CLASSES

Ophthalmological Corticosteroids
Respiratory Corticosteroids
Systemic Corticosteroid Combinations
Systemic Corticosteroids, Plain

DEA CLASS

Rx

DESCRIPTION

An oral, parenteral, and ophthalmic glucocorticoid with little to no mineralocorticoid activity
Used in adult and pediatric patients, for many uses, including cerebral edema, in antiemetic regimens for chemotherapy, and for allergic or inflammatory dermatologic, ophthalmic, or systemic conditions
Systemic dexamethasone is helpful for the treatment of cerebral edema because of its superior ability to penetrate the CNS

COMMON BRAND NAMES

AK-Dex, Baycadron, CUSHINGS SYNDROME DIAGNOSTIC, Decadron, Dexabliss, DexPak Jr TaperPak, DexPak TaperPak, Dextenza, DEXYCU, DoubleDex, Dxevo, Hemady, HiDex, Maxidex, Ozurdex, ReadySharp Dexamethasone, Simplist Dexamethasone, Solurex, TaperDex, ZCORT, Zema-Pak, ZoDex, ZonaCort 11 Day, ZonaCort 7 Day

HOW SUPPLIED

AK-Dex/Decadron/Dexamethasone/Dexamethasone Sodium Phosphate Auricular (Otic) Drops: 0.1%
AK-Dex/Decadron/Dexamethasone/Dexamethasone Sodium Phosphate Auricular (Otic) Sol: 0.1%
AK-Dex/Decadron/Dexamethasone/Dexamethasone Sodium Phosphate Ophthalmic Drops: 0.1%
AK-Dex/Decadron/Dexamethasone/Dexamethasone Sodium Phosphate Ophthalmic Sol: 0.1%
Baycadron/Decadron/Dexamethasone Oral Sol: 0.5mg, 1mg, 1mL, 5mL
CUSHINGS SYNDROME DIAGNOSTIC/Decadron/Dexabliss/Dexamethasone/DexPak Jr TaperPak/DexPak TaperPak/Dxevo/Hemady/HiDex/TaperDex/ZCORT/Zema-Pak/ZoDex/ZonaCort 11 Day/ZonaCort 7 Day Oral Tab: 0.5mg, 0.75mg, 1mg, 1.5mg, 2mg, 4mg, 6mg, 20mg
Decadron/Dexamethasone/Dexamethasone Sodium Phosphate/DoubleDex/ReadySharp Dexamethasone/Simplist Dexamethasone/Solurex Intramuscular Inj Sol: 1mL, 4mg, 10mg
Decadron/Dexamethasone/Dexamethasone Sodium Phosphate/DoubleDex/ReadySharp Dexamethasone/Simplist Dexamethasone/Solurex Intravenous Inj Sol: 1mL, 4mg, 10mg
Decadron/Dexamethasone/Dexamethasone Sodium Phosphate/DoubleDex/Simplist Dexamethasone/Solurex Intra-Articular Inj Sol: 1mL, 4mg, 10mg
Decadron/Dexamethasone/Dexamethasone Sodium Phosphate/DoubleDex/Simplist Dexamethasone/Solurex Intralesional Inj Sol: 1mL, 4mg, 10mg
Decadron/Dexamethasone/Dexamethasone Sodium Phosphate/DoubleDex/Simplist Dexamethasone/Solurex Soft Tissue Inj Sol: 1mL, 4mg, 10mg
Dextenza Ophthalmic Insert: 0.4mg
DEXYCU Intraocular Inj Susp: 9%
Maxidex Ophthalmic Susp: 0.1%
Ozurdex Intravitreal Imp: 0.7mg

DOSAGE & INDICATIONS

†Indicates off-label use

MAXIMUM DOSAGE

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

DOSING CONSIDERATIONS

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

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

ADMINISTRATION

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

Visually inspect parenteral products for particulate matter and discoloration prior to administration whenever solution and container permit.
Some injectable formulations contain benzyl alcohol; avoid the use of these formulations in premature neonates, and use with caution in neonates.

Ophthalmic solution or suspension:
Apply ophthalmic solution or suspension topically to the eye.
For ophthalmic suspensions, shake well prior to each administration.
Instruct patient on appropriate instillation technique.
Do not to touch the tip of the dropper or tube to the eye, fingertips, or other surfaces.
To prevent contamination, each dropper is for 1 individual, do not share among patients.
The initial prescription and renewal of the ophthalmic suspension should be made by a physician only after examination of the patient with the aid of magnification, such as slit lamp biomicroscopy and fluorescein staining (where appropriate). Prescribe no more than 1 bottle at a time.[54348] [61633]
 
Intraocular Administration
For administration by the physician at the end of the ophthalmic surgical procedure.
Dexycu Intraocular Suspension
Preparation of intraocular suspension:
Prepare a sterile field. Remove the components of the administration kit from their respective pouches and place onto the sterile field.
Withdraw the syringe plunger approximately 1 inch. Place the syringe ring on the plunger (slit facing the plunger). Apply slight downward pressure until the syringe ring "snaps" into place.
Place the 18-gauge needle firmly on the syringe. Remove the cap from the needle. Depress the plunger completely and then withdraw the plunger to fill the syringe with air.
Mix using a vortex mixer or vigorously shake the vial sideways for a minimum of 30 seconds; the suspended drug material must be used immediately after shaking.
Remove the blue plastic flip-cap from the vial and wipe the top of the rubber stopper with an alcohol pad. Invert the vial.
Insert the needle into the vial and inject the air into the vial. Making sure the needle tip is immersed in the drug material pooled in the neck of the inverted vial, fill the syringe by slowly withdrawing the plunger approximately 0.2 mL. Remove the needle from the vial and discard the unused portion in the vial.
Remove the needle from the syringe. Firmly place the cannula on the syringe and remove the plastic cap. Hold the syringe vertically with the cannula pointing up. Depress the plunger to expel air bubbles from the syringe.
Affix the syringe guide over the syringe ring on the plunger.
Depress the plunger until the syringe guide/ring mechanism comes gently into contact with the flange of the syringe. Lightly tap/flick the barrel of the syringe to remove any excess drug from the tip of the cannula. Do not wipe or touch the tip of the cannula to remove excess drug.
Remove the syringe guide, leaving the syringe ring in place. CAUTION: DO NOT MOVE THE PLUNGER. The space between the syringe ring and the top of the plunger is the medication injection volume that will be applied to the patient's eye; the syringe is now ready for injection.[48640]
 
Intraocular Administration:
In a single slow-motion, inject 0.005 mL of the drug material behind the iris in the inferior portion of the posterior chamber. If the sphere of the administered drug after intraocular injection appears to be larger than 2 mm in diameter, excess drug material may be removed by irrigation and aspiration in the sterile surgical setting.
Some drug material will remain in the syringe after the injection; this is necessary for accurate dosing. Discard the unused portion remaining in the syringe after administration.[48640]
 
Dextenza Ophthalmic Insert
Intracanalicular Administration:
Do not use if pouch has been damaged or opened. Do not re-sterilize.
Carefully remove foam carrier and transfer to a clean and dry area. If necessary, dilate the punctum with an ophthalmic dilator. Care should be taken not to perforate the canaliculus during dilation or placement of the insert. If perforation occurs, do not place the insert in the eye.
After drying the punctal area, using blunt (non-toothed) forceps, grasp the insert and place into the lower lacrimal canaliculus by pulling the lid temporally and inserting nasally. Ensure the insert is placed just below the punctal opening. Excessive squeezing of the insert with forceps may cause deformation.
To aid in the hydration of the insert, 1 to 2 drops of balanced salt solution can be instilled into the punctum. The insert hydrates quickly upon contact with moisture. If the insert begins to hydrate before fully inserted, discard the product and use a new insert.
The insert can be visualized when illuminated by a blue light source (e.g., slit lamp or hand held blue light) with yellow filter.[63796]
The insert is for single-use only.
Insert is resorbable; removal not required.

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

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

STORAGE

Generic:
- Keep from freezing
- Protect from moisture
- Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
AK-Dex:
- Store at room temperature (between 59 to 86 degrees F)
Baycadron:
- Keep from freezing
- Store at controlled room temperature (between 68 and 77 degrees F)
CUSHINGS SYNDROME DIAGNOSTIC :
- Store at controlled room temperature (between 68 and 77 degrees F)
Decadron:
- Protect from moisture
- Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
Dexabliss:
- Keep from freezing
- Protect from moisture
- Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
DexPak Jr TaperPak:
- Keep from freezing
- Protect from moisture
- Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
DexPak TaperPak:
- Keep from freezing
- Protect from moisture
- Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
Dextenza:
- Do not freeze
- Protect from light
- Refrigerate (between 36 and 46 degrees F)
- Store in original package until time of use
DEXYCU:
- Store at controlled room temperature (between 68 and 77 degrees F)
DoubleDex:
- Discard product if it contains particulate matter, is cloudy, or discolored
- Discard unused portion. Do not store for later use.
- Protect from light
- Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
- Store in carton until time of use
Dxevo:
- Keep from freezing
- Protect from moisture
- Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
Hemady:
- Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
HiDex:
- Keep from freezing
- Protect from moisture
- Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
Maxidex:
- Store between 46 to 80 degrees F
- Store in a cool, dry place
- Store upright
Ozurdex:
- Store at room temperature (between 59 to 86 degrees F)
ReadySharp Dexamethasone:
- Discard product if it contains particulate matter, is cloudy, or discolored
- Protect from freezing
- Protect from light
- Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
- Store in carton until time of use
Simplist Dexamethasone:
- Avoid exposure to heat
- Discard product if it contains particulate matter, is cloudy, or discolored
- Do not autoclave
- Protect from freezing
- Protect from light
- Store at controlled room temperature (between 68 and 77 degrees F)
Solurex:
- Avoid exposure to heat
- Discard product if it contains particulate matter, is cloudy, or discolored
- Do not autoclave
- Protect from freezing
- Protect from light
- Store at controlled room temperature (between 68 and 77 degrees F)
TaperDex:
- Keep from freezing
- Protect from moisture
- Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
ZCORT:
- Keep from freezing
- Protect from moisture
- Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
Zema-Pak:
- Keep from freezing
- Protect from moisture
- Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
ZoDex:
- Keep from freezing
- Protect from moisture
- Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
ZonaCort 11 Day:
- Keep from freezing
- Protect from moisture
- Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
ZonaCort 7 Day:
- Keep from freezing
- Protect from moisture
- Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F

CONTRAINDICATIONS / PRECAUTIONS

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

Dexamethasone is contraindicated in patients with a hypersensitivity to the drug or any of its components. Although true corticosteroid hypersensitivity is rare, 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.

