Decadron
Classes
Ophthalmological Corticosteroids
Respiratory Corticosteroids
Systemic Corticosteroid Combinations
Systemic Corticosteroids, Plain
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.
Dexamethasone Intensol (Oral Solution Concentrate)
1 mg/mL concentrated solution; contains 30% alcohol.
Measure the appropriate dose, using only the calibrated dropper provided with product.
Mix the dose with liquid or semi-solid food such as water, juice, soda, applesauce, or pudding and stir the preparation for a few seconds.
Consume the entire mixture immediately; do not store for future use.
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.
Direct IV injection:
Dexamethasone sodium phosphate solution for injection 4 mg/mL or 10 mg/mL may be given directly from the vial.
Intermittent or continuous IV infusion:
Dexamethasone sodium phosphate solution for injection 4 mg/mL or 10 mg/mL may be added to 5% Dextrose injection or 0.9% Sodium Chloride injection, USP and given by IV infusion.
Use diluted solutions within 24 hours, as infusion solutions generally do not contain preservatives.
Dexamethasone sodium phosphate solution for injection 4 mg/mL or 10 mg/mL may be administered intramuscularly.
Intra-articular, Soft tissue, or Intralesional injection
Dexamethasone sodium phosphate solution for injection 4 mg/mL may be administered into joints, soft tissues, or lesions, but administration of dexamethasone via these routes requires specialized techniques.
Only clinicians familiar with these methods of administration and with management of potential complications should administer dexamethasone by these routes.
Frequent intra-articular injections may result in damage to joint tissues.
Dexamethasone sodium phosphate injection is particularly recommended for use in conjunction with one of the less soluble, longer-acting steroids for intra-articular and soft tissue injection.
Ophthalmic 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.
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
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
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
Dosage And Indications
Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response. NOTE: Parenteral therapy may be needed in acute insufficiency. Hydrocortisone and cortisone are preferred for these conditions; dexamethasone has no mineralocorticoid properties. Dosages required may be variable.
0.15 to 0.375 mg/m2/day PO once daily has been recommended for patients with congenital adrenal hyperplasia. Although most experts recommend hydrocortisone as first-line treatment of adrenal insufficiency in pediatric patients whose linear growth is incomplete due to a lower incidence of growth suppression, other authors have stated that dexamethasone may be used safely with close monitoring and individualization of dose based on growth, bone age, and hormone levels. Liquid formulations of dexamethasone are recommended for more precise titration of doses. 0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Parenteral therapy may be needed in acute insufficiency.
Initially, 0.5 to 9 mg/day IV or IM, divided every 6 to 12 hours. Adjust according to patient response. NOTE: Hydrocortisone and cortisone are preferred for these conditions; dexamethasone has no mineralocorticoid properties. Dosages required may be variable.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.
0.5 mg PO every 6 hours for 48 hours. 24-hour urine collections are made for determination of 17-hydroxycorticosteroid excretion. Alternatively, 1 mg PO at 11:00 p.m. with plasma cortisol concentration measured at 8:00 a.m. the following morning.
25 to 30 mcg/kg/dose PO (Max: 2 mg/dose PO) given at 11:00 p.m. with a plasma cortisol concentration measured at 8:00 a.m. the following morning. A plasma cortisol concentration of less than 5 mcg/dL occurs in normal individuals but not those with Cushing's syndrome. Measure a dexamethasone concentration concurrently with the cortisol concentration to ensure adequacy of the dexamethasone dose.
2 mg PO every 6 hours for 48 hours. 24-hour urine collections are made for determination of 17-hydroxycorticosteroid excretion.
120 mcg/kg/dose PO (Max: 8 mg/dose PO) given at 11:00 p.m. with a plasma cortisol concentration measured at 8:00 a.m. the following morning. A decrease in the morning cortisol of 20% or more from baseline had a 97.5% sensitivity and 100% specificity in distinguishing patients with Cushing's disease from those with primary adrenal disorders in a retrospective study (n = 125, age 3 to 18 years). Measure a dexamethasone concentration concurrently with the cortisol concentration to ensure adequacy of the dexamethasone dose. Alternatively, a 2 day test consisting of 30 mcg/kg/day PO on day 1 and 120 mcg/kg/day PO on day 2, each given in 4 divided doses, has been recommended. Cortisol concentrations are suppressed in patients with pituitary Cushing's syndrome after the larger dose but not the smaller dose; cortisol concentrations are not suppressed after dexamethasone in patients with adrenocorticotropic hormone-independent Cushing syndrome.
4 to 8 mg IM as a single dose on day 1. Then change to oral therapy, 1.5 mg PO twice daily on days 2 and 3; then 0.75 mg PO twice daily on day 4; then 0.75 mg PO once daily on days 5 and 6, then discontinue.
Various dosage regimens have been used. 1 to 6 mg/kg IV or 40 mg IV every 4 to 6 hours while shock persists. Alternatively, 20 mg IV injection followed by an IV infusion of 3 mg/kg over 24 hours. Corticosteroids are given as adjunctive therapy to epinephrine.
Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust according to patient response. Corticosteroids are not indicated as initial treatment for anaphylaxis, but can be given as adjunctive therapy after the administration of epinephrine.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response. Corticosteroids are not indicated as initial treatment for anaphylaxis, but can be given as adjunctive therapy after the administration of epinephrine.
Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.
Initially, 1 to 1.5 mg/kg/dose IV, then 1 to 1.5 mg/kg/day IV in divided doses every 3 to 4 hours was used in conjunction with hyperventilation, control of body temperature, barbiturates, and continuous intracranial and arterial pressure monitoring in pediatric patients with severe head injury (n = 24, age 3 months to 14 years). 0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved dosage range. Adjust according to patient response. Use is not a substitute for neurosurgical evaluation and definitive management such as neurosurgery, etc.
0.02 to 0.3 mg/kg/day PO or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response. Use is not a substitute for neurosurgical evaluation and definitive management such as neurosurgery, etc.
10 mg IV or IM as a single dose, followed by 4 mg IV or IM every 6 hours, until symptoms subside, then reduce dosage. A response should be seen within 12 to 24 hours, and a gradual dose reduction begun after 2 to 4 days, reducing over another 5 to 7 days. Replace with oral dosage as soon as possible. For palliative maintenance therapy when oral therapy is not feasible, 2 mg IM or IV can be given 2 to 3 times per day, if needed. Use is not a substitute for neurosurgical evaluation and definitive management such as neurosurgery, etc.
For cerebral edema, 1 to 3 mg PO three times daily, can follow parenteral therapy; then, taper off over a period of 5 to 7 days. For palliative management of recurrent or inoperable brain tumors, maintenance with 2 mg PO given 2 or 3 times daily may be effective.
Initially, 0.5 to 9 mg/day IV or IM, in divided doses. Adjust according to patient response. Renal transplant guidelines recommend corticosteroids for the initial treatment of acute rejection.
0.06 to 0.3 mg/kg/day or 1.2 to 10 mg/m2/day IM or IV in divided doses every 6 to 12 hours. Renal transplant guidelines recommend corticosteroids for the initial treatment of acute rejection.
0.4 mg/kg/day PO with a taper over 6 to 8 weeks. Guidelines recommend as adjunct therapy for meningitis. Routine use outside of CNS involvement is not recommended; however, select patients may benefit.[54286] [61094] [65619] [65758]
0.3 to 0.6 mg/kg/day PO for 4 to 6 weeks, then taper over 2 to 4 weeks. Guidelines recommend as adjunct therapy for meningitis. Routine use outside of CNS involvement is not recommended; however, select patients may benefit.[54286] [61094] [65619] [65758]
0.4 mg/kg/day IV or IM with a taper over 6 to 8 weeks. Guidelines recommend as adjunct therapy for meningitis. Routine use outside of CNS involvement is not recommended; however, select patients may benefit.
