjunctive treatment of carpal tunnel syndrome†.
    Oral dosage
    Adults

    20 mg PO once daily for 2 weeks, followed by 10 mg PO once daily for 2 additional weeks, has provided relief. NOTE: The definitive treatment for median-nerve entrapment is surgery. Corticosteroids are temporary measures; patients who have intermittent pain and paresthesias without any fixed motor sensory deficits may respond to conservative therapy.

    For the treatment of selected cases of collagen disorders and mixed connective tissue disease†, such as acute rheumatic carditis, systemic dermatomyositis (polymyositis), systemic lupus erythematosus (SLE), temporal arteritis, Churg-Strauss syndrome†, polyarteritis nodosa, relapsing polychondritis, polymyalgia rheumatica, certain cases of vasculitis, or Wegener's granulomatosis†.
    For additional guidance for systemic lupus erythematosus (SLE) in adults.
    Oral dosage
    Adults

    Doses for the various manifestations of SLE vary widely. Initially 20 mg to 40 mg/day PO for moderate illness and 60 mg to 100 mg/day PO for severe illness; some patients may require higher doses, such as 200 to 300 mg/day PO in divided doses. After the disease is controlled, reduce the dose by 10% every 5 to 7 days; a more rapid reduction may result in relapse. Maintenance doses are usually 10 to 20 mg PO once daily or 20 to 40 mg PO every other day.

    For systemic dermatomyositis (polymyositis) when dosed in combination with azathioprine.
    Oral dosage
    Adults

    Initially, large doses (e.g., 60 mg PO once daily) are used, once the muscle disease is controlled, prednisone should be tapered to 5 mg to 10 mg PO every other day.

    For treatment using usual labeled dosage.
    Oral dosage
    Adults

    5 mg/day to 60 mg/day PO, administered in 1 to 4 divided doses, depending upon disease being treated. Individualize dose and titrate to response. Initial doses needed may be high (60 mg/day or more). After symptoms controlled, decrease dose slowly every 5 to 7 days. Maintenance doses for chronic conditions are usually 10 to 20 mg PO once daily or 20 mg to 40 mg PO every other day.

    Children and Adolescents

    0.05 mg/kg/day to 2 mg/kg/day PO in 1 to 4 divided doses. Individualize dose and titrate to response.

    For the treatment of autoimmune hepatitis†.
    Oral dosage
    Adults

    Initially, 20 mg to 30 mg PO once daily has been recommended. Some experts give a combination of prednisone and azathioprine. For maintenance, prednisone 5 mg to 15 mg PO once daily has been recommended.

    For the treatment of primary amyloidosis† not associated with familial Mediterranean fever.
    Oral dosage
    Adults

    0.8 mg/kg PO once daily for 7 days, in combination with melphalan; repeated every 6 weeks. The treatment combination demonstrated superior results over colchicine alone in the treatment of primary amyloidosis.

    For the treatment of idiopathic or viral pericarditis†.
    Oral dosage
    Adults

    20 mg to 80 mg PO once daily. Corticosteroids are contraindicated in pericarditis after myocardial infarction; corticosteroids retard myocardial scar formation and the incidence of rupture may increase.

    For the treatment of acute interstitial nephritis (AIN)†.
    Oral dosage
    Adults, Adolescents, and Children

    There is variation in the literature with regard to dosage regimens. Prednisone 0.75 mg/kg/day to 1 mg/kg/day PO is commonly reported, followed by gradual taper over 3 to 6 weeks. Use of IV methylprednisolone for a few days may precede oral corticosteroid use. NOTE: Following biopsy to confirm diagnosis, corticosteroids are usually instituted soon afterward as an adjunctive measure; removal of the suspected offending agent /cause is the primary treatment. While many case reports suggest a possible net benefit to the use of corticosteroids, some experts advocate for more prospective study of their value.

    For the systemic treatment of ophthalmic inflammatory conditions such as endophthalmitis†, optic neuritis, allergic conjunctivitis, keratitis, allergic corneal ulcer, iritis, chorioretinitis, anterior segment inflammation, uveitis, choroiditis, or sympathetic ophthalmia.
    Oral dosage
    Adults

    5 mg/day to 60 mg/day PO administered in 1 to 4 divided doses, depending upon disease being treated. NOTE: Topically applied corticosteroids are as effective as systemic corticosteroids for anterior ocular inflammation.

    Children and Adolescents

    0.14 mg/kg/day to 2 mg/kg/day PO or 4 mg/m2/day to 60 mg/m2/day PO, given in 1 to 4 divided doses. NOTE: Topically applied corticosteroids are as effective as systemic corticosteroids for anterior ocular inflammation.

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

    A range of 40 mg/day to 80 mg/day PO is suggested. 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 a corticosteroid; many patients with MSCC require corticosteroids to help preserve neurologic function, such as ambulation.

    For the treatment of Bell's palsy†.
    Oral dosage
    Adults

    Common regimens from high-quality clinical trials include a prednisone or prednisolone dose of 60 mg PO per day for 5 days, followed by a 5-day taper or 25 mg PO twice daily for 10 days , in combination with appropriate antiviral treatment. 1 mg/kg (up to 80 mg) PO once per day for 7 to 14 days, with an appropriate antiviral agent against herpes simplex virus (HSV), has also been recommended; if treatment is continued for 14 days, the prednisone dose can be tapered in the second week of treatment. A prednisone dose of 410 mg PO administered in descending doses over 10 days has also been used with efficacy. The American Academy of Neurology notes that for new-onset Bell's palsy, steroids are effective in increasing the probability of complete facial functional recovery according to data derived from class I (high quality) studies.

    For the adjunct treatment of West syndrome (infantile spasms†).
    Oral dosage
    Children up to 21 months and Infants

    The optimal dose of prednisone for infantile spasms has not been determined. The most frequently reported doses in the literature range from 1 mg/kg/day to 3 mg/kg/day PO. One study comparing low dose IM ACTH (20 International Units/m2) with prednisone 2 mg/kg/day PO reported no significant difference in response rates between the groups (spasm cessation in 42% and 33% of patients respectively). Other studies using higher doses of IM ACTH (150 International Units/m2) in patients ranging from 2 to 21 months of age have shown ACTH therapy to be superior to prednisone. Based on the evidence currently available, the American Academy of Neurology and the Child Neurology Society's practice parameters for the treatment of infantile spasms state that there is insufficient evidence that oral corticosteroids are effective in the treatment of infantile spasms.

    For the adjunct treatment of refractory seizures†, including absence seizures†, myoclonic seizures†, Lennox-Gastaut syndrome†, and other intractable seizure disorders†.
    Oral dosage
    Children and Infants 9 months and older

    There are limited data available for the treatment of refractory seizure types in pediatric patients. The optimal dose of prednisone for adjunctive therapy of seizure disorders has not been determined. Doses of 0.3 mg/kg/day to 3 mg/kg/day PO have been used. One case series of 28 pediatric patients ages 2 to 10 years suggests that prednisone therapy may be an effective adjunct treatment for intractable generalized epilepsy. Prednisone 1 mg/kg/day PO was administered for 12 weeks in addition to each patient's regular anticonvulsant regimen. Per parent diary, almost half of the study patients became seizure free, 36% had more than a 50% decrease in seizure frequency, and 18% had no change in seizure frequency. Treatment was most beneficial in those with absence seizures and early Lennox-Gastaut syndrome. In another retrospective case series, 32 mentally retarded children received various steroids for intractable epilepsy. Eight of those, ages 9 months to 6 years, received prednisone at varying doses and duration (0.3 to 3 mg/kg/day for a duration of 7 days to 24 months). Two patients had 100% reduction in seizure frequency, 1 patient had a 50% to 75% reduction, and 5 patients had no change in seizure frequency as reported by parents and confirmed with EEG. All 3 patients who responded had complex partial seizures. Of those 3 patients, 2 relapsed in less than 1 month after prednisone discontinuation. A non-randomized, non-blinded study compared IM ACTH 150 International Units/m2 for 1 week followed by an 11-week taper to prednisone 3 mg/kg/day for 4 weeks followed by 3 mg/kg every other day for 8 weeks, and then a 4-week taper. Infants and children with infantile spasms and children with other types of non-specified intractable seizures were included in the analysis. The mean age of patients in the non-specified intractable seizures group was 42.5 months. The investigators found that prednisone was effective in 59% (n = 13) of patients with infantile spasms who had a hypsarrhythmic EEG abnormality. Prednisone was reported to be ineffective in all 30 patients with other seizure types.