Prolonged administration of pharmacological doses of systemic, nasal, inhaled or topical corticosteroids (resulting in systemic absorption) may result in hypothalamic-pituitary-adrenal (HPA) suppression and/or manifestations of Cushing's syndrome in some patients. Adrenal suppression and increased intracranial pressure have been reported with the use and/or withdrawal of various corticosteroid formulations in pediatric 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 concentrations. Withdraw prolonged systemic corticosteroid therapy (duration of treatment of more than 2 weeks) gradually. HPA suppression can last for up to 12 months following cessation of systemic therapy. Recovery of HPA axis function is generally prompt and complete upon discontinuation of the topical corticosteroid. HPA-suppressed patients may need supplemental corticosteroid treatment during periods of physiologic stress, such as post-surgical stress, acute blood loss, or infectious conditions, even after the corticosteroid has been discontinued. Encourage patients currently receiving chronic corticosteroid therapy or who have had corticosteroids discontinued within the last 12 months to carry identification advising the need for administration of corticosteroids in situations of increased stress. 

Potential adverse effects of chronic corticosteroid therapy should be weighed against the clinical benefits obtained and the availability of other treatment alternatives. Prolonged systemic corticosteroid therapy can lead to osteopenia, osteoporosis, vertebral compression fractures, aseptic necrosis of femoral and humeral heads, and pathologic fractures of long bones secondary to decreased bone formation, increased bone resorption, and protein catabolism in any patient.  A high-protein diet may alleviate or prevent the adverse effects associated with protein catabolism. The elderly, post-menopausal, and pediatric patients may be more susceptible to the effects on bone. Chronic systemic dexamethasone therapy may cause growth inhibition in pediatric patients due to hypothalamic-pituitary-adrenal axis suppression and inhibition of bone growth. Corticosteroids should be titrated to the lowest effective dose. Because bone development is critical in pediatric patients, monitoring is warranted in patients receiving high-dose or chronic corticosteroid treatment. Use of the lowest effective dose is recommended to minimize the occurrence of systemic adverse effects. Monitor growth routinely.  

Patients receiving high-dose (e.g., equivalent to 1 mg/kg or more of prednisone daily) or systemic corticosteroid therapy, such as dexamethasone, for any period of time, particularly in conjunction with corticosteroid-sparing drugs (e.g., troleandomycin) are at risk to develop immunosuppression; however, patients receiving moderate dosages of systemic corticosteroids for short periods or low dosages for prolonged periods also may be at risk. Treatment with topical or inhaled corticosteroids lessens the risk of immunosuppression; although localized effects may be seen in some patients. When given in combination with other immunosuppressive agents, there is a risk of over-immunosuppression.  Intra-articularly injected corticosteroids are systemically absorbed and may cause immunosuppression. Advise patients to contact their health care provider if they develop fever or other signs or symptoms of an infectious process. Local injection of a corticosteroid into a previously infected joint is not usually recommended. Examine any joint fluid to exclude a septic process. Injection into unstable joints is generally not recommended.

If surgery is required, patients should advise their physician that they received prolonged systemic corticosteroid therapy, such as dexamethasone, within the last 12 months and state the disease for which they were being treated. For systemic therapy, identification cards that include disease state, type and dose of corticosteroid, and physician should always be carried with the patient. Long-acting dexamethasone injection preparations, which are no longer marketed in the U.S., are not suitable for use in acute stress situations. To avoid drug-induced adrenal insufficiency, a supportive corticosteroid dosage may be required in times of stress (such as trauma, surgery, or severe illness) both during treatment with these injections and for a year afterward. 

Corticosteroids may increase the risks related to infections with any pathogen, including viral, bacterial, fungal, protozoan, or helminth infection. The degree to which the dose, route, and duration of corticosteroid administration correlate with the specific risks of infection is not well characterized, however, with increasing doses of corticosteroids, the rate of occurrence of infectious complications increases. Corticosteroids may also mask some signs of current infection. Although the FDA-approved product labeling states that corticosteroids are contraindicated in patients with systemic fungal infections, most clinicians believe that systemic corticosteroids can be administered to these patients as long as appropriate therapy is administered simultaneously. Avoid the use in patients with a fungal infection or bacterial infection that is not adequately controlled with anti-infective agents. Activation of latent disease or exacerbation of intercurrent infection due to pathogens such as Amoeba, Candida, Cryptococcus, Mycobacterium, Nocardia, Pneumocystis, or Toxoplasma can occur in patients receiving systemic corticosteroids. Rule out infection with latent or active amebiasis before initiating corticosteroid therapy in patients who have spent time in the tropics or who have unexplained diarrhea. Use corticosteroids with caution in patients with known or suspected Strongyloides (threadworm) infestation as the immunosuppressive effects may lead to disseminated infection, severe enterocolitis, and sepsis. Cases of severe and disseminated strongyloidiasis have been reported following use of corticosteroids in combination with tocilizumab to treat patients with coronavirus disease 2019 (COVID-19). Before giving these drugs together to patients from strongyloidiasis endemic areas, consider administering ivermectin as prophylactic treatment. Reserve systemic corticosteroid therapy in active tuberculosis for patients with fulminating or disseminated disease and only in conjunction with appropriate antituberculosis therapy. Reactivation of tuberculosis may occur in patients with latent tuberculosis or tuberculin reactivity; close observation for disease reactivation is needed if corticosteroids are indicated in such patients. Furthermore, chemoprophylaxis is advised if prolonged corticosteroid therapy is needed. Advise patients receiving immunosuppressive doses of systemic corticosteroids to avoid exposure to persons with a viral infection (i.e., measles or varicella) because these diseases may be more serious or even fatal in immunosuppressed patients. Instruct patients to get immediate medical advice if exposure occurs. If exposed to chickenpox, prophylaxis with varicella-zoster immune globulin may be indicated. If exposed to measles, prophylaxis with pooled intramuscular immunoglobulin may be indicated. Avoid the use of corticosteroids in active ocular herpes infection due to the risk of corneal perforation. Corticosteroids should not be used in cerebral malaria. The use of ophthalmic dexamethasone formulations is contraindicated in most forms of cornea and conjunctiva viral ocular infections including herpes simplex virus epithelial keratitis, ocular vaccinia, and ocular varicella, and also in mycobacterial infection of the eye or fungal diseases of the eye.

Do not use high doses of systemic corticosteroids such as dexamethasone for the treatment of traumatic brain injury. An increase in early mortality (at 2 weeks) and late mortality (at 6 months) was noted in patients with head trauma who were determined not to have other clear indications for corticosteroid treatment; in the trial, patients received methylprednisolone hemisuccinate.

Corticosteroid therapy, including systemic dexamethasone 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. As sodium retention with resultant edema and potassium loss may occur in patients receiving systemic corticosteroids, these agents should be used with caution in patients with congestive heart failure, hypertension, or renal disease or insufficiency.

Systemic corticosteroids, such as dexamethasone, may decrease glucose tolerance, produce hyperglycemia, and aggravate or precipitate diabetes mellitus. This may especially occur in patients predisposed to diabetes mellitus. When corticosteroid therapy is necessary for patients with diabetes mellitus, changes in insulin, oral antidiabetic agent dosage, and/or diet may be required.

An acute myopathy has been observed with the use of high doses of systemic corticosteroids, most often occurring in patients with neuromuscular disease disorders (e.g., myasthenia gravis), or in patients receiving concomitant therapy with neuromuscular blocking drugs. This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis. Elevation of creatinine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years.

Existing emotional instability or psychosis may be aggravated by corticosteroids. Psychiatric derangements may appear when corticosteroids are used, ranging from euphoria, insomnia, mood swings, personality changes, and severe depression, to frank psychosis. Use dexamethasone with caution in patients with a seizure disorder; systemic steroids can lower the seizure threshold.

Metabolic clearance of corticosteroids is decreased in hypothyroidism and increased in hyperthyroidism. Changes in thyroid disease status of a patient may necessitate an adjustment in systemic dexamethasone dosage.

Systemic corticosteroids should be used with caution in patients with active or latent peptic ulcer disease, diverticulitis, fresh intestinal anastomoses, and nonspecific ulcerative colitis, since steroids may increase the risk of a gastrointestinal (GI) perforation. Signs of peritoneal irritation following GI perforation in patients receiving corticosteroids may be minimal or absent. Corticosteroids should not be used in patients where there is a possibility of impending GI perforation, abscess, or pyogenic infection. There is an enhanced effect due to decreased metabolism of systemic corticosteroids in patients with severe hepatic disease with cirrhosis.

Systemic corticosteroids, like dexamethasone, may cause impaired wound healing. Ophthalmic and ocular dosage forms may cause impairment of wound healing within or near the site of application.

Prolonged use of corticosteroids including dexamethasone may result in glaucoma with damage to the optic nerve, defects in visual acuity and fields of vision. Corticosteroids can cause cataracts and exacerbate pre-existing glaucoma. Periodically assess patients receiving corticosteroids chronically for cataract formation, visual disturbance, or increased intraocular pressure. Consider referring patients who develop ocular symptoms or use systemic corticosteroid-containing products for more than 6 weeks to an ophthalmologist for evaluation. Ophthalmic dexamethasone is more likely than other ophthalmic agents to increase intraocular pressure, so intraocular pressure should be measured every 2 to 4 weeks for the first 2 months of therapy, and every 1 to 2 months thereafter. Ophthalmic dexamethasone therapy should be undertaken with caution in patients with a history of open-angle glaucoma, myopia, Krukenberg's spindle, or diabetes because these patients have an increased risk of developing ocular hypertension during therapy. The dexamethasone intravitreal implant is contraindicated in patients with glaucoma who have cup to disc ratio more than 0.8. Ophthalmic dexamethasone should be used with caution in patients with corneal abrasion.   Dexamethasone intravitreal implant is also contraindicated in patients who have a tear or a rupture of posterior ocular lens capsule; these patients with an absent or torn posterior capsule of the lens are at increased risk of migration of the intravitreal implant into the anterior chamber. Laser posterior capsulotomy in pseudophakic patients is not a contraindication for the dexamethasone intravitreal implant. The initial prescription and renewal of the medication order of dexamethasone intravitreal implant should be made only after examination of the patient with the aid of magnification, such as slit lamp biomicroscopy, and, where appropriate, fluorescein staining. If signs and symptoms fail to improve after 2 days, re-evaluate the patient. The safety and efficacy of dexamethasone intravitreal implant, ophthalmic injection suspension, and ophthalmic insert have not been established in pediatric patients.