0.3 to 0.6 mg/kg/day IV or IM for 4 to 6 weeks, then taper over 2 to 4 weeks. Guidelines recommend as adjunct therapy for meningitis. Routine use outside of CNS involvement is not recommended; however, select patients may benefit.
0.3 to 0.4 mg/kg/day PO for 2 to 4 weeks, then taper by 0.1 mg/kg/week until 0.1 mg/kg/day PO, then 4 mg/day PO and taper by 1 mg/week for a total duration of 12 weeks. Guidelines recommend as adjunct therapy for meningitis. Routine use outside of CNS involvement is not recommended; however, select patients may benefit.[34362] [54286] [61094] [65619] [65758]
0.3 to 0.4 mg/kg/day PO for 2 to 4 weeks, then taper by 0.1 mg/kg/week until 0.1 mg/kg/day PO, then 4 mg/day PO and taper by 1 mg/week for a total duration of 12 weeks. Guidelines recommend as adjunct therapy for meningitis. Routine use outside of CNS involvement is not recommended; however, select patients may benefit.[34362] [54286] [61094] [65619] [65758]
0.3 to 0.6 mg/kg/day PO for 4 to 6 weeks, then taper over 2 to 4 weeks. Guidelines recommend as adjunct therapy for meningitis. Routine use outside of CNS involvement is not recommended; however, select patients may benefit. [54286] [61094] [65619] [65758]
0.3 to 0.4 mg/kg/day IV or IM for 2 to 4 weeks, then taper by 0.1 mg/kg/week until 0.1 mg/kg/day IV or IM, then 4 mg/day IV or IM and taper by 1 mg/week for a total duration of 12 weeks. Guidelines recommend as adjunct therapy for meningitis. Routine use outside of CNS involvement is not recommended; however, select patients may benefit.[34362] [61094]
0.3 to 0.4 mg/kg/day IV or IM for 2 to 4 weeks, then taper by 0.1 mg/kg/week until 0.1 mg/kg/day IV or IM, then 4 mg/day IV or IM and taper by 1 mg/week for a total duration of 12 weeks. Guidelines recommend as adjunct therapy for meningitis. Routine use outside of CNS involvement is not recommended; however, select patients may benefit.[34362] [61094]
0.3 to 0.6 mg/kg/day IV or IM for 4 to 6 weeks, then taper over 2 to 4 weeks. Guidelines recommend as adjunct therapy for meningitis. Routine use outside of CNS involvement is not recommended; however, select patients may benefit.
Instill 3 or 4 drops (ophthalmic solution) into the aural canal 2 to 3 times per day. When a favorable response is obtained, reduce dosage gradually and eventually discontinue. If preferred, the aural canal may be packed with a gauze wick saturated with solution. Keep the wick moist with solution and remove from the ear after 12 to 24 hours. May repeat as needed at the discretion of the prescriber. There is no specific otic solution preparation; use ophthalmic solution. Used for steroid responsive inflammatory conditions of the external auditory meatus, such as allergic otitis externa, selected purulent and nonpurulent infective otitis externa when the hazard of steroid use is accepted to decrease edema and inflammation.
Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.
Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust maintenance dosage according to patient response.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.
Dosage ranges from 2 to 4 mg for large joints and 0.8 to 1 mg for small joints. Injection into intervertebral joints should not be attempted at any time and hip joint injection cannot be recommended as an office procedure. Intrasynovial should be employed only when affected areas are limited to 1 or 2 sites. May repeat from once every 3 to 5 days to once every 2 to 3 weeks.
The 4 mg/mL injection strength may be used for intralesional and soft tissue administration. Doses range from 0.2 mg to 4 mg injected as a single dose at the appropriate site. For soft tissue and bursal injections a dose of 2 to 4 mg is recommended. Ganglia require a dose of 1 to 2 mg. A dose of 0.4 to 1 mg is used for injection into tendon sheaths. Usually employed when condition to be treated is limited to 1 or 2 sites. Dosage dependent upon degree of inflammation, size, disease state, and location of affected area. Repeat doses may be given from once every 3 to 5 days to once every 2 to 3 weeks.
Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. For many conditions, the dosing of corticosteroids is highly variable. Adjust according to patient response. In an open study of 10 patients with ITP, pulse dosing produced a sustained improvement in platelet count with a total daily dose of 40 mg/day PO for 4 consecutive days out of each 28 day cycle for 6 consecutive cycles.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.
Initially, 0.5 to 9 mg/day IV or IM, given in 2 to 4 divided doses. For many conditions, the dosing of corticosteroids is highly variable. Adjust according to patient response.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.
Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Dosage of corticosteroids can be highly variable, depending on patient condition. Adjust according to patient response.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response. Administer dexamethasone IV or IM initially for the treatment of severe respiratory conditions or those compromising the airway.
Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Dosage of corticosteroids can be highly variable, depending on patient condition. Adjust according to patient response.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response. Administer dexamethasone IV or IM initially for the treatment of severe respiratory conditions or those compromising the airway.
Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response. Use of dexamethasone for longer than 2 days may increase the potential for metabolic side effects. Use parenteral dexamethasone dosage for severe respiratory conditions or those compromising the airway. Although prednisone, prednisolone, or methylprednisolone are the systemic corticosteroids of choice for the management of moderate to severe asthma exacerbations, other corticosteroids such as dexamethasone, given in equipotent daily doses are likely to be as effective.[33558]
0.6 mg/kg/dose PO as a single dose or once daily for 2 days. Max: 16 mg/dose.[54531] [54533] [59736] [59737] [64934] Administer dexamethasone IV or IM initially for the treatment of severe respiratory conditions or those compromising the airway. Single or 2-day regimens of dexamethasone have shown similar efficacy, less vomiting, and improved compliance when compared to a 5-day course of oral prednisone or prednisolone.[54531] [54533] [59736] [59737] Use of dexamethasone for longer than 2 days may increase the potential for metabolic side effects. Although prednisone, prednisolone, or methylprednisolone are the systemic corticosteroids of choice for the management of moderate to severe asthma exacerbations, other corticosteroids such as dexamethasone, given in equipotent daily doses are likely to be as effective.[33558] Of note, 0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved initial dosage range for dexamethasone; however, this is significantly lower than the range used in clinical practice.[54286]
Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust according to patient response. Use of dexamethasone for longer than 2 days may increase the potential for metabolic side effects. Although prednisone, prednisolone, or methylprednisolone are the systemic corticosteroids of choice for the management of moderate to severe asthma exacerbations, other corticosteroids such as dexamethasone, given in equipotent daily doses are likely to be as effective.[33558]
0.6 mg/kg/dose IV or IM as a single dose or once daily for 2 days. Max: 16 mg/dose.[54357] [59738] [64934] Single-dose regimens ranging from 0.3 to 1.7 mg/kg/dose have been reported. Max: 36 mg/dose.[59736] In a study of young children with moderate exacerbations, a single day regimen of parenteral dexamethasone resulted in similar efficacy as a 5-day course of oral prednisolone.[59738] Use of dexamethasone for longer than 2 days may increase the potential for metabolic side effects. Although prednisone, prednisolone, or methylprednisolone are the systemic corticosteroids of choice for the management of moderate to severe asthma exacerbations, other corticosteroids such as dexamethasone, given in equipotent daily doses are likely to be as effective.[33558] Of note, 0.5 to 9 mg per day IV or IM is the FDA-approved initial dosage range depending on the condition being treated; however, higher doses are sometimes used in clinical practice.[54285] [54286]
Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response until urine is protein-free, then slowly taper as indicated. Some patients may require long-term dosing.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.
Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. For many conditions, the dosing of corticosteroids is highly variable. Adjust to patient response.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.
Dosages vary depending upon the chemotherapy protocol. Common doses include 1.5 to 6 mg/m2/day PO for 8 to 21 days or 8 mg PO every 8 hours for 10 days.
initial, 0.75 to 9 mg orally daily; dose is dependent on the disease being treated and should be individualized based on patient response. Maintenance therapy may be given; use the lowest dose that produces an adequate clinical response. Taper dexamethasone gradually in patients on long-term therapy; do not abruptly stop therapy in these patients.
initial, 0.02 to 0.3 mg/kg (0.6 mg to 9 mg/m2) orally daily in 3 or 4 divided doses. Dose is dependent on the disease being treated and should be individualized based on patient response. Maintenance therapy may be given; use the lowest dose that produces an adequate clinical response. Taper dexamethasone gradually in patients on long-term therapy; do not abruptly stop therapy in these patients.
initial, 0.5 to 9 mg IV daily; dose is dependent on the disease being treated and should be individualized based on patient response. Maintenance therapy may be given; use the lowest dose that produces an adequate clinical response. Taper dexamethasone gradually in patients receiving IV therapy for more than a few days; do not abruptly stop therapy in these patients.
40 mg orally daily on days 1, 2, 3, and 4 in combination with gemcitabine 1,000 mg/m2 IV on days 1 and 8 and cisplatin 75 mg/m2 IV on day 1 (GDP regimen) every 21 days for 2 cycles was evaluated in a randomized, phase III trial (NCIC-CTG LY.12 trial). In patients with CD20-positive lymphoma, rituximab 375 mg/m2 IV was added on day 1 of each treatment cycle (R-GDP regimen). Patients in the trial could receive a third cycle of therapy if they did not achieve a complete or partial response after the second cycle. Patients with CD20-positive lymphoma who received an autologous stem-cell transplant (ASCT) were randomized to receive either rituximab 375 mg/m2 IV every 2 months for 6 cycles or observation starting 28 days post ASCT.
40 mg orally or IV on days 1, 2, 3, and 4 as part of the DHAP regimen with cisplatin 100 mg/m2 as a continuous IV infusion over 24 hours on day 1 and cytarabine 2 grams/m2 IV over 3 hours every 12 hours for 2 doses on day 2 in combination with ofatumumab 1,000 mg IV on days 1 and 8 of cycle 1 then ofatumumab 1,000 mg IV on day 1 of cycles 2 and 3 was evaluated in a randomized, phase III trial (n = 445; the ORCHARRD trial). Cycles were repeated every 21 days for a total of 3 cycles of therapy. Premedication with acetaminophen, diphenhydramine, and an IV glucocorticoid was administered prior to each ofatumumab infusion. If dexamethasone from the DHAP chemotherapy was dosed on the same day as ofatumumab, then the glucocorticoid premedication was omitted and substituted with the 40-mg dose of dexamethasone. Granulocyte colony-stimulating factor use was recommended as follows: filgrastim 5 micrograms (mcg)/kg on days 6 to 13 or pegfilgrastim 6 mg on day 6 on cycles of therapy with no stem-cell mobilization and filgrastim 5 to 10 mcg/kg on days 6 to 13 on cycles of therapy that were followed by stem-cell mobilization. Central nervous system prophylaxis using intrathecal therapy was permitted. Supportive care during treatment consisted of irradiated blood products, oral antibiotics, and antifungal prophylaxis as clinically indicated.
6 to 10 mg/m2/day PO for 14 days as part of induction, consolidation, or intensification combination regimens.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range ; however, doses may vary according to the specific protocol used.
Initially, 0.5 to 9 mg IV or IM daily; dose is dependent on the disease being treated and should be individualized based on patient response. Maintenance therapy may be given; use the lowest dose that produces an adequate response. Taper dexamethasone gradually in patients receiving parenteral therapy for more than a few days; do not abruptly stop treatment.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range ; however, doses may vary according to the specific protocol used.
30 mg/day PO for 7 days, followed by doses of 4 to 12 mg PO every other day for 1 month have been shown to be effective. Controlled clinical trials have shown corticosteroids to be effective in speeding the resolution of acute exacerbations, they do not show that they affect the ultimate outcome or natural history of the disease.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.
NOTE: Dexamethasone has been designated an orphan drug by the FDA for the treatment of multiple myeloma.
For the treatment of multiple myeloma in patients who have received at least 1 prior therapy, in combination with lenalidomide.
NOTE: Lenalidomide is FDA approved in combination with dexamethasone for the treatment of multiple myeloma in patients that have failed at least 1 prior therapy.
Oral dosage Adults
40 mg orally daily on days 1 to 4, 9 to 12, and 17 to 20 every 28 days for the first 4 cycles of therapy, and then 40 mg orally daily on days 1 to 4 every 28 days starting with cycle 5. Given in combination with lenalidomide (25 mg orally daily on days 1 to 21 of each cycle). Continue or modify dosing based on clinical and laboratory findings.
NOTE: Lenalidomide is FDA approved in combination with dexamethasone for this indication.
Oral dosage Adults 75 years and younger
40 mg orally on days 1, 8, 15, and 22; administer in combination with lenalidomide (25 mg orally daily for 21 days followed by 7 days off treatment). Continue 28-day treatment cycles until disease progression in patients who are ineligible for an autologous stem-cell transplantation (ASCT); hematopoietic stem-cell mobilization should occur within four 28-day treatment cycles in patients who are eligible for an ASCT.
20 mg orally on days 1, 8, 15, and 22; administer in combination with lenalidomide (25 mg orally daily for 21 days followed by 7 days off treatment). Continue 28-day treatment cycles until disease progression.
40 mg orally daily on days 1 to 4, days 9 to 12, and days 17 to 20 or dexamethasone 40 mg orally daily on days 1 to 4 on all cycles and days 9 to 12 and days 17 to 20 of cycles 1 and 2 only, plus doxorubicin 9 mg/m2 IV daily and vincristine 0.4 mg IV daily on days 1 to 4 (VAD regimen) has been studied. Doxorubicin and vincristine were administered as a continuous IV infusion over 24 hours/day [49477] or as a daily IV infusion. Cycles were repeated every 4 weeks for 3 to 4 cycles as induction therapy prior to autologous stem-cell transplantation.[49477] [49478]
NOTE: Thalidomide is FDA approved in combination with dexamethasone for this indication.
Oral dosage Adults
40 mg orally daily on days 1 to 4, days 9 to 12, and days 17 to 20 of every 28-day treatment cycle plus thalidomide 200 mg orally daily (given at bedtime and at least 1 hour after the evening meal).
40 mg orally daily on days 1 to 4 during all cycles and on days 9 to 12 for cycles 1 and 2 only plus bortezomib (1.3 mg/m2 IV on days 1, 4, 8, and 11) repeated every 3 weeks for 4 cycles as induction therapy prior to autologous stem-cell transplantation has been evaluated in newly diagnosed multiple myeloma patients in randomized, phase 3 studies.