    For the treatment of heart transplant rejection†.
    Oral dosage
    Adults

    Guidelines recommend 1 mg/kg/day to 3 mg/kg/day PO for 3 to 5 days for asymptomatic mild or moderate acute cellular rejection (ISHLT 1R or 2R). A corticosteroid taper may be considered. Not first-line for symptomatic rejection (ISHLT 1R, 2R, or 3R) or for asymptomatic severe rejection (ISHLT 3R).

    For the management of heart transplant rejection prophylaxis†.
    Oral dosage
    Adults

    One study used prednisone 0.5 mg/kg/day to 1 mg/kg/day PO initially, then 0.3 mg/kg/day to 0.5 mg/kg/day by day 21 after transplantation and at least 0.1 mg/kg/day by month 6 with cyclosporine (up to 12 mg/kg/day divided twice daily) and either azathioprine (1 mg/kg/day to 3 mg/kg/day PO/IV with a maximum of 300 mg/day) or everolimus (0.75 mg or 1.5 mg PO twice daily). Cyclosporine target trough concentrations were 250 to 400 ng/mL for weeks 1 through 4, 200 to 350 ng/mL for weeks 5 through 24, and 100 to 300 ng/mL for weeks 25 through 96. Guidelines state corticosteroid avoidance, early corticosteroid weaning, or very low dose maintenance corticosteroid therapy are all acceptable therapeutic approaches. When corticosteroids are used, if no rejection episodes in the past 6 months have occurred and significant corticosteroid side effects are present, attempt corticosteroid weaning. Corticosteroid withdrawal can be successfully achieved 3 to 6 months after transplantation in many patients such as older patients, non-multiparous women, and those without circulating anti-HLA antibodies or rejection history.

    For adjunct therapy in patients with Mycobacterium avium complex infection† (MAC) experiencing moderate to severe immune reconstitution inflammatory syndrome (IRIS).
    Oral dosage
    Adults

    20 to 40 mg PO once daily for 4 to 8 weeks can be considered for patients with moderate to severe immune reconstitution inflammatory syndrome (IRIS).

    For adjunctive treatment in selected cases of pneumonia† or pneumonitis.
    For the treatment of Pneumocystis pneumonia (PCP)† in HIV patients as adjunctive therapy.
    Oral dosage
    Adults and Adolescents

    40 mg PO twice daily on days 1 to 5; then 40 mg PO once daily on days 6 to 10; then 20 mg PO once daily on days 11 to 21. Begin therapy as early as possible and within 72 hours of PCP therapy. Corticosteroids are recommended in patients with a PaO2 of 70 mmHg or less at room air or with an alveolar-arterial O2 gradient 35 mmHg or more. The benefits of corticosteroid therapy started after 72 hours of PCP therapy are unknown, but some clinicians may recommend for moderate-to-severe PCP.

    For aspiration pneumonitis.
    Oral dosage
    Adults

    5 mg to 60 mg PO per day; administered in 1 to 4 divided doses. Gradually taper after 1 to 2 weeks and discontinue by 4 to 6 weeks, guided by symptoms.

    Children

    0.14 mg/kg to 2 mg/kg PO daily or 4 to 60 mg/m2 PO daily, given in 1 to 4 divided doses. Gradually taper after 1 to 2 weeks and discontinue by 4 to 6 weeks, as guided by symptoms.

    For adjunct therapy in patients with chorioretinitis associated with congenital toxoplasmosis†.
    Oral dosage
    Infants and Children

    0.5 mg/kg/dose PO twice daily (Max: 20 mg/dose) with rapid taper in combination with pyrimethamine, sulfadiazine, and leucovorin is recommended for patients with severe chorioretinitis by the American Academy of Pediatrics (AAP) guidelines.

    Neonates

    0.5 mg/kg/dose PO twice daily in combination with pyrimethamine, sulfadiazine, and leucovorin is recommended for patients with CSF protein 1 g/dL or more or severe chorioretinitis in vision-threatening macular area. Initiate prednisone after 72 hours of anti-Toxoplasma therapy and continue until CSF protein is less than 1 g/dL or resolution of severe chorioretinitis.

    For the treatment of peripheral T-cell lymphoma (PTCL)†.
    For the first-line treatment of PTCL in combination with gemcitabine, cisplatin, and thalidomide†.
    Oral dosage
    Adults and Adolescents 14 years and older

    60 mg/m2 PO on days 1, 2, 3, 4, and 5 in combination with gemcitabine (800 mg/m2 IV over 30 minutes on days 1 and 8), cisplatin (25 mg/m2 IV on days 1, 2, and 3), and thalidomide (200 mg PO daily) repeated every 21 days until disease progression or for up to 6 cycles was evaluated in patients with previously untreated PTCL in a randomized trial. Patients received aspirin 100 mg/day PO during thalidomide therapy. The use of granulocyte colony-stimulation factor was permitted as indicated.

    †Indicates off-label use

    MAXIMUM DOSAGE

    Dosage must be individualized and is highly variable depending on the nature and severity of the disease, and on patient response. Although there is no absolute maximum dosage, the Boston Collaborative Drug Study found that psychiatric events occurred in fewer than 1% of patients when prednisone was prescribed in doses of 30 mg/day or less, whereas the incidence rose to 18% in patients receiving 80 mg/day.

    DOSING CONSIDERATIONS

    Hepatic Impairment

    Specific guidelines for dosage adjustments in hepatic impairment are not available; prednisone is converted to prednisolone, the active moiety, by the liver. The use of oral prednisolone instead of oral prednisone may be preferred in patients with significant hepatic dysfunction (see Prednisolone monograph); doses are equivalent (i.e., 1 mg prednisone is equivalent to 1 mg of prednisolone).

    Renal Impairment

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

    ADMINISTRATION

    Oral Administration

    All oral dosage forms: Administer with food to minimize indigestion or GI irritation.

    Oral Solid Formulations

    Immediate-release tablet: If given once daily or every other day, administer in the morning to coincide with the body's normal cortisol secretion.
    Delayed-release tablet (Rayos): Administer the delayed-release tablets once daily by having the patient swallow them whole; do not break, divide or chew. When deciding the administration time for the delayed-release tablets, consider the pharmacokinetics and the disease or condition being treated. Prednisone is released from the tablet beginning approximately 4 hours after intake of the first dose.

    Oral Liquid Formulations

    Oral solution or syrup: Administer using a calibrated measuring device for accurate measurement of the dose.