Corticosteroid therapy usually does not contraindicate vaccination with live-virus vaccines when such therapy is of short-term (less than 2 weeks); low to moderate dose; long-term alternate-day treatment with short-acting preparations; maintenance physiologic doses (replacement therapy); ophthalmic administration, 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 a 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 or more 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 or more weeks, it is recommended to wait at least 3 months after discontinuation of therapy before administering a live-virus vaccine.

There are no adequate, well-controlled studies for the use of dexamethasone in pregnant women; therefore, the manufacturers recommend that the drug be used during pregnancy only if the potential benefit to the mother outweighs the potential risk to the fetus. For COVID-19, the National Institutes of Health (NIH) recommends use of the drug in pregnant patients, if indicated, as the potential benefit of decreased maternal mortality justifies the low risk of fetal adverse effects with the short course of therapy. Corticosteroids have been shown to be teratogenic in many species when given in systemic doses equivalent to the human dose. Animal studies in which corticosteroids have been given to pregnant mice, rats, and rabbits have yielded an increased incidence of cleft palate in the offspring. In addition, dexamethasone has been shown to be teratogenic in mice and rabbits following topical ophthalmic application in multiples of the therapeutic dose. Topical ocular administration of dexamethasone to pregnant mice and rabbits during organogenesis produced embryofetal lethality, cleft palate and multiple visceral malformations. Topical and otic corticosteroids should not be used in large amounts, on large areas, or for prolonged periods of time in pregnant women. Dexamethasone injections have been used medically later in pregnancy to induce fetal lung maturation in patients at risk for pre-term delivery; use is for select circumstances and for a limited duration of time. An infant who is born to a woman receiving large doses of systemic corticosteroids during pregnancy should be monitored for signs of adrenal insufficiency, and appropriate therapy should be initiated, if necessary.

Systemic use of dexamethasone has not been studied during breast-feeding; corticosteroids appear in human milk and could suppress growth, interfere with endogenous corticosteroid production, or cause other untoward effects. Caution is warranted, and some manufacturers recommend discontinuing breast-feeding if systemic dexamethasone treatment is needed. However, experts generally consider inhaled corticosteroids and oral corticosteroids (e.g., prednisone and prednisolone), acceptable to use during breast-feeding. There is no information regarding dexamethasone effects on breastfed infants or milk production or its presence in human milk following placement of the intravitreal implant or intracanalicular insert to inform risk to an infant during lactation. However, the systemic concentration of dexamethasone following administration of the intracanalicular insert is low. It is not known whether topical ophthalmic administration of dexamethasone could result in sufficient systemic absorption to produce detectable quantities in breast milk. For COVID-19, the National Institutes of Health (NIH) recommends dexamethasone be offered to lactating mothers who qualify for therapy without interruption of breast-feeding. Consider the benefits of breast-feeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition.

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

Use systemic corticosteroids with caution in the geriatric patient; the risks and benefits of therapy should be considered for any individual patient. Geriatric and debilitated patients are especially susceptible to corticosteroid-induced decreases in bone mineral density and resultant fractures. Detrimental effects on bone metabolism, such as osteoporosis, are a risk with chronic, systemically-administered corticosteroids.  According to the Beers Criteria, systemic corticosteroids are considered potentially inappropriate medications (PIMs) for use in geriatric patients with delirium or at high risk for delirium and should be avoided in these patient populations due to the possibility of new-onset delirium or exacerbation of the current condition. The Beers expert panel notes that oral and parenteral corticosteroids may be required for conditions such as exacerbation of chronic obstructive pulmonary disease (COPD) but should be prescribed in the lowest effective dose and for the shortest possible duration. The federal Omnibus Budget Reconciliation Act (OBRA) regulates medication use in residents of long-term care facilities (LTCFs); the need for continued use of a systemic glucocorticoid should be documented, along with monitoring for adverse consequences with intermediate or longer-term use.

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

Dexamethasone ophthalmic solutions are sometimes used off-label in the ear for otic conditions. Otic dexamethasone use is contraindicated for use in patients with tympanic membrane perforation.

ADVERSE REACTIONS

ocular hemorrhage / Delayed / 6.0-23.0
exfoliative dermatitis / Delayed / Incidence not known
increased intracranial pressure / Early / Incidence not known
papilledema / Delayed / Incidence not known
avascular necrosis / Delayed / Incidence not known
tendon rupture / Delayed / Incidence not known
bone fractures / Delayed / Incidence not known
GI bleeding / Delayed / Incidence not known
esophageal ulceration / Delayed / Incidence not known
pancreatitis / Delayed / Incidence not known
GI perforation / Delayed / Incidence not known
peptic ulcer / Delayed / Incidence not known
anaphylactoid reactions / Rapid / Incidence not known
skin atrophy / Delayed / Incidence not known
angioedema / Rapid / Incidence not known
heart failure / Delayed / Incidence not known
seizures / Delayed / Incidence not known
stroke / Early / Incidence not known
arachnoiditis / Early / Incidence not known
visual impairment / Early / Incidence not known
macular edema / Delayed / Incidence not known
corneal erosion / Delayed / Incidence not known
retinopathy / Delayed / Incidence not known
ocular hypertension / Delayed / Incidence not known
keratoconjunctivitis / Early / Incidence not known
endophthalmitis / Delayed / Incidence not known
optic neuritis / Delayed / Incidence not known
retinal detachment / Delayed / Incidence not known
keratitis / Delayed / Incidence not known
bradycardia / Rapid / Incidence not known
vasculitis / Delayed / Incidence not known
myocardial infarction / Delayed / Incidence not known
thrombosis / Delayed / Incidence not known
thromboembolism / Delayed / Incidence not known
pulmonary edema / Early / Incidence not known
cardiomyopathy / Delayed / Incidence not known
cardiac arrest / Early / Incidence not known
arrhythmia exacerbation / Early / Incidence not known

iritis / Delayed / 5.0-15.0
conjunctival hyperemia / Early / 1.0-7.0
photophobia / Early / 0-1.0
hyperemia / Delayed / 0-1.0
corneal edema / Early / 1.0-1.0
hyperglycemia / Delayed / 10.0
hypotension / Rapid / Incidence not known
physiological dependence / Delayed / Incidence not known
pseudotumor cerebri / Delayed / Incidence not known
withdrawal / Early / Incidence not known
adrenocortical insufficiency / Delayed / Incidence not known
hypothalamic-pituitary-adrenal (HPA) suppression / Delayed / Incidence not known
Cushing's syndrome / Delayed / Incidence not known
diabetes mellitus / Delayed / Incidence not known
glycosuria / Early / Incidence not known
osteoporosis / Delayed / Incidence not known
growth inhibition / Delayed / Incidence not known
myopathy / Delayed / Incidence not known
osteopenia / Delayed / Incidence not known
myasthenia / Delayed / Incidence not known
gastritis / Delayed / Incidence not known
esophagitis / Delayed / Incidence not known
immunosuppression / Delayed / Incidence not known
candidiasis / Delayed / Incidence not known
erythema / Early / Incidence not known
skin ulcer / Delayed / Incidence not known
impaired wound healing / Delayed / Incidence not known
sodium retention / Delayed / Incidence not known
fluid retention / Delayed / Incidence not known
hypokalemia / Delayed / Incidence not known
hypernatremia / Delayed / Incidence not known
edema / Delayed / Incidence not known
hypertension / Early / Incidence not known
hypocalcemia / Delayed / Incidence not known
metabolic alkalosis / Delayed / Incidence not known
euphoria / Early / Incidence not known
delirium / Early / Incidence not known
neuritis / Delayed / Incidence not known
EEG changes / Delayed / Incidence not known
impaired cognition / Early / Incidence not known
depression / Delayed / Incidence not known
mania / Early / Incidence not known
meningitis / Delayed / Incidence not known
peripheral neuropathy / Delayed / Incidence not known
amnesia / Delayed / Incidence not known
paresis / Delayed / Incidence not known
psychosis / Early / Incidence not known
hallucinations / Early / Incidence not known
memory impairment / Delayed / Incidence not known
conjunctivitis / Delayed / Incidence not known
exophthalmos / Delayed / Incidence not known
ocular inflammation / Early / Incidence not known
cataracts / Delayed / Incidence not known
ocular infection / Delayed / Incidence not known
blurred vision / Early / Incidence not known
palpitations / Early / Incidence not known
sinus tachycardia / Rapid / Incidence not known
angina / Early / Incidence not known
hypercholesterolemia / Delayed / Incidence not known
phlebitis / Rapid / Incidence not known
hepatomegaly / Delayed / Incidence not known
elevated hepatic enzymes / Delayed / Incidence not known