40 mg orally on days 1, 2, 4, 5, 8, 9, 11, and 12 plus bortezomib (1.3 mg/m2 IV on days 1, 4, 8, and 11) and thalidomide (100 mg orally daily for the first 14 days during cycle 1 only, and then 200 mg orally daily thereafter). Regimen is known as the VTD regimen. Repeated every 21 days for 3 cycles prior to a double (tandem) autologous stem-cell transplant (ASCT). This regimen was studied in a multicenter, randomized, phase 3 study. Patients randomized to induction therapy with VTD also received two 35-day consolidation cycles with VTD (bortezomib 1.3 mg/m2 on days 1, 8, 15, and 22 plus thalidomide 100 mg orally daily and dexamethasone 40 mg orally on days 1, 2, 8, 9, 15, 16, 22, and 23) following the second transplantation. Patients also received maintenance therapy with dexamethasone 40 mg orally on days 1 to 4 every 28 days until relapse or disease progression.[49746] Additionally in a randomized, phase 3 study, dexamethasone 40 mg orally daily on days 1 to 4 and 9 to 12 plus bortezomib (1.3 mg/m2 on days 1, 4, 8, and 11) and thalidomide (200 mg orally daily after dose escalation as follows in the first cycle: thalidomide 50 mg/day on days 1 to 14 and 100 mg/day on days 15 to 28) repeated every 4 weeks for 6 cycles prior to an ASCT was studied. In this study, patients who received up to 3 years of maintenance therapy (starting 3 months after ASCT) with bortezomib (1.3 mg/m2 IV on days 1, 4, 8, and 11 repeated every 3 months) plus thalidomide (100 mg/day) had significantly improved 2-year progression-free survival compared with thalidomide or interferon alfa-2b maintenance therapy.[49747]
NOTE: Panobinostat is FDA approved in combination with bortezomib and dexamethasone this indication.
Oral dosage Adults
20 mg orally on days 1, 2, 4, 5, 8, 9, 11, and 12 during cycles 1 to 8, then dexamethasone 20 mg orally on days 1, 2, 8, and 9 during cycles 9 to 16. Administer in combination with bortezomib (1.3 mg/m2 IV bolus over 3 to 5 seconds on days 1, 4, 8, and 11 in cycles 1 to 8) then bortezomib (1.3 mg/m2 on days 1 and 8 in cycles 9 to 16) and panobinostat (20 mg orally on days 1, 3, 5, 8, 10, and 12). Continue every 21-day treatment cycles for up to 8 cycles; consider giving up to an additional 8 cycles (maximum of 16 treatment cycles) in patients who experience clinical benefit without unresolved severe or medically significant toxicity.[58821] Treatment with panobinostat, bortezomib, and dexamethasone (n = 387; median therapy duration of 5 months) was compared with placebo, bortezomib, and dexamethasone (n = 381; median therapy duration of 6.1 months) in patients with relapsed or relapsed and refractory multiple myeloma who had received 1 to 3 prior therapies in a multinational, randomized, phase 3 trial (the PANORAMA1 trial). The median patient age was 63 years (range, 56 to 69 years), about 51% of patients had received 1 prior therapy, and approximately 57% of patients had previously received a stem-cell transplantation. Patients with primary refractory or bortezomib-refractory disease were ineligible for this study. At a median follow-up time of 6.47 months (interquartile range, 1.81 to 13.47 months), the median progression-free survival time (primary endpoint) was significantly improved in the panobinostat arm (11.99 months) compared with the placebo arm (8.08 months; hazard ratio (HR) = 0.63; 95% CI, 0.52 to 0.76; p less than 0.0001). The overall survival (OS) time was not significantly improved in the panobinostat arm (33.64 months vs. 30.39 months; HR = 0.87; 95% CI, 0.69 to 1.1); however, OS data are not mature. Crossover from the placebo arm to the panobinostat arm was not permitted.[58822]
NOTE: Carfilzomib is FDA approved in combination with lenalidomide and dexamethasone for this indication.
Oral and Intravenous dosage Adults
40 mg PO or IV on days 1, 8, 15, and 22 in combination with lenalidomide (25 mg orally daily for 21 days) and carfilzomib as specified in the protocol. Treatment cycles are repeated every 28 days until disease progression or unacceptable toxicity; maximum of 18 cycles for carfilzomib only. CYCLE 1: carfilzomib 20 mg/m2 IV over 10 minutes on days 1 and 2; if tolerated, increase to a target dose of 27 mg/m2 IV over 10 minutes on days 8, 9, 15, and 16. CYCLES 2 to 12: carfilzomib 27 mg/m2 IV over 10 minutes on days 1, 2, 8, 9, 15, and 16. CYCLES 13 to 18: carfilzomib 27 mg/m2 IV over 10 minutes on days 1, 2, 15, and 16. Dose carfilzomib at a maximum body surface area (BSA) of 2.2 m2; dose adjustment is not necessary for patients with a weight change of 20% or less. Give dexamethasone 30 minutes to 4 hours prior to the carfilzomib (on carfilzomib dosing days only). Give hydration with both oral fluids and IV fluids prior to each carfilzomib dose in cycle 1. Additional IV hydration may be given after the carfilzomib infusion in cycle 1. Oral and/or IV hydration may be continued as needed in subsequent cycles; adjust hydration to individual patient needs. Thromboprophylaxis is recommended. Consider giving an antiviral agent and an antacid medication. In a prespecified interim analysis of a multinational, randomized, open-label, phase 3 trial (n = 792; the ASPIRE trial), the median progression-free survival time (primary endpoint) was significantly increased with carfilzomib plus lenalidomide/dexamethasone (26.3 months) compared with lenalidomide/dexamethasone alone (17.6 months; hazard ratio (HR) = 0.69; 95% CI, 0.57 to 0.83; p = 0.0001) in patients with relapsed multiple myeloma who had received 1 to 3 prior therapies (age range, 31 to 91 years; median of 2 prior therapies). In this study, some patients had previously received bortezomib (65.8%) and/or lenalidomide (19.8%). The median overall survival (OS) time had not been reached in either study arm at the time of the interim analysis (median follow-up: carfilzomib arm, 32.3 months; lenalidomide/dexamethasone alone, 31.5 months). The estimated 24-month OS rates were 73.3% and 65% in the carfilzomib/lenalidomide/dexamethasone and lenalidomide/dexamethasone arms, respectively (HR = 0.79; 95% CI, 0.63 to 0.99; p = 0.04); prespecified criteria for stopping the study due to OS benefit was not met and this study is ongoing.
NOTE: Daratumumab is FDA approved in combination with bortezomib and dexamethasone for this indication.
Oral or Intravenous dosage Adults 75 years or younger
20 mg orally or IV on days 1, 2, 4, 5, 8, 9, 11, and 12 (or 20 mg orally/IV once weekly in patients with a body-mass index less than 18.5, poorly controlled diabetes mellitus, or a prior intolerance to glucocorticoid therapy) repeated every 3 weeks for 8 cycles in combination with daratumumab and bortezomib. The bortezomib dosage is 1.3 mg/m2 as a subcutaneous injection or IV infusion on days 1, 4, 8, and 11 repeated every 3 weeks for 8 cycles. The daratumumab dosage is 16 mg/kg (actual body weight) IV weekly on weeks 1 to 9 (9 doses), 16 mg/kg IV every 3 weeks on weeks 10 to 24 (5 doses), and then 16 mg/kg IV every 4 weeks starting on week 25 until disease progression. Administer standard pre-and post-infusion medications with daratumumab infusions. Give dexamethasone prior to the daratumumab infusion when these drugs are scheduled on the same day.