    STORAGE

    Generic:
    - Store at controlled room temperature (between 68 and 77 degrees F)
    Deltasone:
    - Store at controlled room temperature (between 68 and 77 degrees F)
    Predone:
    - Store at controlled room temperature (between 68 and 77 degrees F)
    RAYOS:
    - Protect from light
    - Protect from moisture
    - Store at 77 degrees F; excursions permitted to 59-86 degrees F
    Sterapred:
    - Store at controlled room temperature (between 68 and 77 degrees F)
    Sterapred DS:
    - Store at controlled room temperature (between 68 and 77 degrees F)

    CONTRAINDICATIONS / PRECAUTIONS

    General Information

    Increased dosages of rapid-acting corticosteroids like prednisone may be necessary for patients undergoing physiologic stress. The corticosteroid should be administered before, during, and after the stressful situation.

    Infection, surgery

    Patients should be instructed to notify their physician immediately if signs of infection or injury occur, both during treatment, or up to 12 months following the cessation of prednisone therapy. Dosages should be adjusted, or glucocorticoid therapy reintroduced, if required. If surgery is required, patients should advise the attending physician of the corticosteroid they have received within the last 12 months, and the disease for which they were being treated. Identification cards which include the name of the patient's disease, the currently administered type and dose of corticosteroid, and the patient's physician should be carried with the patient at all times.

    Fungal infection

    The manufacturers state that prednisone is contraindicated in patients with systemic fungal infection, but many clinicians believe that corticosteroids can be administered to patients with any type of known infection as long as appropriate therapy is administered simultaneously.

    Herpes infection, measles, tuberculosis, varicella, viral infection

    Corticosteroid therapy, including prednisone therapy, can mask the symptoms of infection and should not be used in cases of viral infection or bacterial infection which are not adequately controlled by anti-infective agents. Secondary infections are common during corticosteroid therapy. Corticosteroids may 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 corticosteroids should be advised to avoid exposure to measles or varicella, and if exposed to these diseases, to seek medical advice immediately. In general, corticosteroids should not be used in patients with herpes infection.

    Myocardial infarction

    Corticosteroid therapy, including prednisone therapy, has been associated with left ventricular free-wall rupture in patients with recent myocardial infarction, and should therefore be used cautiously in these patients.

    Heart failure, hypertension

    Corticosteroids, such as prednisone, cause edema, which may exacerbate congestive heart failure or hypertension, and should be used with caution in these patients.

    Cataracts, glaucoma, visual disturbance

    Corticosteroids, such as prednisone, should be used cautiously in patients with glaucoma or other visual disturbance. Corticosteroids are well known to cause cataracts and can exacerbate glaucoma during long-term administration. Patients receiving topical or systemic corticosteroids chronically should be periodically assessed for cataract formation.

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

    Corticosteroids, such as prednisone, should be used with caution in patients with GI disease, diverticulitis, intestinal anastomosis (because of the possibility of perforation), or hepatic disease causing hypoalbuminemia such as cirrhosis. 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.

    Diabetes mellitus, hypothyroidism, osteoporosis, psychosis, renal disease, seizure disorder

    Corticosteroids, such as prednisone, should be used with extreme caution in patients with psychosis, emotional instability, herpes simplex ocular infections, renal disease, osteoporosis, diabetes mellitus, and seizure disorder, because the drugs may exacerbate these conditions. Patients with hypothyroidism may have an exaggerated response to corticosteroids, thus any steroid should be used with caution in these patients.

    Myasthenia gravis

    Glucocorticoids, such as prednisone, should be used with caution in patients with myasthenia gravis who are being treated with anticholinesterase agents (see Interactions). Muscle weakness may be transiently increased during the initiation of glucocorticoid therapy in patients with myasthenia gravis, necessitating respiratory support.

    Coagulopathy, thromboembolic disease

    Glucocorticoids such as prednisone may rarely increase blood coagulability and cause intravascular thrombosis, thrombophlebitis, and thromboembolism. Therefore, corticosteroids should be used with caution in patients with coagulopathy or thromboembolic disease.

    Pregnancy

    There have been no adequate and well-controlled studies on the use of corticosteroids, including prednisone, in human pregnancy. If these drugs must be used during pregnancy, the potential risks should be discussed with the patient. Complications including cleft palate, still birth, and premature abortion have been reported when corticosteroids were administered during pregnancy. Babies born to women receiving large doses of corticosteroids during pregnancy should be monitored for signs of adrenal insufficiency and appropriate therapy initiated, if necessary.

    Breast-feeding

    Corticosteroids distribute into breast milk, and the manufacturer states that because of the potential for serious adverse reactions in nursing babies, a decision should be made whether to discontinue nursing or to discontinue the drug. However, prednisone concentrations in breast milk are low, and no adverse effects have been reported in the breast-fed infant with maternal use of any corticosteroid during breast-feeding; prednisone is generally considered compatible to use during lactation. Published case reports of systemic prednisone use during pregnancy that indicate little risk to a nursing infant due to lack of reported side effects. Prednisone is converted to prednisolone in vivo, and peak concentrations in human milk appear in about 1 hour after a dose; the total daily dose reaching the infant is approximately 0.1% of the mother's total daily dose. Prednisolone and methylprednisolone have similar data available regarding systemic use during lactation. At higher daily prednisone doses, avoidance of breast-feeding during times of peak milk concentrations can help limit infant exposure; however, such adjustments are rarely necessary. 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 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 via topical administration (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.

    Growth inhibition, increased intracranial pressure, neonates

    Prednisone has been used in infants, children, and adolescents; however, consider pediatric-specific issues before initiating treatment. Safety and efficacy have not been established for the use of corticosteroids in neonates. Adverse effects in newborns have included complications of treatment such as gastrointestinal bleeding, intestinal perforation, hyperglycemia, and hypertension. The potential for growth inhibition in any pediatric patient should be monitored during prolonged therapy, 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. Pediatric patients may be more susceptible to developing systemic toxicity; adrenal suppression and increased intracranial pressure have been reported with the use and/or withdrawal of various corticosteroid formulations in young patients. Further, children receiving corticosteroids are immunosuppressed, and are therefore more susceptible to infection. Normally innocuous infections can become fatal in these children, and care should be taken to avoid exposure to these diseases. Published studies provide evidence of efficacy and safety in pediatric patients for the treatment of nephrotic syndrome (pediatric patients more than 2 years of age), and aggressive lymphomas and leukemias (patients greater than 1 month of age). Other indications for pediatric use of corticosteroids (e.g., severe asthma and wheezing) are based on adequate and well-controlled trials conducted in adults, on the premises that the course of the diseases and their pathophysiology are considered to be substantially similar in both populations.

    Cushing's syndrome

    As glucocorticoids can produce or aggravate Cushing's syndrome, glucocorticoids, such as prednisone, should be avoided in patients with Cushing's disease.

    Abrupt discontinuation, hypothalamic-pituitary-adrenal (HPA) suppression

    Systemic corticosteroids, such as prednisone, can aggravate Cushing's syndrome; avoid use in patients with Cushing's syndrome. Pharmacological doses of systemic corticosteroids administered for prolonged periods may result in hypothalamic-pituitary-adrenal (HPA) suppression and/or manifestations of Cushing's syndrome in some patients. 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. Withdraw prolonged systemic corticosteroid therapy (greater than 2 weeks) gradually. HPA suppression can last for up to 12 months following cessation of systemic chronic therapy. Recovery of HPA axis function is generally prompt and complete upon discontinuation of short-term or topical corticosteroid therapy. HPA-suppressed patients may need supplemental corticosteroid treatment during periods of physiologic stress, such as surgery, acute blood loss, or infectious conditions, even after the corticosteroid has been discontinued. Encourage patients currently receiving chronic corticosteroid therapy or who have had chronic corticosteroids discontinued within the last 12 months to carry identification advising the need for administration of corticosteroids in situations of increased stress.