ocular pain / Early / 1.0-8.0
xerophthalmia / Early / 5.0-5.0
headache / Early / 1.0-4.0
ptosis / Delayed / 2.0-2.0
ocular discharge / Delayed / 1.0-1.0
lacrimation / Early / 1.0-1.0
malaise / Early / Incidence not known
fever / Early / Incidence not known
lethargy / Early / Incidence not known
menstrual irregularity / Delayed / Incidence not known
hirsutism / Delayed / Incidence not known
hypertrichosis / Delayed / Incidence not known
myalgia / Early / Incidence not known
weakness / Early / Incidence not known
arthropathy / Delayed / Incidence not known
arthralgia / Delayed / Incidence not known
nausea / Early / Incidence not known
abdominal pain / Early / Incidence not known
hiccups / Early / Incidence not known
weight gain / Delayed / Incidence not known
appetite stimulation / Delayed / Incidence not known
vomiting / Early / Incidence not known
leukocytosis / Delayed / Incidence not known
infection / Delayed / Incidence not known
rash / Early / Incidence not known
urticaria / Rapid / Incidence not known
pruritus / Rapid / Incidence not known
alopecia / Delayed / Incidence not known
skin hyperpigmentation / Delayed / Incidence not known
hyperhidrosis / Delayed / Incidence not known
striae / Delayed / Incidence not known
perineal pain / Early / Incidence not known
acneiform rash / Delayed / Incidence not known
purpura / Delayed / Incidence not known
injection site reaction / Rapid / Incidence not known
skin hypopigmentation / Delayed / Incidence not known
ecchymosis / Delayed / Incidence not known
telangiectasia / Delayed / Incidence not known
petechiae / Delayed / Incidence not known
xerosis / Delayed / Incidence not known
acne vulgaris / Delayed / Incidence not known
irritability / Delayed / Incidence not known
insomnia / Early / Incidence not known
paresthesias / Delayed / Incidence not known
anxiety / Delayed / Incidence not known
dizziness / Early / Incidence not known
restlessness / Early / Incidence not known
emotional lability / Early / Incidence not known
vertigo / Early / Incidence not known
ocular hypotonia / Delayed / Incidence not known
ocular irritation / Rapid / Incidence not known
foreign body sensation / Rapid / Incidence not known
ocular pruritus / Rapid / Incidence not known
mydriasis / Early / Incidence not known
syncope / Early / Incidence not known