20 mg orally or IV once weekly repeated every 3 weeks for 8 cycles in combination with daratumumab and bortezomib. The bortezomib dosage is 1.3 mg/m2 as a subcutaneous injection or IV infusion on days 1, 4, 8, and 11 repeated every 3 weeks for 8 cycles. The daratumumab dosage is 16 mg/kg (actual body weight) IV weekly on weeks 1 to 9 (9 doses), 16 mg/kg IV every 3 weeks on weeks 10 to 24 (5 doses), and then 16 mg/kg IV every 4 weeks starting on week 25 until disease progression. Administer standard pre-and post-infusion medications with daratumumab infusions. Give dexamethasone prior to the daratumumab infusion when these drugs are scheduled on the same day.
NOTE: Daratumumab is FDA-approved in combination with lenalidomide and dexamethasone for this indication.
Oral or Intravenous dosage Adults 75 years or younger
40 mg orally or IV once weekly (or 20 mg orally or IV once weekly for patients with a body-mass index less than 18.5) in combination with lenalidomide and daratumumab until disease progression or unacceptable toxicity. The lenalidomide dosage is 25 mg orally daily on days 1 to 21 repeated every 28 days in patients with creatinine clearance (CrCl) greater than 60 mL/min and 10 mg orally daily on days 1 to 21 repeated every 28 days in patients with a CrCl of 30 to 60 mL/min. The daratumumab dosage is 16 mg/kg (actual body weight) IV weekly on weeks 1 to 8 (8 doses), 16 mg/kg IV every other week on weeks 9 to 24 (8 doses), and then 16 mg/kg IV every 4 weeks starting on week 25 until disease progression. Administer standard pre-and post-infusion medications with daratumumab infusions. In patients receiving full dose dexamethasone, administer as 20 mg IV prior to the daratumumab infusion and then 20 mg PO the next day when these drugs are scheduled on the same week; patients receiving a 20 mg/week dexamethasone dose should receive the entire dose administered prior to the daratumumab infusion.[61407] [60311]
20 mg orally or IV once weekly in combination with lenalidomide and daratumumab until disease progression or unacceptable toxicity. The lenalidomide dosage is 25 mg orally daily on days 1 to 21 repeated every 28 days in patients with creatinine clearance (CrCl) greater than 60 mL/min and 10 mg orally daily on days 1 to 21 repeated every 28 days in patients with a CrCl of 30 to 60 mL/min. The daratumumab dosage is 16 mg/kg (actual body weight) IV weekly on weeks 1 to 8 (8 doses), 16 mg/kg IV every 2 weeks on weeks 9 to 24 (8 doses), and then 16 mg/kg IV every 4 weeks starting on week 25 until disease progression. Administer standard pre-and post-infusion medications with daratumumab infusions. Give dexamethasone prior to the daratumumab infusion when these drugs are scheduled on the same week.
20 mg orally on days 1, 2, 4, 5, 8, 9, 11, and 12 repeated every 21 days for 8 cycles (SWOG S0777 trial); 20 mg orally on days 1, 2, 4, 5, 8, 9, 11, and 12 repeated every 21 days for 3 cycles prior to stem-cell transplantation (SCT) followed by 10 mg orally on days 1, 2, 4, 5, 8, 9, 11, and 12 repeated every 21 days for 2 cycles after SCT (IFM 2009 trial); and 20 mg orally on days 1, 2, 4, 5, 8, 9, 11, and 12 repeated every 21 days for 4 cycles, 10 mg orally on days 1, 2, 4, 5, 8, 9, 11, and 12 on cycles 5 to 9, and then 10 mg orally on days 1, 2, 8, and 9 on cycles 9 to 12 (ENDURANCE trial) in combination with bortezomib and lenalidomide (VRd regimen) have been evaluated in 3 randomized, phase 3 trials. Maintenance therapy consisted of lenalidomide and dexamethasone or lenalidomide only.
NOTE: Daratumumab is FDA-approved in combination with pomalidomide and dexamethasone for this indication.
Oral or Intravenous dosage Adults 75 years or younger
40 mg orally or IV once weekly (or 20 mg IV/PO once weekly for patients with a body-mass index less than 18.5) in combination with pomalidomide (4 mg orally daily on days 1 to 21 repeated every 28 days) and daratumumab (16 mg/kg of actual body weight IV weekly on weeks 1 to 8 (8 doses), 16 mg/kg IV every other week on weeks 9 to 24 (8 doses), and then 16 mg/kg IV every
4 weeks starting on week 25) until disease progression was evaluated in a nonrandomized, phase 1b trial (n = 103; EQUULEUS trial). Administer standard pre-and post-infusion medications with daratumumab infusions. In patients receiving full dose dexamethasone, administer as 20 mg IV prior to the daratumumab infusion and then 20 mg orally the next day when these drugs are scheduled on the same week; patients receiving a 20 mg/week dexamethasone dose should receive the entire dose administered prior to the daratumumab infusion. [60311]Geriatric Adults over 75 years
20 mg orally or IV once weekly in combination with pomalidomide (4 mg orally daily on days 1 to 21 repeated every 28 days) and daratumumab (16 mg/kg of actual body weight IV weekly on weeks 1 to 8 (8 doses), 16 mg/kg IV every other week on weeks 9 to 24 (8 doses), and then 16 mg/kg IV every 4 weeks starting on week 25) until disease progression was evaluated in a nonrandomized, phase 1b trial (n = 103; EQUULEUS trial). Administer standard pre-and post-infusion medications with daratumumab infusions. Give dexamethasone prior to the daratumumab infusion when these drugs are scheduled on the same week.
Elotuzumab is FDA approved in combination with pomalidomide and dexamethasone for this indication.
Oral dosage Adults 75 years or younger
28 mg orally (at 3 to 24 hours prior to elotuzumab) on days 1, 8, 15, and 22 on cycles 1 and 2 and on day 1 of subsequent cycles in combination with elotuzumab 10 mg/kg IV once weekly on cycles 1 and 2 (on days 1, 8, 15, and 22) followed by 20 mg/kg IV every 4 weeks (on day 1) starting on cycle 3 and pomalidomide 4 mg orally daily on days 1 through 21. Additionally, give dexamethasone 40 mg (at 3 to 24 hours prior to elotuzumab) on days 8, 15, and 22 of cycles 3 and beyond. Repeat treatment cycles every 28 days until disease progression. Administer the following premedications 45 to 90 minutes prior to each elotuzumab infusion: acetaminophen 650 to 1,000 mg orally, diphenhydramine 25 to 50 mg orally or IV (or equivalent), ranitidine 50 mg IV or 150 mg orally (or equivalent), and dexamethasone 8 mg IV. At a minimum follow-up time of 9.1 months, the median investigator-assessed progression-free survival time was significantly improved with elotuzumab plus pomalidomide and dexamethasone (median number of treatment cycles, 9) compared with pomalidomide and dexamethasone alone (10.25 months vs. 4.67 months; hazard ratio (HR) = 0.54; 95% CI, 0.34 to 0.86; p = 0.0078) in patients with relapsed or refractory multiple myeloma in a randomized, phase 2 trial (n = 117; the ELOQUENT-3 trial). In this study, patients had received a median of 3 prior therapies; 70% of patients had refractory disease after both lenalidomide and a proteasome inhibitor and 55% of patients had previously received an autologous stem cell transplantation.