    Corticosteroid hypersensitivity

    Prednisone is contraindicated in patients with a hypersensitivity to prednisone or to any components of the formulation. Although true corticosteroid hypersensitivity is rare, patients who have demonstrated a prior hypersensitivity reaction to prednisone should not receive any form of prednisone or prednisolone. 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 such as prednisone with caution in the geriatric patient; the risks and benefits of therapy should be considered for any individual patient, particularly with chronic use. 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. According to the OBRA guidelines, 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

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

    Moderate

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

    Mild

    weakness / Early / Incidence not known
    arthralgia / Delayed / Incidence not known
    myalgia / Early / Incidence not known
    infection / Delayed / Incidence not known
    headache / Early / Incidence not known
    malaise / Early / Incidence not known
    paresthesias / Delayed / Incidence not known
    insomnia / Early / Incidence not known
    restlessness / 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
    menstrual irregularity / Delayed / Incidence not known
    dysmenorrhea / Delayed / Incidence not known
    amenorrhea / Delayed / Incidence not known
    anorexia / Delayed / Incidence not known
    weight loss / Delayed / Incidence not known
    abdominal pain / Early / Incidence not known
    hiccups / Early / Incidence not known
    appetite stimulation / Delayed / Incidence not known
    nausea / Early / Incidence not known
    vomiting / Early / Incidence not known
    diarrhea / Early / Incidence not known
    weight gain / Delayed / Incidence not known
    ecchymosis / Delayed / Incidence not known
    rash (unspecified) / Early / Incidence not known
    acne vulgaris / Delayed / Incidence not known
    hirsutism / Delayed / Incidence not known
    alopecia / Delayed / Incidence not known
    striae / Delayed / Incidence not known
    perineal pain / Early / Incidence not known
    petechiae / Delayed / Incidence not known
    acneiform rash / Delayed / Incidence not known
    telangiectasia / Delayed / Incidence not known
    diaphoresis / Early / Incidence not known
    purpura / Delayed / Incidence not known
    urticaria / Rapid / Incidence not known
    xerosis / Delayed / Incidence not known
    fever / Early / Incidence not known
    lethargy / Early / Incidence not known
    syncope / Early / Incidence not known
    dizziness / 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 prednisone. Butalbital is a CYP3A4 inducer; prednisone is a CYP3A4 substrate. Monitor for decreased response to prednisone during concurrent use.
    Acetaminophen; Butalbital; Caffeine: (Moderate) Coadministration may result in decreased exposure to prednisone. Butalbital is a CYP3A4 inducer; prednisone is a CYP3A4 substrate. Monitor for decreased response to prednisone during concurrent use.
    Acetaminophen; Butalbital; Caffeine; Codeine: (Moderate) Coadministration may result in decreased exposure to prednisone. Butalbital is a CYP3A4 inducer; prednisone is a CYP3A4 substrate. Monitor for decreased response to prednisone 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.
    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.
    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. In clinical efficacy trials, concurrent treatment of alefacept with these types of agents did not occur. The duration of the period following treatment with alefacept that is appropriate before starting other immunosuppressive therapy has not been evaluated.
    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; 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.
    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.
    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; 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.
    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.
    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.
    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: (Moderate) Use caution if prednisone and aprepitant, fosaprepitant are used concurrently and monitor for an increase in prednisone-related adverse effects for several days after administration of a multi-day aprepitant regimen. The active metabolite of prednisone, prednisolone, 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 and may increase plasma concentrations of prednisone. For example, a 5-day oral aprepitant regimen increased the AUC of another CYP3A4 substrate, midazolam (single dose), by 2.3-fold on day 1 and by 3.3-fold on day 5. After a 3-day oral aprepitant regimen, the AUC of midazolam (given on days 1, 4, 8, and 15) increased by 25% on day 4, and then decreased by 19% and 4% on days 8 and 15, respectively. As a single 125 mg or 40 mg oral dose, the inhibitory effect of aprepitant on CYP3A4 is weak, with the AUC of midazolam increased by 1.5-fold and 1.2-fold, respectively. After administration, fosaprepitant is rapidly converted to aprepitant and shares many of the same drug interactions. However, as a single 150 mg intravenous dose, fosaprepitant only weakly inhibits CYP3A4 for a duration of 2 days; there is no evidence of CYP3A4 induction. Fosaprepitant 150 mg IV as a single dose increased the AUC of midazolam (given on days 1 and 4) by approximately 1.8-fold on day 1; there was no effect on day 4. Less than a 2-fold increase in the midazolam AUC is not considered clinically important.
    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.
    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.
    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 prednisone. Butalbital is a CYP3A4 inducer; prednisone is a CYP3A4 substrate. Monitor for decreased response to prednisone 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 prednisone. Butalbital is a CYP3A4 inducer; prednisone is a CYP3A4 substrate. Monitor for decreased response to prednisone 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) 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: (Moderate) Coadministration of prednisone with atazanavir may cause elevated prednisone serum concentrations, potentially resulting in Cushing's syndrome and adrenal suppression. Prednisone is a CYP3A4 substrate; atazanavir is a strong inhibitor of CYP3A4. 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: (Moderate) Coadministration of prednisone with atazanavir may cause elevated prednisone serum concentrations, potentially resulting in Cushing's syndrome and adrenal suppression. Prednisone is a CYP3A4 substrate; atazanavir is a strong inhibitor of CYP3A4. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. (Moderate) Coadministration of prednisone with cobicistat may cause elevated prednisone serum concentrations, potentially resulting in Cushing's syndrome and adrenal suppression. Cobicistat is a CYP3A4 and P-glycoprotein (P-gp) inhibitor, while prednisone is a CYP3A4 and P-gp substrate. 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 prednisone. Phenobarbital is a CYP3A4 inducer; prednisone is a CYP3A4 substrate. Monitor for decreased response to prednisone during concurrent use.
    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: (Minor) Prednisone is a substrate of P-glycoprotein (P-gp) and azithromycin is a P-gp inhibitor; therefore, prednisone 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.
    Belladonna Alkaloids; Ergotamine; Phenobarbital: (Moderate) Coadministration may result in decreased exposure to prednisone. Phenobarbital is a CYP3A4 inducer; prednisone is a CYP3A4 substrate. Monitor for decreased response to prednisone 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.
    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: (Major) Concurrent administration of systemic corticosteroids, such as prednisone, and boceprevir is not recommended. If prednisone and boceprevir are coadministered, close monitoring for corticosteroid-related adverse events and for decreased boceprevir efficacy is advised. If prednisone dose adjustments are made, re-adjust the dose upon completion of boceprevir treatment. Predictions about the interaction can be made based on the metabolic pathway of prednisone. Prednisone is metabolized by the hepatic isoenzyme CYP3A4 and the drug efflux transporter P-glycoprotein (P-gp); boceprevir inhibits both the isoenzyme and the drug efflux pump. Coadministration may result in elevated prednisone plasma concentrations.
    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 prednisone may be necessary if bosentan is initiated or withdrawn during therapy. Bosentan may increase the metabolism of prednisone resulting in decreased exposure. Bosentan is an inducer of CYP3A4; prednisone is a CYP3A4 substrate.
    Brigatinib: (Moderate) Monitor for decreased efficacy of prednisone if coadministration with brigatinib is necessary. Prednisolone, the active metabolite of prednisone, is a CYP3A substrate; brigatinib induces CYP3A in vitro. Plasma concentrations of prednisolone may decrease.
    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.
    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.
    Butabarbital: (Moderate) Coadministration may result in decreased exposure to prednisone. Butabarbital is a CYP3A4 inducer; prednisone is a CYP3A4 substrate. Monitor for decreased response to prednisone during concurrent use.
    Cabozantinib: (Moderate) Monitor for an increase in prednisone-related adverse events if concomitant use with cabozantinib is necessary, as plasma concentrations of prednisone may be increased. Cabozantinib is a P-glycoprotein (P-gp) inhibitor and prednisone is a substrate of P-gp in vitro; 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 prednisone. Dosage adjustments may be necessary, and closer monitoring of clinical and/or adverse effects is warranted when carbamazepine is used with prednisone.