DRUG INTERACTIONS

Abatacept: (Moderate) Concomitant use of immunosuppressives, as well as long-term corticosteroids, may potentially increase the risk of serious infection in abatacept treated patients. Advise patients taking abatacept to seek immediate medical advice if they develop signs and symptoms suggestive of infection.
Abemaciclib: (Major) Avoid coadministration of dexamethasone with abemaciclib due to decreased exposure to abemaciclib and its active metabolites, which may lead to reduced efficacy. Consider alternative treatments. Abemaciclib is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Coadministration with moderate CYP3A4 inducers is predicted to decrease the relative potency adjusted unbound AUC of abemaciclib plus its active metabolites (M2, M18, and M20) by 53%, 41%, and 29% respectively.
Acetaminophen; Aspirin, ASA; Caffeine: (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.
Acetaminophen; Aspirin: (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.
Acetaminophen; Aspirin; Diphenhydramine: (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.
Acetaminophen; Caffeine; Dihydrocodeine: (Moderate) Concomitant use of dihydrocodeine with dexamethasone can decrease dihydrocodeine levels, resulting in less metabolism by CYP2D6 and decreased dihydromorphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. If coadministration is necessary, monitor for reduced efficacy of dihydrocodeine and signs of opioid withdrawal; consider increasing the dose of dihydrocodeine as needed. If dexamethasone is discontinued, consider a dose reduction of dihydrocodeine and frequently monitor for signs or respiratory depression and sedation. Dexamethasone is a moderate inducer of CYP3A4, an isoenzyme partially responsible for the metabolism of dihydrocodeine.
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 : (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; Codeine: (Moderate) Concomitant use of codeine with dexamethasone can decrease codeine levels, resulting in less metabolism by CYP2D6 and decreased morphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when codeine is being used for cough. If coadministration is necessary, monitor for reduced efficacy of codeine and signs of opioid withdrawal; consider increasing the dose of codeine as needed. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs or respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A4 to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a moderate CYP3A4 inducer.
Acetaminophen; Dextromethorphan; Guaifenesin; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
Acetaminophen; Dextromethorphan; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
Acetaminophen; Guaifenesin; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
Acetaminophen; Hydrocodone: (Moderate) Concomitant use of hydrocodone with dexamethasone can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when hydrocodone is being used for cough. If coadministration is necessary, monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs or respiratory depression and sedation. Hydrocodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer.
Acetaminophen; Oxycodone: (Moderate) Monitor for reduced efficacy of oxycodone and signs of opioid withdrawal if coadministration with dexamethasone is necessary; consider increasing the dose of oxycodone as needed. If dexamethasone is discontinued, consider a dose reduction of oxycodone and frequently monitor for signs of respiratory depression and sedation. Oxycodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Concomitant use with CYP3A4 inducers can decrease oxycodone concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
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) Monitor blood glucose during concomitant corticosteroid and sulfonylurea use; a sulfonylurea dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells.
Adagrasib: (Moderate) Monitor for steroid-related adverse reactions if coadministration of adagrasib with dexamethasone is necessary, due to increased dexamethasone exposure; Cushing's syndrome and adrenal suppression could potentially occur with long-term use. Consider the use of corticosteroids such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A inhibitors, especially for long-term use. Adagrasib is a strong CYP3A inhibitor and dexamethasone is primarily metabolized by CYP3A. Another strong CYP3A inhibitor has been reported to decrease the metabolism of certain corticosteroids by up to 60%, leading to increased risk of corticosteroid side effects.
Albendazole: (Minor) Concomitant administration of albendazole with dexamethasone increases the plasma concentration of albendazole sulfoxide, presumably via reduction in albendazole sulfoxide clearance.
Albiglutide: (Moderate) Monitor blood glucose during concomitant corticosteroid and incretin mimetic use; an incretin mimetic dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells.
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.
Alemtuzumab: (Moderate) Concomitant use of alemtuzumab with immunosuppressant doses of corticosteroids may increase the risk of immunosuppression. Monitor patients carefully for signs and symptoms of infection.
Aliskiren; Hydrochlorothiazide, HCTZ: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.
Alogliptin; Metformin: (Moderate) Monitor blood glucose during concomitant corticosteroid and metformin use; a metformin dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells.
Alosetron: (Minor) Dexamethasone can induce the activity of CYP3A4 and increase the metabolism of alosetron by increasing the metabolism of the drug, thus potentially reducing the effect of alosetron.
Alpha-glucosidase Inhibitors: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells.
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: (Moderate) Concomitant use of anticholinesterase agents, such as ambenonium chloride, and corticosteroids may produce severe weakness in patients with myasthenia gravis. If possible, anticholinesterase agents used to treat myasthenia should be withdrawn at least 24 hours before initiating corticosteroid therapy.
Amifampridine: (Moderate) Carefully consider the need for concomitant treatment with systemic corticosteroids and amifampridine, as coadministration may increase the risk of seizures. If coadministration occurs, closely monitor patients for seizure activity. Seizures have been observed in patients without a history of seizures taking amifampridine at recommended doses. Systemic corticosteroids may increase the risk of seizures in some patients.
Amiloride; Hydrochlorothiazide, HCTZ: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.
Aminolevulinic Acid: (Minor) Corticosteroids administered prior to or concomitantly with photosensitizing agents used in photodynamic therapy may decrease the efficacy of the treatment.
Aminosalicylate sodium, Aminosalicylic acid: (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.
Amiodarone: (Major) Use caution when coadministering amiodarone with drugs which may induce hypokalemia and, or hypomagnesemia, including corticosteroids. Since antiarrhythmic drugs may be ineffective or may be arrhythmogenic in patients with hypokalemia, any potassium or magnesium deficiency should be corrected before instituting and during amiodarone therapy.
Amlodipine: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased.
Amlodipine; Atorvastatin: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased.
Amlodipine; Benazepril: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased.
Amlodipine; Celecoxib: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased.
Amlodipine; Olmesartan: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased.
Amlodipine; Valsartan: (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased.
Amlodipine; Valsartan; Hydrochlorothiazide, HCTZ: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss. (Minor) Coadministration of CYP3A4 inducers with amlodipine can theoretically increase the hepatic metabolism of amlodipine (a CYP3A4 substrate). Caution should be used when CYP3A4 inducers, such as dexamethasone, are coadministered with amlodipine. Monitor therapeutic response; the dosage requirements of amlodipine may be increased.
Amoxicillin; Clarithromycin; Omeprazole: (Major) Coadministration of dexamethasone and clarithromycin may decrease clarithromycin serum concentrations due to CYP3A4 enzyme induction. While the 14-OH-clarithromycin active metabolite concentrations are increased, this metabolite has different antimicrobial activity compared to clarithromycin. The intended therapeutic effect of clarithromycin could be decreased. It is not clear if clarithromycin activity against other organisms would be reduced, but reduced efficacy is possible. Alternatives to clarithromycin should be considered in patients who are taking CYP3A4 inducers. Additionally, clarithromycin inhibits CYP3A4 and has the potential to result in increased plasma concentrations of dexamethasone. Increased blood concentrations and physiologic activity may necessitate a decrease in corticosteroid dosage. (Moderate) Monitor for decreased efficacy of omeprazole if coadministration with dexamethasone is necessary. Omeprazole is metabolized by CYP2C19 and CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. The manufacturer of omeprazole recommends avoidance with strong inducers because decreased exposure of omeprazole can occur. Recommendations are not available for concomitant use with moderate inducers of CYP3A4.
Amphotericin B 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.
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.
Apalutamide: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with apalutamide is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A4 substrate and apalutamide is a strong CYP3A4 inducer.
Aprepitant, Fosaprepitant: (Minor) Aprepitant, fosaprepitant is indicated for the treatment of chemotherapy-induced nausea/vomiting (CINV) in combination with dexamethasone and a 5HT3 antagonist; the pharmacokinetic interactions discussed here are accounted for in the recommended dosing for this indication. No dosage adjustment is needed when dexamethasone is used in combination with a single 40-mg dose of oral aprepitant. Dexamethasone is a CYP3A4 substrate. Aprepitant, when administered as a 3-day oral regimen (125 mg/80 mg/80 mg), is a moderate CYP3A4 inhibitor and inducer. The AUC of dexamethasone (8 mg PO on days 1, 2, and 3) was increased by approximately 2-fold on days 1 and 2 when given with a single 150-mg dose of IV fosaprepitant. After a 5-day regimen of oral aprepitant (125 mg/80 mg/80 mg/80 mg/80 mg), the AUC of dexamethasone increased 2.2-fold on days 1 and 5. A single dose of aprepitant 40 mg increased the AUC of dexamethasone by 1.45-fold, which was not considered clinically significant.
Aripiprazole: (Moderate) Because aripiprazole is metabolized by CYP3A4, concurrent use of CYP3A4 inducers such as dexamethasone may result in decreased plasma concentrations of aripiprazole. If these agents are used in combination, the patient should be carefully monitored for a decrease in aripiprazole efficacy. An increase in aripiprazole dosage may be clinically warranted in some patients. Avoid concurrent use of Abilify Maintena with a CYP3A4 inducer when the combined treatment period exceeds 14 days because aripiprazole blood concentrations decline and may become suboptimal. There are no dosing recommendations for Aristada or Aristada Initio during concurrent use of a mild or moderate CYP3A4 inducer.
Armodafinil: (Minor) Armodafinil is partially metabolized via CYP3A4/5 isoenzymes. CYP3A4 inducers, such as dexamethasone, may potentially increase the metabolism of armodafinil. Decreased serum levels of armodafinil could potentially result in decreased efficacy of the drug.
Arsenic Trioxide: (Moderate) Caution is advisable during concurrent use of arsenic trioxide and corticosteroids as electrolyte imbalance caused by corticosteroids may increase the risk of QT prolongation with arsenic trioxide.
Artemether; Lumefantrine: (Major) Dexamethasone is a substrate/inducer and both components of artemether; lumefantrine are substrates of the CYP3A4 isoenzyme; therefore, coadministration may lead to decreased artemether; lumefantrine concentrations. Concomitant use warrants caution due to a possible reduction in antimalarial activity.
Articaine; Epinephrine: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and epinephrine use due to risk for additive hypokalemia; potassium supplementation may be necessary. Corticosteroids may potentiate the hypokalemic effects of epinephrine.
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) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.
Aspirin, ASA; Butalbital; Caffeine: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Butalbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use. (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.
Aspirin, ASA; Caffeine: (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.
Aspirin, ASA; Caffeine; Orphenadrine: (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.
Aspirin, ASA; Carisoprodol: (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.
Aspirin, ASA; Carisoprodol; Codeine: (Moderate) Concomitant use of codeine with dexamethasone can decrease codeine levels, resulting in less metabolism by CYP2D6 and decreased morphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when codeine is being used for cough. If coadministration is necessary, monitor for reduced efficacy of codeine and signs of opioid withdrawal; consider increasing the dose of codeine as needed. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs or respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A4 to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a moderate CYP3A4 inducer. (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.
Aspirin, ASA; Citric Acid; Sodium Bicarbonate: (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.
Aspirin, ASA; Dipyridamole: (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.
Aspirin, ASA; Omeprazole: (Moderate) Monitor for decreased efficacy of omeprazole if coadministration with dexamethasone is necessary. Omeprazole is metabolized by CYP2C19 and CYP3A4. Dexamethasone is a moderate CYP3A4 inducer. The manufacturer of omeprazole recommends avoidance with strong inducers because decreased exposure of omeprazole can occur. Recommendations are not available for concomitant use with moderate inducers of CYP3A4. (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.