8 mg orally (at 3 to 24 hours prior to elotuzumab) on days 1, 8, 15, and 22 on cycles 1 and 2 and on day 1 of subsequent cycles in combination with elotuzumab 10 mg/kg IV once weekly on cycles 1 and 2 (on days 1, 8, 15, and 22) followed by 20 mg/kg IV every 4 weeks (on day 1) starting on cycle 3 and pomalidomide 4 mg orally daily on days 1 through 21. Additionally, give dexamethasone 20 mg orally (at 3 to 24 hours prior to elotuzumab) on days 8, 15, and 22 of cycles 3 and beyond. Repeat treatment cycles every 28 days until disease progression. Administer the following premedications 45 to 90 minutes prior to each elotuzumab infusion: acetaminophen 650 to 1,000 mg orally, diphenhydramine 25 to 50 mg orally or IV (or equivalent), ranitidine 50 mg IV or 150 mg orally (or equivalent), and dexamethasone 8 mg IV. At a minimum follow-up time of 9.1 months, the median investigator-assessed progression-free survival time was significantly improved with elotuzumab plus pomalidomide and dexamethasone (median number of treatment cycles, 9) compared with pomalidomide and dexamethasone alone (10.25 months vs. 4.67 months; hazard ratio (HR) = 0.54; 95% CI, 0.34 to 0.86; p = 0.0078) in patients with relapsed or refractory multiple myeloma in a randomized, phase 2 trial (n = 117; the ELOQUENT-3 trial). In this study, patients had received a median of 3 prior therapies; 70% of patients had refractory disease after both lenalidomide and a proteasome inhibitor and 55% of patients had previously received an autologous stem cell transplantation.[60354]
Elotuzumab is FDA approved in combination with lenalidomide and dexamethasone for this indication.
Oral dosage Adults
28 mg orally (taken 3 to 24 hours prior to elotuzumab) on days 1, 8, 15, and 22 on cycles 1 and 2 and on days 1 and 15 of subsequent cycles in combination with lenalidomide 25 mg orally daily on days 1 through 21 and elotuzumab 10 mg/kg IV once weekly on cycles 1 and 2 (on days 1, 8, 15, and 22), then 10 mg/kg IV every 2 weeks (on days 1 and 15) thereafter. Give dexamethasone 40 mg orally on days 8 and 22 of cycles 3 and beyond. Repeat treatment cycles every 28 days until disease progression. Administer the following premedications 45 to 90 minutes prior to each elotuzumab infusion: acetaminophen 650 to 1,000 mg PO, diphenhydramine 25 to 50 mg PO or IV (or equivalent), ranitidine 50 mg IV or 150 mg PO (or equivalent), and dexamethasone 8 mg IV.[60354] At a median follow-up time of 24.5 months, the median progression-free survival time was significantly improved with elotuzumab plus lenalidomide and dexamethasone (median duration of therapy, 17 months) compared with lenalidomide and dexamethasone alone (19.4 months vs. 14.9 months; hazard ratio (HR) = 0.7; 95% CI, 0.57 to 0.85; p less than 0.001) in patients with relapsed and/or refractory multiple myeloma in a planned interim analysis of a multicenter, randomized, open-label, phase 3 trial (n = 646; the ELOQUENT-2 trial). In this study, patients had received a median of 2 prior therapies (range, 1 to 4 therapies); 35% of patients had refractory disease to the last therapy and 54% of patients had previously received an autologous stem cell transplantation.[60353] The overall survival time was improved in the elotuzumab-containing arm (48.3 months vs. 39.6 months; HR = 0.82; 95% CI, 0.68 to 1) at the final analysis (minimum follow-up time of 70.6 months). In subgroup analyses, the median OS times were significantly improved in elotuzumab-treated patients who had received 2 or 3 prior therapies (51 months vs. 33.6 months; HR = 0.71; 95% CI, 0.54 to 0.92), were refractory to their most recent therapy (40.4 months vs. 25.9 months; HR = 0.67; 95% CI, 0.49 to 0.91), or were less than 65 years of age (63.5 months vs. 47.7 months; HR = 0.7; 95% CI, 0.52 to 0.96).
NOTE: Daratumumab is FDA-approved in combination with lenalidomide and dexamethasone for this indication.
Oral or Intravenous dosage Adults 75 years or younger
40 mg orally or IV once weekly (or 20 mg orally or IV once weekly for patients with a body-mass index less than 18.5) in combination with lenalidomide and daratumumab until disease progression or unacceptable toxicity. Give dexamethasone IV prior to the first infusion; oral administration may be considered thereafter. Give the treatment dexamethasone dose as the daratumumab premedication steroid when these drugs are scheduled on the same day. Consider giving a low-dose oral corticosteroid (equivalent to methylprednisolone 20 mg or less) on the day after every infusion. The lenalidomide dosage is 25 mg orally daily on days 1 to 21 repeated every 28 days in patients with creatinine clearance (CrCl) greater than 50 mL/min and 10 mg orally daily on days 1 to 21 repeated every 28 days in patients with a CrCl of 30 to 50 mL/min. The daratumumab dosage is 16 mg/kg (actual body weight) IV weekly on weeks 1 to 8 (8 doses), 16 mg/kg IV every 2 weeks on weeks 9 to 24 (8 doses), and then 16 mg/kg IV every 4 weeks starting on week 25 until disease progression. Administer standard pre-and post-infusion medications with daratumumab infusions.[60311] In the MAIA trial (median follow-up, 56.2 months), the median progression-free survival (time not reached vs. 34.4 months; hazard ratio (HR) = 0.53; 95% CI, 0.43 to 0.66, p less than 0.0001) and overall survival (time not reached in either arm; HR = 0.68; 95% CI, 0.53 to 0.86) times were significantly improved in the daratumumab plus lenalidomide and dexamethasone arm compared with the lenalidomide and dexamethasone arm in patients (median age, 73 years; range, 45 to 90 years) with newly diagnosed multiple myeloma who were ineligible for a stem-cell transplant.
20 mg orally or IV once weekly in combination with lenalidomide and daratumumab until disease progression or unacceptable toxicity. Give dexamethasone IV prior to the first infusion; oral administration may be considered thereafter. Give the treatment dexamethasone dose as the daratumumab premedication steroid when these drugs are scheduled on the same day. Consider giving a low-dose oral corticosteroid (equivalent to methylprednisolone 20 mg or less) on the day after every infusion. The lenalidomide dosage is 25 mg orally daily on days 1 to 21 repeated every 28 days in patients with creatinine clearance (CrCl) greater than 50 mL/min and 10 mg orally daily on days 1 to 21 repeated every 28 days in patients with a CrCl of 30 to 50 mL/min. The daratumumab dosage is 16 mg/kg (actual body weight) IV weekly on weeks 1 to 8 (8 doses), 16 mg/kg IV every 2 weeks on weeks 9 to 24 (8 doses), and then 16 mg/kg IV every 4 weeks starting on week 25 until disease progression. Administer standard pre-and post-infusion medications with daratumumab infusions. Give dexamethasone prior to the daratumumab infusion when these drugs are scheduled on the same week.[60311] In the MAIA trial (median follow-up, 56.2 months), the median progression-free survival (time not reached vs. 34.4 months; hazard ratio (HR) = 0.53; 95% CI, 0.43 to 0.66, p less than 0.0001) and overall survival (time not reached in either arm; HR = 0.68; 95% CI, 0.53 to 0.86) times were significantly improved in the daratumumab plus lenalidomide and dexamethasone arm compared with the lenalidomide and dexamethasone arm in patients (median age, 73 years; range, 45 to 90 years) with newly diagnosed multiple myeloma who were ineligible for a stem-cell transplant.