    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) 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; 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.
    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 prednisone may occur if it is coadministered with carvedilol; exercise caution. Carvedilol is a P-glycoprotein (P-gp) inhibitor and prednisone is a P-gp substrate.
    Ceritinib: (Moderate) Monitor for an increase in corticosteroid-related adverse reactions if coadministration of prednisone with ceritinib is necessary. Ceritinib is a CYP3A4 inhibitor and the active metabolite of prednisone, prednisolone, is metabolized by CYP3A4. Strong CYP3A4 inhibitors have been reported to significantly decrease the metabolism of certain corticosteroids by up to 60%, leading to an increased risk of corticosteroid side effects. The degree of CYP3A4 inhibition 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; Hydrocodone; 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; 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, such as prednisone.
    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.
    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.
    Clindamycin: (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.
    Cobicistat: (Moderate) Coadministration of prednisone with cobicistat may cause elevated prednisone serum concentrations, potentially resulting in Cushing's syndrome and adrenal suppression. Cobicistat is a CYP3A4 and P-glycoprotein (P-gp) inhibitor, while prednisone is a CYP3A4 and P-gp substrate. 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: (Moderate) Coadministration of prednisone with cobicistat may cause elevated prednisone serum concentrations, potentially resulting in Cushing's syndrome and adrenal suppression. Cobicistat is a CYP3A4 and P-glycoprotein (P-gp) inhibitor, while prednisone is a CYP3A4 and P-gp substrate. 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 Disoproxil Fumarate: (Moderate) Coadministration of prednisone with cobicistat may cause elevated prednisone serum concentrations, potentially resulting in Cushing's syndrome and adrenal suppression. Cobicistat is a CYP3A4 and P-glycoprotein (P-gp) inhibitor, while prednisone is a CYP3A4 and P-gp substrate. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use.
    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) Avoid coadministration of conivaptan, a CYP3A4/P-glycoprotein (P-gp) inhibitor and prednisone, a CYP3A4/P-gp substrate. Concurrent use may result in elevated prednisone serum concentrations. According to the manufacturer of conivaptan, concomitant use of conivaptan, a strong CYP3A4 inhibitor, and CYP3A substrates, such as prednisone, should be avoided. Coadministration of conivaptan with other CYP3A substrates (midazolam, simvastatin, amlodipine) has resulted in increased mean AUC values (2 to 3 times). Theoretically, similar pharmacokinetic effects could be seen with prednisone. Treatment with prednisone 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.
    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.
    Daclatasvir: (Moderate) Systemic exposure of prednisone, a P-glycoprotein (P-gp) substrate, may be increased when administered concurrently with daclatasvir, a P-gp inhibitor. Taking these drugs together could increase or prolong the therapeutic effects of prednisone; monitor patients for potential adverse effects.
    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.
    Darunavir: (Moderate) Coadministration of prednisone with darunavir may cause elevated prednisone serum concentrations, potentially resulting in Cushing's syndrome and adrenal suppression. Prednisone is a CYP3A4 and P-glycoprotein (P-gp) substrate; darunavir is a strong inhibitor of CYP3A4 and P-gp. 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: (Moderate) Coadministration of prednisone with cobicistat may cause elevated prednisone serum concentrations, potentially resulting in Cushing's syndrome and adrenal suppression. Cobicistat is a CYP3A4 and P-glycoprotein (P-gp) inhibitor, while prednisone is a CYP3A4 and P-gp substrate. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. (Moderate) Coadministration of prednisone with darunavir may cause elevated prednisone serum concentrations, potentially resulting in Cushing's syndrome and adrenal suppression. Prednisone is a CYP3A4 and P-glycoprotein (P-gp) substrate; darunavir is a strong inhibitor of CYP3A4 and P-gp. 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: (Moderate) Coadministration of prednisone with ritonavir (a strong CYP3A4 inhibitor) may cause prednisone serum concentrations to increase, potentially resulting in Cushing's syndrome and adrenal suppression. Consider use of an alternative corticosteroid whose concentrations are less affected by strong CYP3A4 inhibitors, such as beclomethasone and prednisolone, especially during long-term treatment.
    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.
    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.
    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.
    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.
    Diltiazem: (Moderate) Prednisone is metabolized by the liver to the active metabolite prednisolone. Prednisolone is metabolized by CYP3A4 to inactive compounds. As diltiazem is both a substrate and an inhibitor of CYP3A4, monitor patients for corticosteroid-related side effects if prednisone and diltiazem are taken.
    Diphenhydramine; Hydrocodone; 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.
    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.
    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.
    Dronedarone: (Moderate) Dronedarone is metabolized by and is an inhibitor of CYP3A; dronedarone also inhibits P-gp. Prednisone is a substrate for CYP3A4 and P-gp. The concomitant administration of dronedarone with CYP3A4 and P-gp substrates may result in increased exposure of the substrate and should, therefore, be undertaken with caution.
    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.
    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: (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, such as linagliptin, 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.
    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.
    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.
    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.
    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.
    Etravirine: (Moderate) Etravirine is a CYP3A4 inducer/substrate and a P-glycoprotein (PGP) inhibitor and prednisone is a CYP3A4 and PGP substrate. Caution is warranted if these drugs are coadministered.
    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.
    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.
    Fosamprenavir: (Moderate) Concomitant use of prednisone and fosamprenavir may result in altered prednisone plasma concentrations. Prednisone is a substrate of the hepatic isoenzyme CYP3A4 and drug transporter P-glycoprotein (P-gp). Amprenavir, the active metabolite of fosamprenavir, is an inducer of P-gp and a potent inhibitor and moderate inducer of CYP3A4.
    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: (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.
    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 prednisone as coadministration may increase serum concentrations of prednisone and increase the risk of adverse effects. Prednisone is a substrate of P-glycoprotein (P-gp); glecaprevir is a P-gp inhibitor. (Moderate) Caution is advised with the coadministration of pibrentasvir and prednisone as coadministration may increase serum concentrations of prednisone and increase the risk of adverse effects. Prednisone 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; 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.
    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.
    Hydantoins: (Moderate) Hydantoin anticonvulsants induce hepatic microsomal enzymes and may increase the metabolism of prednisone, 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; 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.
    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.
    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.
    Idelalisib: (Major) Avoid concomitant use of idelalisib, a strong CYP3A inhibitor, with prednisone, a CYP3A substrate, as prednisone toxicities may be significantly increased. The AUC of a sensitive CYP3A substrate was increased 5.4-fold when coadministered with idelalisib. 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 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. If coadministration is necessary, close clinical monitoring is advised and therapy should be accompanied by appropriate antimicrobial therapies as indicated.
    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) 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.
    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.
    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.
    Isavuconazonium: (Moderate) Concomitant use of isavuconazonium with prednisone may result in increased serum concentrations of prednisone. Prednisolone, the active metabolite of prednisone, is a substrate of the hepatic isoenzyme CYP3A4; additionally prednisone is a substrate of the drug transporter P-glycoprotein (P-gp). Isavuconazole, the active moiety of isavuconazonium, is an inhibitor of CYP3A4 and P-gp. Caution and close monitoring for adverse effects, such as corticosteroid-related side effects, are advised if these drugs are used together.
    Isoniazid, INH; Pyrazinamide, PZA; Rifampin: (Moderate) A dose adjustment of prednisone may be necessary when administered concurrently with rifamycins, due to the potential for decreased exposure of prednisone. Rifamycins are inducers of CYP3A4; prednisone is a CYP3A4 substrate.