Aspirin, ASA; Oxycodone: (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance. (Moderate) Monitor for reduced efficacy of oxycodone and signs of opioid withdrawal if coadministration with dexamethasone is necessary; consider increasing the dose of oxycodone as needed. If dexamethasone is discontinued, consider a dose reduction of oxycodone and frequently monitor for signs of respiratory depression and sedation. Oxycodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Concomitant use with CYP3A4 inducers can decrease oxycodone concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
Aspirin, ASA; Pravastatin: (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.
Atazanavir: (Major) Avoid concurrent use of dexamethasone with atazanavir. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance to atazanavir; consider use of an alternative corticosteroid. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; atazanavir is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone) whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use.
Atazanavir; Cobicistat: (Major) Avoid concurrent use of dexamethasone with atazanavir. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance to atazanavir; consider use of an alternative corticosteroid. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; atazanavir is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone) whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. (Major) Avoid concurrent use of dexamethasone with cobicistat containing regimens. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; cobicistat is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use.
Atenolol; Chlorthalidone: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.
Atogepant: (Major) Avoid use of atogepant and dexamethasone when atogepant is used for chronic migraine. Use an atogepant dose of 30 or 60 mg PO once daily for episodic migraine if coadministered with dexamethasone. Concurrent use may decrease atogepant exposure and reduce efficacy. Atogepant is a CYP3A substrate and dexamethasone is a moderate CYP3A inducer.
Atracurium: (Moderate) Limit the period of use of neuromuscular blockers and corticosteroids and only use when the specific advantages of the drugs outweigh the risks for acute myopathy. An acute myopathy has been observed with the use of high doses of corticosteroids in patients receiving concomitant long-term therapy with neuromuscular blockers. Clinical improvement or recovery after stopping therapy may require weeks to years.
Atropine; Benzoic Acid; Hyoscyamine; Methenamine; Methylene Blue; Phenyl Salicylate: (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.
Avacopan: (Major) Avoid concomitant use of avacopan and dexamethasone due to the risk of decreased avacopan exposure which may reduce its efficacy. Avacopan is a CYP3A substrate and dexamethasone is a moderate CYP3A inducer.
Avanafil: (Minor) Avanafil is primarily metabolized by CYP3A4, and although no studies have been performed, concomitant administration of CYP3A4 inducers, such as dexamethasone, may decrease avanafil plasma levels. Concomitant use is not recommended.
Avapritinib: (Major) Avoid coadministration of avapritinib with dexamethasone due to the risk of decreased avapritinib efficacy. Avapritinib is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Coadministration with another moderate CYP3A4 inducer is predicted to decrease the AUC and Cmax of avapritinib by 62% and 55%, respectively.
Axitinib: (Major) Avoid coadministration of axitinib with dexamethasone due to the risk of decreased efficacy of axitinib. Selection of a concomitant medication with no or minimal CYP3A4 induction potential is recommended. Axitinib is a CYP3A4/5 substrate and dexamethasone is a CYP3A4 inducer. Coadministration with a strong CYP3A4/5 inducer significantly decreased the plasma exposure of axitinib in healthy volunteers.
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) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.
Basiliximab: (Minor) Because systemically administered corticosteroids have immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives.
Bedaquiline: (Major) Avoid concurrent use of dexamethasone with bedaquiline. Dexamethasone is a CYP3A4 inducer, which may result in decreased bedaquiline systemic exposure (AUC) and possibly reduced therapeutic effect.
Benazepril; Hydrochlorothiazide, HCTZ: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.
Bendroflumethiazide; Nadolol: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.
Benzhydrocodone; Acetaminophen: (Moderate) Concurrent use of benzhydrocodone with dexamethasone may decrease hydrocodone plasma concentrations, decrease opioid efficacy, and potentially lead to a withdrawal syndrome in those with physical dependence to opioid agonists. If concomitant use is necessary, consider increasing the benzhydrocodone dosage until stable drug effects are achieved. Monitor for signs of opioid withdrawal. Discontinuation of dexamethasone may increase the risk of increased opioid-related adverse reactions, such as fatal respiratory depression. If dexamethasone is discontinued, consider a benzhydrocodone dosage reduction and monitor patients for respiratory depression and sedation at frequent intervals. Benzhydrocodone is a prodrug of hydrocodone. Dexamethasone is an inducer of CYP3A4, an isoenzyme partially responsible for the metabolism of hydrocodone.
Benzoic Acid; Hyoscyamine; Methenamine; Methylene Blue; Phenyl Salicylate: (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.
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) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.
Bismuth Subsalicylate; Metronidazole; Tetracycline: (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.
Bisoprolol; Hydrochlorothiazide, HCTZ: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.
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.
Brentuximab vedotin: (Moderate) Concomitant administration of brentuximab vedotin and dexamethasone may decrease the exposure of monomethyl auristatin E (MMAE), one of the 3 components released from brentuximab vedotin. MMAE is a CYP3A4 substrate and dexamethasone is a potent CYP3A4 inducer; therefore, the efficacy of brentuximab may be reduced.
Brexpiprazole: (Moderate) Because brexpiprazole is partially metabolized by CYP3A4, concurrent use of CYP3A4 inducers such as dexamethasone may result in decreased plasma concentrations of brexpiprazole. If these agents are used in combination, the patient should be carefully monitored for a decrease in brexpiprazole efficacy. An increase in brexpiprazole dosage may be clinically warranted in some patients.
Brigatinib: (Moderate) Avoid coadministration of brigatinib with dexamethasone due to decreased plasma exposure to brigatinib which may result in decreased efficacy. If concomitant use is unavoidable, after 7 days of concomitant treatment with dexamethasone, increase the dose of brigatinib as tolerated in 30 mg increments to a maximum of twice the original brigatinib dose. After discontinuation of dexamethasone, resume the brigatinib dose that was tolerated prior to initiation of dexamethasone. Brigatinib is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Coadministration with a moderate CYP3A inducer is predicted to decrease the AUC of brigatinib by approximately 50%.
Bromocriptine: (Moderate) Caution and close monitoring are advised if bromocriptine and dexamethasone are used together. Concurrent use may decrease the plasma concentrations of bromocriptine resulting in loss of efficacy. Bromocriptine is extensively metabolized by the liver via CYP3A4; dexamethasone is a moderate inducer of CYP3A4.
Brompheniramine; 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.
Brompheniramine; 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.
Budesonide: (Moderate) Theoretically, induction of the cytochrome P450 (CYP) 3A4 isoenzyme may result in a lowering of budesonide plasma concentrations, reducing the clinical effect. Drugs known to induce the 3A4 isoenzyme include dexamethasone.
Budesonide; Formoterol: (Moderate) Theoretically, induction of the cytochrome P450 (CYP) 3A4 isoenzyme may result in a lowering of budesonide plasma concentrations, reducing the clinical effect. Drugs known to induce the 3A4 isoenzyme include dexamethasone.
Budesonide; Glycopyrrolate; Formoterol: (Moderate) Theoretically, induction of the cytochrome P450 (CYP) 3A4 isoenzyme may result in a lowering of budesonide plasma concentrations, reducing the clinical effect. Drugs known to induce the 3A4 isoenzyme include dexamethasone.
Bupivacaine; Epinephrine: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and epinephrine use due to risk for additive hypokalemia; potassium supplementation may be necessary. Corticosteroids may potentiate the hypokalemic effects of epinephrine.
Bupivacaine; Lidocaine: (Moderate) Concomitant use of systemic lidocaine and dexamethasone may decrease lidocaine plasma concentrations. Higher lidocaine doses may be required; titrate to effect. Lidocaine is a CYP3A4 and CYP1A2 substrate; dexamethasone induces CYP3A4.
Bupropion: (Moderate) Monitor for seizure activity during concomitant bupropion and corticosteroid use. Bupropion is associated with a dose-related seizure risk; concomitant use of other medications that lower the seizure threshold, such as systemic corticosteroids, increases the seizure risk.
Bupropion; Naltrexone: (Moderate) Monitor for seizure activity during concomitant bupropion and corticosteroid use. Bupropion is associated with a dose-related seizure risk; concomitant use of other medications that lower the seizure threshold, such as systemic corticosteroids, increases the seizure risk.
Buspirone: (Moderate) Potent inducers of hepatic cytochrome P450 3A4, such as dexamethasone, may increase the rate of buspirone metabolism.
Butabarbital: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Butabarbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use.
Butalbital; Acetaminophen: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Butalbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use.
Butalbital; Acetaminophen; Caffeine: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Butalbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use.
Butalbital; Acetaminophen; Caffeine; Codeine: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Butalbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use. (Moderate) Concomitant use of codeine with dexamethasone can decrease codeine levels, resulting in less metabolism by CYP2D6 and decreased morphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when codeine is being used for cough. If coadministration is necessary, monitor for reduced efficacy of codeine and signs of opioid withdrawal; consider increasing the dose of codeine as needed. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs or respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A4 to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a moderate CYP3A4 inducer.
Butalbital; Aspirin; Caffeine; Codeine: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Butalbital is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use. (Moderate) Concomitant use of codeine with dexamethasone can decrease codeine levels, resulting in less metabolism by CYP2D6 and decreased morphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when codeine is being used for cough. If coadministration is necessary, monitor for reduced efficacy of codeine and signs of opioid withdrawal; consider increasing the dose of codeine as needed. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs or respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A4 to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a moderate CYP3A4 inducer. (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.
Cabotegravir; Rilpivirine: (Contraindicated) Concurrent use of dexamethasone (more than 1 dose) and rilpivirine is contraindicated. When these drugs are coadministered, there is a potential for treatment failure and/or the development of rilpivirine or NNRTI resistance. Dexamethasone is an inducer of CYP3A4, which is primarily responsible for the metabolism of rilpivirine. Coadministration may result in decreased rilpivirine serum concentrations, which could cause impaired virologic response to rilpivirine.
Cabozantinib: (Minor) Monitor for an increase in dexamethasone-related adverse reactions if coadministration with cabozantinib is necessary. Dexamethasone is a P-glycoprotein (P-gp) substrate. Cabozantinib is a P-gp inhibitor and has the potential to increase plasma concentrations of P-gp substrates; however, the clinical relevance of this finding is unknown.
Caffeine; Sodium Benzoate: (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.
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; Famotidine; 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; 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; Magnesium Hydroxide; Simethicone: (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 Carbonate; Simethicone: (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) Monitor blood glucose during concomitant corticosteroid and SGLT2 inhibitor use; a SGLT2 inhibitor dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells.
Canagliflozin; Metformin: (Moderate) Monitor blood glucose during concomitant corticosteroid and metformin use; a metformin dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. (Moderate) Monitor blood glucose during concomitant corticosteroid and SGLT2 inhibitor use; a SGLT2 inhibitor dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells.
Candesartan; Hydrochlorothiazide, HCTZ: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.
Capmatinib: (Major) Avoid coadministration of capmatinib and dexamethasone due to the risk of decreased capmatinib exposure, which may reduce its efficacy. Capmatinib is a CYP3A substrate and dexamethasone is a moderate CYP3A4 inducer. Coadministration with another moderate CYP3A4 inducer decreased capmatinib exposure by 44%.
Captopril; Hydrochlorothiazide, HCTZ: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.
Carbamazepine: (Moderate) Hepatic microsomal enzyme inducers, including carbamazepine, can increase the metabolism of dexamethasone. Dosage adjustments may be necessary, and closer monitoring of clinical and/or adverse effects is warranted when carbamazepine is used with dexamethasone.
Carbinoxamine; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
Cariprazine: (Major) Cariprazine and its active metabolites are extensively metabolized by CYP3A4. Concurrent use of cariprazine with CYP3A4 inducers, such as dexamethasone, has not been evaluated and is not recommended because the net effect on active drug and metabolites is unclear.
Carmustine, BCNU: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
Carvedilol: (Minor) Increased concentrations of dexamethasone may occur if it is coadministered with carvedilol; exercise caution. Carvedilol is a P-glycoprotein (P-gp) inhibitor and dexamethasone is a P-gp substrate.