20 mg orally on days 1, 2, 4, 5, 8, 9, 11, and 12 repeated every 21 days on cycles 1 to 8 and then 20 mg orally on days 1, 2, 8, and 9 starting on cycle 9 in combination with pomalidomide (4 mg orally daily on days 1 to 14) and bortezomib was evaluated in a randomized, phase 3 trial (n = 559; the OPTIMISMM trial). Bortezomib was administered as follows: 1.3 mg/m2 IV or subcutaneously on days 1, 4, 8, and 11 on cycles 1 to 8 then 1.3 mg/m2 IV or subcutaneously on days 1 and 8 starting on cycle 9. Treatment cycles were repeated every 21 days until disease progression.
10 mg orally on days 1, 2, 4, 5, 8, 9, 11, and 12 repeated every 21 days on cycles 1 to 8 and then 10 mg orally on days 1, 2, 8, and 9 starting on cycle 9 in combination with pomalidomide (4 mg orally daily on days 1 to 14) and bortezomib. Bortezomib was administered as follows: 1.3 mg/m2 IV or subcutaneously on days 1, 4, 8, and 11 on cycles 1 to 8 then 1.3 mg/m2 IV or subcutaneously on days 1 and 8 starting on cycle 9. Treatment cycles were repeated every 21 days until disease progression.[64412]
NOTE: Daratumumab is FDA approved in combination with bortezomib, thalidomide, and dexamethasone for this indication.
Oral and Intravenous dosage Adults 65 years and younger
40 mg orally or IV on days 1, 2, 8, 9, 15, 16, 22, and 23 in induction cycles 1 and 2; 40 mg orally or IV on days 1 and 2 and 20 mg PO or IV on days 8, 9, 15, and 16 in induction cycles 3 and 4; and 20 mg orally or IV on days 1, 2, 8, 9, 15, and 16 for 2 consolidation cycles in combination with daratumumab, bortezomib, and thalidomide was evaluated in a multicenter, randomized, phase 3 trial (n = 1,085; the CASSIOPEIA trial). In this trial, dexamethasone was administered for up to four 28-day induction therapy cycles and two 28-day consolidation therapy cycles with daratumumab (16 mg/kg IV weekly in induction cycles 1 and 2 then 16 mg/kg IV every 2 weeks in induction cycles 3 and 4 and for both consolidation cycles; bortezomib 1.3 mg/m2 subcutaneously on days 1, 4, 8, and 11 in each induction and consolidation cycle; and thalidomide 100 mg orally daily. Consolidation therapy was begun after hematopoietic reconstitution but not earlier than 30 days after transplant.[64528]
NOTE: Isatuximab is FDA approved in combination with pomalidomide and dexamethasone for this indication.
Oral and Intravenous dosage Adults 74 years and younger
40 mg IV or orally on days 1, 8, 15, and 22 repeated every 28 days until disease progression. Give in combination with isatuximab 10 mg/kg (actual body weight) IV on days 1, 8, 15, and 22 on cycle 1 and isatuximab 10 mg/kg (actual body weight) IV on days 1 and 15 starting on cycle 2 and pomalidomide 4 mg orally daily on days 1 to 21. The scheduled dexamethasone dose should be given prior to isatuximab and pomalidomide on days these drugs are given together. At a median follow-up time of 11.6 months, the median progression-free survival time (evaluated by an independent response committee) was significantly improved in patients with relapsed or refractory multiple myeloma who received isatuximab, pomalidomide, and low-dose dexamethasone compared with pomalidomide and low-dose dexamethasone alone (11.5 months vs. 6.5 months; hazard ratio (HR) = 0.596; 95% CI, 0.44 to 0.81; p = 0.001) in a multinational, randomized, phase 3 trial (the ICARIA-MM trial; n = 307). Patients (median age, 67 years) in this study had received a median of 3 prior therapies including lenalidomide and a proteasome inhibitor; 56% of patients had previously received an autologous stem-cell transplantation. At a second interim analysis (median follow-up, 35.3 months), the median overall survival time was 24.6 months in patients who received isatuximab, pomalidomide, and dexamethasone compared with 17.7 months in patients who received pomalidomide and dexamethasone (HR = 0.76; 95% CI, 0.57 to 1.01). Subsequent therapy was given at disease progression in 60% and 72% of patients in the isatuximab-containing and control arms, respectively. Of patients who received subsequent therapy, fewer patients received daratumumab in the isatuximab-containing arm (24% vs. 58%).
20 mg IV or orally on days 1, 8, 15, and 22 repeated every 28 days until disease progression. Give in combination with isatuximab 10 mg/kg (actual body weight) IV on days 1, 8, 15, and 22 on cycle 1 and isatuximab 10 mg/kg (actual body weight) IV on days 1 and 15 starting on cycle 2 and pomalidomide 4 mg orally daily on days 1 to 21. The scheduled dexamethasone dose should be given prior to isatuximab and pomalidomide on days these drugs are given together. At a median follow-up time of 11.6 months, the median progression-free survival was significantly improved in patients with relapsed or refractory multiple myeloma who received isatuximab, pomalidomide, and low-dose dexamethasone compared with pomalidomide and low-dose dexamethasone alone (11.5 months vs. 6.5 months; hazard ratio = 0.596; 95% CI, 0.44 to 0.81; p = 0.001) in a multinational, randomized, phase 3 trial (the ICARIA-MM trial; n = 307). Patients (median age, 67 years) in this study had received a median of 3 prior therapies including lenalidomide and a proteasome inhibitor; 56% of patients had previously received an autologous stem-cell transplantation.
NOTE: Daratumumab; hyaluronidase is FDA approved in combination with lenalidomide and dexamethasone for this indication.
Oral and Intravenous dosage Adults 75 years or younger
40 mg IV/PO (or 20 mg PO/IV in patients with a body-mass index less than 18.5) once weekly plus lenalidomide 25 mg PO daily on days 1 to 21 repeated every 28 days in combination with 1,800 mg daratumumab and 30,000 units hyaluronidase subcutaneously weekly on weeks 1 to 8 (8 doses), 1,800 mg daratumumab and 30,000 units hyaluronidase every other week on weeks 9 to 24 (8 doses), and then 1,800 mg daratumumab and 30,000 units hyaluronidase every 4 weeks starting on week 25 until disease progression was evaluated in a single-arm cohort (n = 65) of a multicohort, open-label trial (the PLEIADES trial). The overall response rate was 91% in patients with relapsed or refractory multiple myeloma who received daratumumab/hyaluronidase, lenalidomide, and dexamethasone.
20 mg PO/IV once weekly plus lenalidomide 25 mg PO daily on days 1 to 21 repeated every 28 days in combination with 1,800 mg daratumumab and 30,000 units hyaluronidase subcutaneously weekly on weeks 1 to 8 (8 doses), 1,800 mg daratumumab and 30,000 units hyaluronidase every other week on weeks 9 to 24 (8 doses), and then 1,800 mg daratumumab and 30,000 units hyaluronidase every 4 weeks starting on week 25 until disease progression was evaluated in a single-arm cohort (n = 65) of a multicohort, open-label trial (the PLEIADES trial). The overall response rate was 91% in patients with relapsed or refractory multiple myeloma who received daratumumab/hyaluronidase, lenalidomide, and dexamethasone.
NOTE: Carfilzomib and daratumumab are FDA approved in combination with dexamethasone for this indication.