    Isoniazid, INH; Rifampin: (Moderate) A dose adjustment of prednisone may be necessary when administered concurrently with rifamycins, due to the potential for decreased exposure of prednisone. Rifamycins are inducers of CYP3A4; prednisone is a CYP3A4 substrate.
    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) Prednisone is metabolized by the liver to the active metabolite prednisolone. Itraconazole is a potent inhibitor of CYP3A4, and prednisolone is a CYP3A4 substrate. Monitor patients for corticosteroid-related side effects if both prednisone and itraconazole are taken.
    Ivacaftor: (Moderate) Use caution when administering ivacaftor and prednisone concurrently. Ivacaftor is an inhibitor of CYP3A and P-glycoprotein (Pgp); prednisone is a substrate of Pgp and it's active metabolite, prednisolone, is metabolized by CYP3A. Co-administration can increase prednisone exposure leading to increased or prolonged therapeutic effects and adverse events; however, the clinical impact of this has not yet been determined.
    Ixabepilone: (Minor) Ixabepilone is a weak inhibitor of P-glycoprotein (Pgp). Prednisone is a Pgp substrate, and concomitant use of ixabepilone with a Pgp substrate may cause an increase in prednisone concentrations. Use caution if ixabepilone is coadministered with a Pgp substrate.
    Ketoconazole: (Moderate) Ketoconazole can decrease the hepatic clearance of prednisone, resulting in increased plasma concentrations. The interaction may be due to the inhibition of cytochrome P-450 3A4 isoenzyme by ketoconazole, and subsequent decreases in corticosteroid metabolism by the same isoenzyme. The dose of corticosteroid should be titrated to avoid steroid toxicity. Prednisolone and prednisone pharmacokinetics appear less susceptible than methylprednisolone to CYP3A4 inhibitory interactions. Ketoconazole also can enhance the adrenal suppressive effects of corticosteroids.
    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 prednisone-associated adverse reactions is advised with concomitant administration of ledipasvir. Prednisone is a substrate of the drug transporter P-glycoprotein (P-gp); ledipasvir is a P-gp inhibitor. Taking these drugs together may increase prednisone 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.
    Linagliptin: (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, such as linagliptin, should be closely monitored for signs indicating loss of diabetic control when corticosteroids are instituted.
    Linagliptin; 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, such as linagliptin, 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.
    Lopinavir; Ritonavir: (Moderate) Coadministration of prednisone with ritonavir (a strong CYP3A4 inhibitor) may cause prednisone serum concentrations to increase, potentially resulting in Cushing's syndrome and adrenal suppression. Consider use of an alternative corticosteroid whose concentrations are less affected by strong CYP3A4 inhibitors, such as beclomethasone and prednisolone, especially during long-term treatment.
    Lumacaftor; Ivacaftor: (Moderate) Lumacaftor; ivacaftor may reduce the efficacy of prednisone and prednisolone by decreasing systemic exposure of the corticosteroid. If used together, a higher systemic corticosteroid dose may be required to obtain the desired therapeutic effect. Prednisolone, the active metabolite of prednisone, is a CYP3A4 substrate, and lumacaftor is a strong CYP3A inducer. (Moderate) Use caution when administering ivacaftor and prednisone concurrently. Ivacaftor is an inhibitor of CYP3A and P-glycoprotein (Pgp); prednisone is a substrate of Pgp and it's active metabolite, prednisolone, is metabolized by CYP3A. Co-administration can increase prednisone exposure leading to increased or prolonged therapeutic effects and adverse events; however, the clinical impact of this has not yet been determined.
    Lumacaftor; Ivacaftor: (Moderate) Lumacaftor; ivacaftor may reduce the efficacy of prednisone and prednisolone by decreasing systemic exposure of the corticosteroid. If used together, a higher systemic corticosteroid dose may be required to obtain the desired therapeutic effect. Prednisolone, the active metabolite of prednisone, is a CYP3A4 substrate, and lumacaftor is a strong CYP3A inducer.
    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.
    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.
    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 prednisone. Mephobarbital is a CYP3A4 inducer; prednisone is a CYP3A4 substrate. Monitor for decreased response to prednisone 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.
    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: (Moderate) Use caution if mitotane and prednisone are used concomitantly, and monitor for decreased efficacy of prednisone and a possible change in dosage requirements. Mitotane is a strong CYP3A4 inducer and prednisone is a CYP3A4 substrate; coadministration may result in decreased plasma concentrations of prednisone.
    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.
    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.
    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.
    Nevirapine: (Moderate) In a clinical trial, concomitant use of prednisone was associated with an increase in incidence and severity of rash during the first 6 weeks of nevirapine therapy. Therefore, the use of prednisone to prevent nevirapine-associated rash is not recommended.
    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.
    Ombitasvir; Paritaprevir; Ritonavir: (Moderate) Coadministration of prednisone with ritonavir (a strong CYP3A4 inhibitor) may cause prednisone serum concentrations to increase, potentially resulting in Cushing's syndrome and adrenal suppression. Consider use of an alternative corticosteroid whose concentrations are less affected by strong CYP3A4 inhibitors, such as beclomethasone and prednisolone, especially during long-term treatment.
    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: (Moderate) Prednisolone is metabolized by CYP3A4; oritavancin is a weak CYP3A4 inducer. Plasma concentrations and efficacy of prednisolone may be reduced if these drugs are administered concurrently.
    Oxymetholone: (Moderate) Concomitant use of oxymetholone with corticosteroids or corticotropin, ACTH may cause increased edema. Manage edema with diuretic and/or digitalis therapy.
    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: (Moderate) Pazopanib is a weak inhibitor of CYP3A4. Coadministration of pazopanib and prednisone, a CYP3A4 substrate, may cause an increase in systemic concentrations of prednisone. Use caution when administering these drugs concomitantly. In addition, concomitant administration may predispose the patient to over-immunosuppression resulting in an increased risk for the development of severe infections.
    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.
    Phenobarbital: (Moderate) Coadministration may result in decreased exposure to prednisone. Phenobarbital is a CYP3A4 inducer; prednisone is a CYP3A4 substrate. Monitor for decreased response to prednisone 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 prednisone 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 prednisone. Further, both prednisone 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 prednisone, 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.
    Primidone: (Moderate) Coadministration may result in decreased exposure to prednisone. Primidone is a CYP3A4 inducer; prednisone is a CYP3A4 substrate. Monitor for decreased response to prednisone 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.
    Propylthiouracil, PTU: (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.
    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.
    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 prednisone is necessary, as the systemic exposure of prednisone may be increased resulting in increase in treatment-related adverse reactions. Ribociclib is a moderate CYP3A4 inhibitor. Prednisolone, the active metabolite of prednisone, is a CYP3A4 substrate.
    Ribociclib; Letrozole: (Moderate) Use caution if coadministration of ribociclib with prednisone is necessary, as the systemic exposure of prednisone may be increased resulting in increase in treatment-related adverse reactions. Ribociclib is a moderate CYP3A4 inhibitor. Prednisolone, the active metabolite of prednisone, is a CYP3A4 substrate.
    Rifabutin: (Moderate) A dose adjustment of prednisone may be necessary when administered concurrently with rifamycins, due to the potential for decreased exposure of prednisone. Rifamycins are inducers of CYP3A4; prednisone is a CYP3A4 substrate.
    Rifampin: (Moderate) A dose adjustment of prednisone may be necessary when administered concurrently with rifamycins, due to the potential for decreased exposure of prednisone. Rifamycins are inducers of CYP3A4; prednisone is a CYP3A4 substrate.
    Rifamycins: (Moderate) A dose adjustment of prednisone may be necessary when administered concurrently with rifamycins, due to the potential for decreased exposure of prednisone. Rifamycins are inducers of CYP3A4; prednisone is a CYP3A4 substrate.
    Rifapentine: (Moderate) A dose adjustment of prednisone may be necessary when administered concurrently with rifamycins, due to the potential for decreased exposure of prednisone. Rifamycins are inducers of CYP3A4; prednisone is a CYP3A4 substrate.
    Rilonacept: (Moderate) Patients receiving immunosuppressives along with rilonacept may be at a greater risk of developing an infection.