Caspofungin: (Major) Data suggest that coadministration of inducers or mixed inducers/inhibitors of hepatic drug clearance along with caspofungin may result in reduced caspofungin blood concentrations. The reductions may be clinically significant. It is not known how caspofungin drug clearance is induced. Drugs that may lead to reductions in caspofungin concentrations include dexamethasone. For adult patients receiving dexamethasone, an increase in the caspofungin dose to 70 mg/day should be considered. For pediatric patients receiving dexamethasone, a daily dosage of 70 mg/m2, not to exceed 70 mg, should be considered.
Cenobamate: (Minor) A dose adjustment of systemic dexamethasone may be necessary if cenobamate is initiated or withdrawn during therapy. Cenobamate may increase the metabolism of dexamethasone resulting in decreased exposure. Cenobamate is a moderate inducer of CYP3A4; dexamethasone is a CYP3A4 substrate.
Ceritinib: (Moderate) Monitor for steroid-related adverse reactions if coadministration of ceritinib with dexamethasone is necessary, due to increased dexamethasone exposure; Cushings syndrome and adrenal suppression could potentially occur with long-term use. Consider the use of corticosteroids such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, especially for long-term use. Ceritinib is a strong CYP3A4 inhibitor and dexamethasone is primarily metabolized by CYP3A4. Another strong CYP3A4 inhibitor has been reported to decrease the metabolism of certain corticosteroids by up to 60%, leading to increased risk of corticosteroid side effects.
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.
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) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.
Chlorpheniramine; Codeine: (Moderate) Concomitant use of codeine with dexamethasone can decrease codeine levels, resulting in less metabolism by CYP2D6 and decreased morphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when codeine is being used for cough. If coadministration is necessary, monitor for reduced efficacy of codeine and signs of opioid withdrawal; consider increasing the dose of codeine as needed. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs or respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A4 to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a moderate CYP3A4 inducer.
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) Concomitant use of dihydrocodeine with dexamethasone can decrease dihydrocodeine levels, resulting in less metabolism by CYP2D6 and decreased dihydromorphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. If coadministration is necessary, monitor for reduced efficacy of dihydrocodeine and signs of opioid withdrawal; consider increasing the dose of dihydrocodeine as needed. If dexamethasone is discontinued, consider a dose reduction of dihydrocodeine and frequently monitor for signs or respiratory depression and sedation. Dexamethasone is a moderate inducer of CYP3A4, an isoenzyme partially responsible for the metabolism of dihydrocodeine. (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: (Moderate) Concomitant use of hydrocodone with dexamethasone can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when hydrocodone is being used for cough. If coadministration is necessary, monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs or respiratory depression and sedation. Hydrocodone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer.
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) Monitor blood glucose during concomitant corticosteroid and sulfonylurea use; a sulfonylurea dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells.
Chlorthalidone: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.
Chlorthalidone; Clonidine: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.
Cholestyramine: (Moderate) Cholestyramine may increase the clearance of corticosteroids.
Choline Salicylate; Magnesium Salicylate: (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.
Cisapride: (Moderate) Cisapride is metabolized by the hepatic cytochrome P450 enzyme system, specifically the CYP3A4 isoenzyme. Inducers of CYP3A4, such as dexamethasone, may increase the clearance of cisapride.
Cisatracurium: (Moderate) Limit the period of use of neuromuscular blockers and corticosteroids and only use when the specific advantages of the drugs outweigh the risks for acute myopathy. An acute myopathy has been observed with the use of high doses of corticosteroids in patients receiving concomitant long-term therapy with neuromuscular blockers. Clinical improvement or recovery after stopping therapy may require weeks to years.
Clarithromycin: (Major) Coadministration of dexamethasone and clarithromycin may decrease clarithromycin serum concentrations due to CYP3A4 enzyme induction. While the 14-OH-clarithromycin active metabolite concentrations are increased, this metabolite has different antimicrobial activity compared to clarithromycin. The intended therapeutic effect of clarithromycin could be decreased. It is not clear if clarithromycin activity against other organisms would be reduced, but reduced efficacy is possible. Alternatives to clarithromycin should be considered in patients who are taking CYP3A4 inducers. Additionally, clarithromycin inhibits CYP3A4 and has the potential to result in increased plasma concentrations of dexamethasone. Increased blood concentrations and physiologic activity may necessitate a decrease in corticosteroid dosage.
Clofarabine: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
Clozapine: (Moderate) Caution is advisable during concurrent use of dexamethasone and clozapine. Dexamethasone is an inducer of CYP3A4, one of the isoenzymes responsible for the metabolism of clozapine. According to the manufacturer, patients receiving clozapine in combination with a weak to moderate CYP3A4 inducer should be monitored for loss of effectiveness. Consideration should be given to increasing the clozapine dose if necessary. Concurrent use with strong CYP3A4 inducers is not recommended. Topical corticosteroids are not likely to interact.
Cobicistat: (Major) Avoid concurrent use of dexamethasone with cobicistat containing regimens. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; cobicistat is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use.
Cobimetinib: (Major) Avoid the concurrent use of cobimetinib with dexamethasone due to decreased cobimetinib efficacy. Cobimetinib is a CYP3A substrate in vitro, and dexamethasone is a moderate inducer of CYP3A. Based on simulations, cobimetinib exposure would decrease by 73% when coadministered with a moderate CYP3A inducer.
Codeine: (Moderate) Concomitant use of codeine with dexamethasone can decrease codeine levels, resulting in less metabolism by CYP2D6 and decreased morphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when codeine is being used for cough. If coadministration is necessary, monitor for reduced efficacy of codeine and signs of opioid withdrawal; consider increasing the dose of codeine as needed. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs or respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A4 to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a moderate CYP3A4 inducer.
Codeine; Guaifenesin: (Moderate) Concomitant use of codeine with dexamethasone can decrease codeine levels, resulting in less metabolism by CYP2D6 and decreased morphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when codeine is being used for cough. If coadministration is necessary, monitor for reduced efficacy of codeine and signs of opioid withdrawal; consider increasing the dose of codeine as needed. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs or respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A4 to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a moderate CYP3A4 inducer.
Codeine; Guaifenesin; Pseudoephedrine: (Moderate) Concomitant use of codeine with dexamethasone can decrease codeine levels, resulting in less metabolism by CYP2D6 and decreased morphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when codeine is being used for cough. If coadministration is necessary, monitor for reduced efficacy of codeine and signs of opioid withdrawal; consider increasing the dose of codeine as needed. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs or respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A4 to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a moderate CYP3A4 inducer.
Codeine; Phenylephrine; Promethazine: (Moderate) Concomitant use of codeine with dexamethasone can decrease codeine levels, resulting in less metabolism by CYP2D6 and decreased morphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when codeine is being used for cough. If coadministration is necessary, monitor for reduced efficacy of codeine and signs of opioid withdrawal; consider increasing the dose of codeine as needed. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs or respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A4 to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a moderate CYP3A4 inducer. (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.
Codeine; Promethazine: (Moderate) Concomitant use of codeine with dexamethasone can decrease codeine levels, resulting in less metabolism by CYP2D6 and decreased morphine concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. It is recommended to avoid this combination when codeine is being used for cough. If coadministration is necessary, monitor for reduced efficacy of codeine and signs of opioid withdrawal; consider increasing the dose of codeine as needed. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs or respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A4 to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a moderate CYP3A4 inducer.
Corticorelin, Ovine: (Major) Patients pretreated with dexamethasone have demonstrated an inhibited or blunted response to corticotropin, ovine. Patients receiving corticotropin, ovine should not be pretreated with dexamethasone; no specific guidelines are available.
Cyclosporine: (Moderate) Convulsions have been reported during concurrent use of cyclosporine and other corticosteroids. In addition, mutual inhibition of metabolism occurs with concurrent use of cyclosporine and dexamethasone; therefore, the potential for adverse events associated with either drug may be increased. Coadministration should be approached with caution.
Dabrafenib: (Major) Use dabrafenib and dexamethasone together with caution; concentrations of either agent may be decreased. Use an alternate agent in place of dexamethasone if possible. If concomitant use cannot be avoided, monitor patients for loss of dexamethasone efficacy. Dexamethasone and dabrafenib are both CYP3A4 substrates and moderate CYP3A4 inducers.
Daclatasvir: (Major) The dose of daclatasvir, a CYP3A4 substrate, must be increased to 90 mg PO once daily when administered in combination with moderate CYP3A4 inducers, such as dexamethasone. Taking these drugs together may decrease daclatasvir serum concentrations, potentially resulting in reduced antiviral efficacy and antimicrobial resistance. Conversely, the therapeutic effects of dexamethasone, a P-glycoprotein (P-gp) substrate, may be increased by daclatasvir, a P-gp inhibitor.
Dapagliflozin: (Moderate) Monitor blood glucose during concomitant corticosteroid and SGLT2 inhibitor use; a SGLT2 inhibitor dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells.
Dapagliflozin; Metformin: (Moderate) Monitor blood glucose during concomitant corticosteroid and metformin use; a metformin dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. (Moderate) Monitor blood glucose during concomitant corticosteroid and SGLT2 inhibitor use; a SGLT2 inhibitor dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells.
Dapagliflozin; Saxagliptin: (Moderate) Monitor blood glucose during concomitant corticosteroid and SGLT2 inhibitor use; a SGLT2 inhibitor dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells.
Dapsone: (Moderate) Closely monitor for a reduction in dapsone efficacy and signs of hemolytic anemia if coadministration with dexamethasone is necessary. Dapsone is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Coadministration may decrease plasma concentrations of dapsone and increase the formation of dapsone hydroxylamine (a metabolite associated with hemolysis).
Daridorexant: (Major) Avoid concomitant use of daridorexant and dexamethasone. Coadministration may decrease daridorexant exposure which may reduce its efficacy. Daridorexant is a CYP3A substrate and dexamethasone is a moderate CYP3A inducer. Concomitant use of another moderate CYP3A inducer decreased daridorexant overall exposure by over 50%.
Darunavir: (Major) Avoid concurrent use of darunavir with dexamethasone. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance to darunavir; consider use of an alternative corticosteroid. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; darunavir is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use.
Darunavir; Cobicistat: (Major) Avoid concurrent use of darunavir with dexamethasone. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance to darunavir; consider use of an alternative corticosteroid. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; darunavir is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. (Major) Avoid concurrent use of dexamethasone with cobicistat containing regimens. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; cobicistat is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use.
Darunavir; Cobicistat; Emtricitabine; Tenofovir alafenamide: (Major) Avoid concurrent use of darunavir with dexamethasone. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance to darunavir; consider use of an alternative corticosteroid. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; darunavir is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. (Major) Avoid concurrent use of dexamethasone with cobicistat containing regimens. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; cobicistat is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use.
Dasabuvir; Ombitasvir; Paritaprevir; Ritonavir: (Contraindicated) Concurrent administration of dexamethasone with dasabuvir; ombitasvir; paritaprevir; ritonavir is contraindicated. Taking these drugs together could result in elevated dexamethasone plasma concentrations and decreased concentrations of dasabuvir, paritaprevir, and ritonavir. Antiviral efficacy could be affected. Dexamethasone is a P-glycoprotein (P-gp) substrate and a CYP3A4 substrate/inducer. Ritonavir is a P-gp inhibitor and a CYP3A4 substrate/potent inhibitor. Both paritaprevir and dasabuvir (minor) are CYP3A4 substrates. (Contraindicated) Concurrent administration of dexamethasone with dasabuvir; ombitasvir; paritaprevir; ritonavir or ombitasvir; paritaprevir; ritonavir is contraindicated. Taking these drugs together could result in elevated dexamethasone plasma concentrations and decreased concentrations of dasabuvir, paritaprevir, and ritonavir. Antiviral efficacy could be affected. Dexamethasone is a P-glycoprotein (P-gp) substrate and a CYP3A4 substrate/inducer. Ritonavir is a P-gp inhibitor and a CYP3A4 substrate/potent inhibitor. Both paritaprevir and dasabuvir (minor) are CYP3A4 substrates. (Moderate) Close monitoring of therapeutic and adverse effects is required when dexamethasone is coadministered with ritonavir. Ritonavir inhibits CYP3A4 and dexamethasone is a CYP3A4 substrate.
Deferasirox: (Moderate) Because gastric ulceration and GI bleeding have been reported in patients taking deferasirox, use caution when coadministering with other drugs known to increase the risk of peptic ulcers or gastric hemorrhage including corticosteroids.
Deflazacort: (Major) Avoid concomitant use of deflazacort and dexamethasone. Concurrent use may significantly decrease concentrations of 21-desDFZ, the active metabolite of deflazacort, resulting in loss of efficacy. Deflazacort is a CYP3A4 substrate; dexamethasone is a moderate inducer of CYP3A4. Administration of deflazacort with multiple doses of rifampin (a strong CYP3A4 inducer) resulted in geometric mean exposures that were approximately 95% lower compared to administration alone.
Delavirdine: (Minor) Since dexamethasone may induce metabolism of delavirdine, concomitant use of these agents should be done with caution. Delavirdine therapy may be less effective due to decreased plasma levels in patients taking these drugs concomitantly.
Denileukin Diftitox: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
Denosumab: (Moderate) The safety and efficacy of denosumab use in patients with immunosuppression have not been evaluated. Patients receiving immunosuppressives along with denosumab may be at a greater risk of developing an infection.
Desmopressin: (Major) Desmopressin is contraindicated with concomitant inhaled or systemic corticosteroid use due to an increased risk of hyponatremia. Desmopressin can be started or resumed 3 days or 5 half-lives after the corticosteroid is discontinued, whichever is longer.
Dextromethorphan; Bupropion: (Moderate) Monitor for seizure activity during concomitant bupropion and corticosteroid use. Bupropion is associated with a dose-related seizure risk; concomitant use of other medications that lower the seizure threshold, such as systemic corticosteroids, increases the seizure risk.
Dextromethorphan; Diphenhydramine; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
Dextromethorphan; Guaifenesin; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
Dextromethorphan; Quinidine: (Moderate) Quinidine is a substrate of the CYP3A4 isoenzyme. Inducers of CYP3A4 such as dexamethasone may increase hepatic elimination of quinidine with the potential for reduced efficacy of quinidine.
Dipeptidyl Peptidase-4 Inhibitors: (Moderate) Monitor blood glucose during concomitant corticosteroid and dipeptidyl peptidase-4 (DPP-4) inhibitor use; a DPP-4 dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells.
Diphenhydramine; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
Dofetilide: (Major) Corticosteroids can cause increases in blood pressure, sodium and water retention, and hypokalemia, predisposing patients to interactions with certain other medications. Corticosteroid-induced hypokalemia could also enhance the proarrhythmic effects of dofetilide.
Dolutegravir; Rilpivirine: (Contraindicated) Concurrent use of dexamethasone (more than 1 dose) and rilpivirine is contraindicated. When these drugs are coadministered, there is a potential for treatment failure and/or the development of rilpivirine or NNRTI resistance. Dexamethasone is an inducer of CYP3A4, which is primarily responsible for the metabolism of rilpivirine. Coadministration may result in decreased rilpivirine serum concentrations, which could cause impaired virologic response to rilpivirine.
Doravirine: (Moderate) Concurrent administration of doravirine and dexamethasone may result in decreased doravirine exposure, resulting in potential loss of virologic control. Doravirine is a CYP3A4 substrate; dexamethasone is a moderate CYP3A4 inducer.
Doravirine; Lamivudine; Tenofovir disoproxil fumarate: (Moderate) Concurrent administration of doravirine and dexamethasone may result in decreased doravirine exposure, resulting in potential loss of virologic control. Doravirine is a CYP3A4 substrate; dexamethasone is a moderate CYP3A4 inducer.
Doxacurium: (Moderate) Limit the period of use of neuromuscular blockers and corticosteroids and only use when the specific advantages of the drugs outweigh the risks for acute myopathy. An acute myopathy has been observed with the use of high doses of corticosteroids in patients receiving concomitant long-term therapy with neuromuscular blockers. Clinical improvement or recovery after stopping therapy may require weeks to years.
Dronabinol: (Moderate) Use caution if coadministration of dronabinol with dexamethasone is necessary, and monitor for a decrease in the efficacy of dronabinol. Dronabinol is a CYP2C9 and 3A4 substrate; dexamethasone is a moderate inducer of CYP3A4. Concomitant use may result in decreased plasma concentrations of dronabinol.
Dronedarone: (Major) The concomitant use of dronedarone and CYP3A4 inducers should be avoided. Dronedarone is metabolized by CYP3A and is an inhibitor of CYP3A and P-gp. Dexamethasone induces CYP3A4 and is a substrate for CYP3A4 and P-gp. Coadministration of CYP3A4 inducers, such as dexamethasone, with dronedarone may result in reduced plasma concentration and subsequent reduced effectiveness of dronedarone therapy; the plasma concentrations of dexamethasone may also be increased.
Droperidol: (Moderate) Caution is advised when using droperidol in combination with corticosteroids which may lead to electrolyte abnormalities, especially hypokalemia or hypomagnesemia, as such abnormalities may increase the risk for QT prolongation or cardiac arrhythmias.
Dulaglutide: (Moderate) Monitor blood glucose during concomitant corticosteroid and incretin mimetic use; an incretin mimetic dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells.
Duvelisib: (Major) Avoid concomitant use of duvelisib with dexamethasone. Coadministration may decrease the exposure of duvelisib, which may reduce the efficacy of duvelisib. If concomitant use is necessary, increase the dose of duvelisib on day 12 of coadministration from 25 mg PO twice daily to 40 mg PO twice daily; or from 15 mg PO twice daily to 25 mg PO twice daily. When dexamethasone has been discontinued for at least 14 days, resume duvelisib at the dose taken prior to initiating treatment with dexamethasone. Duvelisib is a CYP3A substrate; dexamethasone is a moderate CYP3A inducer. Coadministration of duvelisib with another moderate CYP3A inducer for 12 days decreased duvelisib exposure by 35%.
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.
Elacestrant: (Major) Avoid concurrent use of elacestrant and dexamethasone due to the risk of decreased elacestrant exposure which may reduce its efficacy. Elacestrant is a CYP3A substrate and dexamethasone is a moderate CYP3A inducer. Concomitant use with another moderate CYP3A inducer reduced elacestrant overall exposure by 55% to 73%.
Elagolix: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with elagolix is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A4 substrate and elagolix is a weak to moderate CYP3A4 inducer.
Elagolix; Estradiol; Norethindrone acetate: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with elagolix is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A4 substrate and elagolix is a weak to moderate CYP3A4 inducer.
Elbasvir; Grazoprevir: (Major) If possible, avoid concurrent administration of elbasvir with dexamethasone. Dexamethasone is a moderate CYP3A inducer, while elbasvir is a substrate of CYP3A. Use of these drugs together is expected to decrease the plasma concentrations of elbasvir, and may result in decreased virologic response. (Major) If possible, avoid concurrent administration of grazoprevir with dexamethasone. Dexamethasone is a moderate CYP3A inducer, while grazoprevir is a substrate of CYP3A. Use of these drugs together is expected to decrease the plasma concentrations of grazoprevir, and may result in decreased virologic response. Conversely, concentrations of dexamethasone (also a CYP3A substrate) may be increased when given with grazoprevir (a weak CYP3A inhibitor).
Eliglustat: (Moderate) Coadministration of dexamethasone and eliglustat may result in increased plasma concentrations of dexamethasone. Monitor patients closely for corticosteroid-related adverse effects; if appropriate, consider reducing the dexamethasone dosage and titrating to clinical effect. Dexamethasone is a P-glycoprotein (P-gp) substrate; eliglustat is a P-gp inhibitor.
Elvitegravir; Cobicistat; Emtricitabine; Tenofovir Alafenamide: (Major) Avoid concurrent use of dexamethasone with cobicistat containing regimens. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; cobicistat is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. (Major) Avoid concurrent use of dexamethasone with elvitegravir. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance to elvitegravir; consider use of an alternative corticosteroid, such as beclomethasone and prednisolone. Dexamethasone induces CYP3A4, and elvitegravir is a substrate of this enzyme.
Elvitegravir; Cobicistat; Emtricitabine; Tenofovir Disoproxil Fumarate: (Major) Avoid concurrent use of dexamethasone with cobicistat containing regimens. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance. In addition, serum concentrations of dexamethasone may be increased, potentially resulting in Cushing's syndrome and adrenal suppression. Dexamethasone is a CYP3A4 substrate and inducer; cobicistat is a substrate of this enzyme as well as a strong CYP3A inhibitor. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. (Major) Avoid concurrent use of dexamethasone with elvitegravir. Coadministration may result in a reduction of antiretroviral efficacy and the potential development of viral resistance to elvitegravir; consider use of an alternative corticosteroid, such as beclomethasone and prednisolone. Dexamethasone induces CYP3A4, and elvitegravir is a substrate of this enzyme.
Empagliflozin: (Moderate) Monitor blood glucose during concomitant corticosteroid and SGLT2 inhibitor use; a SGLT2 inhibitor dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells.
Empagliflozin; Linagliptin: (Moderate) Monitor blood glucose during concomitant corticosteroid and SGLT2 inhibitor use; a SGLT2 inhibitor dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells.
Empagliflozin; Linagliptin; Metformin: (Moderate) Monitor blood glucose during concomitant corticosteroid and metformin use; a metformin dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. (Moderate) Monitor blood glucose during concomitant corticosteroid and SGLT2 inhibitor use; a SGLT2 inhibitor dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells.
Empagliflozin; Metformin: (Moderate) Monitor blood glucose during concomitant corticosteroid and metformin use; a metformin dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells. (Moderate) Monitor blood glucose during concomitant corticosteroid and SGLT2 inhibitor use; a SGLT2 inhibitor dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells.
Emtricitabine; Rilpivirine; Tenofovir alafenamide: (Contraindicated) Concurrent use of dexamethasone (more than 1 dose) and rilpivirine is contraindicated. When these drugs are coadministered, there is a potential for treatment failure and/or the development of rilpivirine or NNRTI resistance. Dexamethasone is an inducer of CYP3A4, which is primarily responsible for the metabolism of rilpivirine. Coadministration may result in decreased rilpivirine serum concentrations, which could cause impaired virologic response to rilpivirine.
Emtricitabine; Rilpivirine; Tenofovir Disoproxil Fumarate: (Contraindicated) Concurrent use of dexamethasone (more than 1 dose) and rilpivirine is contraindicated. When these drugs are coadministered, there is a potential for treatment failure and/or the development of rilpivirine or NNRTI resistance. Dexamethasone is an inducer of CYP3A4, which is primarily responsible for the metabolism of rilpivirine. Coadministration may result in decreased rilpivirine serum concentrations, which could cause impaired virologic response to rilpivirine.
Enalapril; Hydrochlorothiazide, HCTZ: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.
Encorafenib: (Major) Avoid coadministration of encorafenib and dexamethasone due to decreased encorafenib exposure and potential loss of efficacy. Encorafenib is a CYP3A4 substrate; dexamethasone is a moderate CYP3A4 inducer. Coadministration with CYP3A4 inducers has not been studied with encorafenib; however, in clinical trials, steady-state encorafenib exposures were lower than encorafenib exposures after the first dose, suggesting CYP3A4 auto-induction.
Entrectinib: (Major) Avoid coadministration of entrectinib with dexamethasone due to decreased entrectinib exposure and risk of decreased efficacy. Entrectinib is a CYP3A4 substrate; dexamethasone is a moderate CYP3A4 inducer. Coadministration of a moderate CYP3A4 inducer is predicted to reduce the entrectinib AUC by 56%.
Enzalutamide: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with enzalutamide is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A4 substrate and enzalutamide is a strong CYP3A4 inducer.
Ephedrine: (Moderate) Ephedrine may enhance the metabolic clearance of corticosteroids. Decreased blood concentrations and lessened physiologic activity may necessitate an increase in corticosteroid dosage.
Ephedrine; Guaifenesin: (Moderate) Ephedrine may enhance the metabolic clearance of corticosteroids. Decreased blood concentrations and lessened physiologic activity may necessitate an increase in corticosteroid dosage.
Epinephrine: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and epinephrine use due to risk for additive hypokalemia; potassium supplementation may be necessary. Corticosteroids may potentiate the hypokalemic effects of epinephrine.
Eprosartan; Hydrochlorothiazide, HCTZ: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.
Erdafitinib: (Major) If coadministration of erdafitinib and dexamethasone is necessary at the initiation of erdafitinib therapy, administer the dose of erdafitinib as recommended (8 mg once daily with potential to increase the dose to 9 mg on days 14 to 21 based on phosphate levels and tolerability). If dexamethasone must be added to erdafitinib therapy after the initial dose inc