    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) Coadministration of prednisone with ritonavir (a strong CYP3A4 inhibitor) may cause prednisone serum concentrations to increase, potentially resulting in Cushing's syndrome and adrenal suppression. Consider use of an alternative corticosteroid whose concentrations are less affected by strong CYP3A4 inhibitors, such as beclomethasone and prednisolone, especially during long-term treatment.
    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.
    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.
    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.
    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 prednisone as coadministration may result in increased systemic exposure of prednisone. Prednisone 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 prednisone.
    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.
    Simeprevir: (Minor) Simeprevir, a P-glycoprotein (P-gp) inhibitor and a mild intestinal CYP3A4 inhibitor, may increase the side effects of prednisone, which is a P-gp and CYP3A4 substrate. Monitor patients for adverse effects of prednisone, such as enhanced adrenal suppression.
    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.
    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 Iodide: (Moderate) Corticosteroids, such as prednisone, are known to decrease the uptake of iodide into thyroid tissue. In order to increase thyroid uptake and optimize exposure of thyroid tissue to the radionucleotide sodium iodide I-131, consider withholding prednisone prior to treatment with sodium iodide I-131.
    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; Voxilaprevir: (Moderate) Plasma concentrations of prednisone, a P-glycoprotein (P-gp) substrate, may be increased when administered concurrently with voxilaprevir, a P-gp inhibitor. Monitor patients for increased side effects if these drugs are administered concurrently.
    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.
    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: (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.
    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: (Major) Concurrent administration of systemic corticosteroids, such as prednisone, and telaprevir is not recommended. If prednisone and telaprevir are coadministered, close monitoring for corticosteroid-related adverse events is advised. If prednisone dose adjustments are made, re-adjust the dose upon completion of telaprevir treatment. Predictions about the interaction can be made based on the metabolic pathway of prednisone. Prednisone is metabolized by the hepatic isoenzyme CYP3A4 and the drug efflux transporter P-glycoprotein (P-pg); telaprevir inhibits both the isoenzyme and the drug efflux pump. Coadministration may result in elevated prednisone plasma concentrations.
    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: (Moderate) Increased prednisone active metabolite concentrations are expected with telithromycin coadministration. Prednisone is metabolized by the liver to the active metabolite prednisolone through the 11b-hydroxydehydrogenase enzyme (which is not part of the CYP system). Prednisolone is metabolized by the CYP3A4-mediated 6b-hydroxylase enzyme to inactive compounds. Telithromycin is a known inhibitor of CYP3A4, and prednisolone is a CYP3A4 substrate. Additionally, prednisone is a substrate of P-glycoprotein (PGP) and telithromycin may be a PGP inhibitor. Monitor patients for corticosteroid-related side effects if both prednisone and telithromycin are taken.
    Telotristat Ethyl: (Moderate) Use caution if coadministration of telotristat ethyl and prednisone is necessary, as the systemic exposure of prednisone may be decreased resulting in reduced efficacy. If these drugs are used together, monitor patients for suboptimal efficacy of prednisone; consider increasing the dose of prednisone if necessary. Prednisolone, the active metabolite of prednisone, 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: (Minor) Use caution if coadministration of temsirolimus with prednisone is necessary, and monitor for an increase in prednisone-related adverse reactions. Temsirolimus is a P-glycoprotein (P-gp) inhibitor in vitro, and prednisone is an in vitro P-gp substrate. Pharmacokinetic data are not available for concomitant use of temsirolimus with P-gp substrates, but exposure to prednisone is likely to increase.
    Tesamorelin: (Moderate) Use caution when coadministering tesamorelin with prednisone as their concurrent use may decrease the effectiveness of the steroids. Tesamorelin stimulates the production of growth hormone, which is known to inhibit the enzyme 11-beta-hydroxysteroid dehydrogenase type 1 (11-beta-HSD-1); cortisone and prednisone require the 11-beta-HSD-1 enzyme for conversion to their active metabolites. Patients with hypoadrenalism receiving treatment with cortisone or prednisone may required increased maintenance or stress doses after initiation of tesamorelin.
    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.
    Theophylline, Aminophylline: (Minor) Serum theophylline concentrations have been reported to be lower during concomitant administration of prednisone, but the actual magnitude of the interaction was slight.
    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.
    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 systemiccorticosteroids.
    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.
    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.
    Trandolapril; Verapamil: (Minor) The absorption of verapamil can also be reduced by the cyclophosphamide, vincristine, procarbazine, prednisone (COPP) chemotherapeutic drug regimen.
    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: (Minor) In vitro data indicate that ulipristal may be an inhibitor of P-glycoprotein (P-gp) at clinically relevant concentrations. Thus, co-administration of ulipristal and P-gp substrates such as prednisone may increase prednisone concentrations. With single doses of ulipristal for emergency contraception it is not clear this interaction will have clinical consequence. In the absence of clinical data, co-administration of ulipristal (when given daily) and P-gp substrates is not recommended.
    Vancomycin: (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.
    Vandetanib: (Moderate) Use caution if coadministration of vandetanib with prednisone is necessary, due to a possible increase in prednisone-related adverse reactions. Prednisone is a substrate of P-glycoprotein (P-gp) in vitro. Coadministration with vandetanib increased the Cmax and AUC of digoxin, another P-gp substrate, by 29% and 23%, respectively.
    Varicella-Zoster 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.
    Vecuronium: (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.
    Vemurafenib: (Minor) Concomitant use of vemurafenib and prednisone may result in altered concentrations of prednisone or its active metabolite, prednisolone. Vemurafenib is an inhibitor of P-glycoprotein (PGP) and an inducer of CYP3A4. Prednisone is a substrate of PGP and its active metabolite, prednisolone, is a CYP3A4 substrate. Use caution and monitor patients for toxicity and efficacy.
    Verapamil: (Minor) The absorption of verapamil can also be reduced by the cyclophosphamide, vincristine, procarbazine, prednisone (COPP) chemotherapeutic drug regimen.
    Vigabatrin: (Major) Vigabatrin should not be used with corticosteroids, which are associated with serious ophthalmic effects (e.g., retinopathy or glaucoma) unless the benefit of treatment clearly outweighs the risks.
    Vinblastine: (Minor) Use caution when administering vinblastine concurrently with a CYP3A4 inducer such as dexamethasone. Vinblastine is metabolized by CYP3A4 and dexamethasone may decrease vinblastine plasma 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.
    Vincristine Liposomal: (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia.
    Voriconazole: (Moderate) Prednisone is metabolized by the liver to the active metabolite prednisolone. Prednisolone is metabolized by CYP3A4 to inactive compounds. Voriconazole is a known inhibitor of CYP3A4. Monitor patients for corticosteroid-related side effects if both prednisone and voriconazole are taken.
    Vorinostat: (Moderate) Use vorinostat and corticosteroids together with caution; the risk of QT prolongation and arrhythmias may be increased if electrolyte abnormalities occur. Corticosteroids may cause electrolyte imbalances; hypomagnesemia, hypokalemia, or hypocalcemia and may increase the risk of QT prolongation with vorinostat. Frequently monitor serum electrolytes if concomitant use of these drugs is necessary.
    Warfarin: (Moderate) The effect of corticosteroids on oral anticoagulants (e.g., warfarin) is variable. There are reports of enhanced as well as diminished effects of anticoagulants when given concurrently with corticosteroids; however, limited published data exist, and the mechanism of the interaction is not well described. High-dose corticosteroids appear to pose a greater risk for increased anticoagulant effect. In addition, corticosteroids have been associated with a risk of peptic ulcer and gastrointestinal bleeding. Thus corticosteroids should be used cautiously and with appropriate clinical monitoring in patients receiving oral anticoagulants; coagulation indices (e.g., INR, etc.) should be monitored to maintain the desired anticoagulant effect. During high-dose corticosteroid administration, daily laboratory monitoring may be desirable.
    Yellow Fever 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.
    Zafirlukast: (Minor) Zafirlukast inhibits the CYP3A4 isoenzymes and should be used cautiously in patients stabilized on drugs metabolized by CYP3A4, such as corticosteroids.
    Zileuton: (Minor) Zileuton is metabolized by the cytochrome P450 isoenzyme 3A4. Although administration of zileuton with other drugs metabolized by CYP3A4 has not been studied, zileuton may inhibit CYP3A4 isoenzymes. Zileuton could potentially compete with other CYP3A4 substrates.

    PREGNANCY AND LACTATION

    Pregnancy

    There have been no adequate and well-controlled studies on the use of corticosteroids, including prednisone, in human pregnancy. If these drugs must be used during pregnancy, the potential risks should be discussed with the patient. Complications including cleft palate, still birth, and premature abortion have been reported when corticosteroids were administered during pregnancy. Babies born to women receiving large doses of corticosteroids during pregnancy should be monitored for signs of adrenal insufficiency and appropriate therapy initiated, if necessary.

    Corticosteroids distribute into breast milk, and the manufacturer states that because of the potential for serious adverse reactions in nursing babies, a decision should be made whether to discontinue nursing or to discontinue the drug. However, prednisone concentrations in breast milk are low, and no adverse effects have been reported in the breast-fed infant with maternal use of any corticosteroid during breast-feeding; prednisone is generally considered compatible to use during lactation. Published case reports of systemic prednisone use during pregnancy that indicate little risk to a nursing infant due to lack of reported side effects. Prednisone is converted to prednisolone in vivo, and peak concentrations in human milk appear in about 1 hour after a dose; the total daily dose reaching the infant is approximately 0.1% of the mother's total daily dose. Prednisolone and methylprednisolone have similar data available regarding systemic use during lactation. At higher daily prednisone doses, avoidance of breast-feeding during times of peak milk concentrations can help limit infant exposure; however, such adjustments are rarely necessary. 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 drug, healthcare providers are encouraged to report the adverse effect to the FDA.

    MECHANISM OF ACTION

    Mechanism of Action: Glucocorticoids are naturally occurring hormones that prevent or suppress inflammation and immune responses when administered at pharmacological doses. At a molecular level, unbound glucocorticoids readily cross cell membranes and bind with high affinity to specific cytoplasmic receptors. This binding induces a response by modifying transcription and, ultimately protein synthesis to achieve the steroid's intended action. Such actions may include: inhibition of leukocyte infiltration at the site of inflammation, interference in the function of mediators of inflammatory response, and suppression of humoral immune responses. Some of the net effects include reduction in edema or scar tissue, as well as a general suppression in immune response. The degree of clinical effect is normally related to the dose administered. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, collectively called lipocortins. Lipocortins, in turn, control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of the precursor molecule arachidonic acid. Likewise, the numerous adverse effects related to corticosteroid use are usually related to the dose administered and the duration of therapy.

    PHARMACOKINETICS

    Prednisone is administered orally as immediate-release (IR) tablets, an oral solution, or delayed-release tablets.
     
    Affected cytochrome P450 isoenzymes and drug transporters: P-gp, CYP3A4
    In vitro, prednisone was identified as a substrate of p-glycoprotein (P-gp). The circulating drug binds extensively to the plasma proteins albumin and transcortin, with only the unbound portion of a dose active. Systemic prednisone is quickly distributed into the kidneys, intestines, skin, liver, and muscle. Corticosteroids distribute into the breast milk and cross the placenta. Prednisone is metabolized by the liver to the active metabolite prednisolone, which has a 4—6 fold higher exposure than that of prednisone. Prednisolone is formed through the 11b-hydroxydehydrogenase enzyme, which is not part of the CYP system, but prednisolone is metabolized by the CYP3A4-mediated 6b-hydroxylase enzyme to inactive compounds. These inactive metabolites, as well as a small portion of unchanged drug, are excreted in the urine. The plasma elimination half-life is 1 hour whereas the biological half-life of prednisone is 18—36 hours.
     
    The pharmacokinetic profile of delayed-release tablets has an approximately 4-hour lag time from that of IR formulations. The distribution and elimination processes are comparable between the two formulations. After oral administration of the delayed-release tablets, the terminal half-life of both prednisone and prednisolone was 2—3 hours, which is comparable to that from the IR formulation.

    Oral Route

    Prednisone immediate-release (IR) tablets: Following oral administration, prednisone is rapidly absorbed across the GI membrane. In vitro, prednisone was identified as a substrate of p-glycoprotein. Peak effects can be observed after 1—2 hours.
    Prednisone delayed-release tablets (Rayos): While the pharmacokinetic profile of prednisone delayed-release tablets when given with food differs in terms of lag time from prednisone IR, its absorption process is comparable. Following oral administration with food, prednisone delayed-release is released approximately 4 hours after oral ingestion. This causes a delay in the time until peak plasma concentrations (Tmax) are achieved. In 27 healthy male subjects, the median Tmax of prednisone delayed-release tablets was 6—6.5 hours compared to 2 hours for a prednisone IR formulation. The rate of absorption was similar for both formulations. The peak plasma concentrations (Cmax) and exposure were comparable for both formulations when administered 2.5 hours after a light meal or with normal meal. Food was shown to significantly affect the absorption of delayed-release tablets during a study in 24 heathy subjects. Under standard fasting conditions, both the Cmax and the bioavailability of delayed-release tablets were significantly lower than under fed conditions, shortly after intake of a high fat meal. When the delayed-release tablets were administered at 1 mg, 2 mg, and 5 mg, dose-proportionality in terms of Cmax and systemic exposure were evident for the parent drug prednisone as well as for the active metabolite prednisolone.