Oral and Intravenous dosage Adults 75 years or younger
20 mg PO/IV on days 1, 2, 8, 9, 15, and 16 and 40 mg PO/IV on day 22 repeated every 28 days in combination with IV carfilzomib (20 mg/m2 and 56 mg/m2 twice weekly regimen) and IV daratumumab until disease progression or unacceptable toxicity. Alternatively, dexamethasone may be given as follows: 20 mg PO/IV on days 1, 2, 8, 9, 15, 16, 22, and 23 in cycles 1 and 2; 20 mg PO/IV on days 1, 2, 15, and 16 and 40 mg PO/IV on days 8 and 22 in cycles 3, 4, 5, and 6; and 20 mg PO/IV on days 1 and 2 and 40 mg PO/IV on days 8, 15, and 22 in cycles 7 and beyond in combination with IV carfilzomib (20 mg/m2 and 70 mg/m2 once weekly regimen) and IV daratumumab until disease progression or unacceptable toxicity. Treatment cycles are repeated every 28 days. Give dexamethasone 30 minutes to 4 hours prior to the carfilzomib dose and 1 to 3 hours prior to daratumumab. At a median follow-up time of about 17 months, the median progression-free survival was significantly improved in patients with relapsed or refractory multiple myeloma who received carfilzomib 20 mg/m2 and 56 mg/m2 twice weekly regimen, daratumumab, and dexamethasone compared with carfilzomib and dexamethasone alone (median time not reached vs. 15.8 months; hazard ratio = 0.63; 95% CI, 0.46 to 0.85; p = 0.0027) in a multicenter, randomized (2:1), open-label, phase 3 trial (n = 466; the CANDOR trial). At a median follow-up time of 16.6 months (range, 0.5 to 27.4 months), the overall response rate was 84% (complete response rate, 33%) in patients with relapsed or refractory multiple myeloma who received carfilzomib 20 mg/m2 and 70 mg/m2 once weekly regimen, daratuzumab, and dexamethasone in a multicenter, multi-arm, phase 1b trial (n = 85; EQUULEUS trial).
20 mg PO/IV on days 1 and 2 of cycle 1 only and then 20 mg PO/IV weekly in combination with IV carfilzomib and IV daratumumab until disease progression or unacceptable toxicity. Treatment cycles are repeated every 28 days. Give dexamethasone 30 minutes to 4 hours prior to the carfilzomib dose and 1 to 3 hours prior to daratumumab. At a median follow-up time of about 17 months, the median progression-free survival was significantly improved in patients with relapsed or refractory multiple myeloma who received carfilzomib 20 mg/m2 and 56 mg/m2 twice weekly regimen, daratumumab, and dexamethasone compared with carfilzomib and dexamethasone alone (median time not reached vs. 15.8 months; hazard ratio = 0.63; 95% CI, 0.46 to 0.85; p = 0.0027) in a multicenter, randomized (2:1), open-label, phase 3 trial (n = 466; the CANDOR trial). At a median follow-up time of 16.6 months (range, 0.5 to 27.4 months), the overall response rate was 84% (complete response rate, 33%) in patients with relapsed or refractory multiple myeloma who received carfilzomib 20 mg/m2 and 70 mg/m2 once weekly regimen, daratuzumab, and dexamethasone in a multicenter, multi-arm, phase 1b trial (n = 85; EQUULEUS trial).
20 mg on days 1, 2, 8, 9, 15, and 16 repeated every 21 days on cycles 1, 2, 3, and 4 followed by high-dose chemotherapy and an autologous stem-cell transplant and then 2 additional cycles of dexamethasone 20 mg on days 1, 2, 8, 9, 15, and 16 repeated every 21 days (cycles 5 and 6) plus lenalidomide 25 mg orally daily on days 1 to 14 and bortezomib 1.3 mg/m2 subcutaneously on days 1, 4, 8, and 11 repeated every 21 days for 6 cycles (VRd regimen) with daratumumab was evaluated in a randomized, phase 2 trial (the GRIFFIN trial; n = 207). Daratumumab treatment consisted of 16 mg/kg IV on days 1, 8, and 15 repeated every 21 days on cycles 1, 2, 3, and 4 and 16 mg/kg IV day 1 repeated every 21 days on cycles 5 and 6. Maintenance therapy was given for up to 2 years and consisted of daratumumab 16 mg/kg IV on day 1 repeated every 4 or 8 weeks and lenalidomide 10 mg orally daily on days 1 to 21 (increased to 15 mg after 3 cycles if tolerated) repeated every 28 days.
NOTE: Selinexor is FDA approved in combination with bortezomib and dexamethasone for this indication.
Oral dosage Adults
20 mg PO on days 1 and 2 in combination with selinexor 100 mg orally on day 1 once weekly and bortezomib 1.3 mg/m2 subcutaneously on day 1 once weekly for 4 weeks followed by 1 week off; repeat cycles until disease progression. Treatment with a once-weekly regimen of selinexor plus bortezomib, and dexamethasone (SVd regimen) led to a significantly improved median progression-free survival time compared with bortezomib and dexamethasone (13.93 months vs. 9.46 months; hazard ratio (HR) = 0.7; 95% CI, 0.53 to 0.93) in a randomized, phase 3 trial (n = 402; the Boston trial). At a median follow-up of 17.3 months, the median overall survival (OS) time was not significantly improved in the SVd arm (HR = 0.84; 95% CI, 0.57 to 1.23); however, OS data was not mature at the time of this analysis. Patients (median age, 67 years) in this trial had received a median of 2 prior regimens (range, 1 to 2 regimens) and approximately 70% of patients had received prior bortezomib therapy; 35% of patients had previously received a stem-cell transplant.
NOTE: Melphalan flufenamide is FDA approved in combination with dexamethasone for this indication.
Oral and Intravenous dosage Adults younger than 75 years
40 mg orally or IV on days 1, 8, 15, and 22 in combination with melphalan flufenamide 40 mg IV on day 1 repeated every 28 days until disease progression. Treatment with melphalan flufenamide plus dexamethasone resulted in an overall response rate of 23.7% in 97 patients with multiple myeloma who had received 4 or more previous lines of therapy and were refractory to at least 1 proteasome inhibitor, 1 immunomodulatory agent, and a CD38-directed monoclonal antibody in a nonrandomized phase 2 trial (the HORIZON trial). No patient achieved a complete response. In this trial, the median duration of response was 4.2 months. Patients (median age, 65 years; range, 35 to 86 years) had received a median of 6 prior regimens (range, 4 to 12 regimens); 75% of patients had alkylator refractory disease and 70% of patients had previously received a stem-cell transplant.
20 mg orally or IV on days 1, 8, 15, and 22 in combination with melphalan flufenamide 40 mg IV on day 1 repeated every 28 days until disease progression. Treatment with melphalan flufenamide plus dexamethasone resulted in an overall response rate of 23.7% in 97 patients with multiple myeloma who had received 4 or more previous lines of therapy and were refractory to at least 1 proteasome inhibitor, 1 immunomodulatory agent, and a CD38-directed monoclonal antibody in a nonrandomized phase 2 trial (the HORIZON trial). No patient achieved a complete response. In this trial, the median duration of response was 4.2 months. Patients (median age, 65 years; range, 35 to 86 years) had received a median of 6 prior regimens (range, 4 to 12 regimens); 75% of patients had alkylator refractory disease and 70% of patients had previously received a stem-cell transplant.
NOTE: Isatuximab and carfilzomib are FDA approved in combination with dexamethasone for this indication.
Oral or Intravenous dosage Adults
20 mg on days 1, 2, 8, 9, 15, 16, 22, and 23 in combination with isatuximab (cycle 1: 10 mg/kg IV on days 1, 8, 15, and 22; cycle 2 and beyond: 10 mg/kg IV on days 1 and 15) and carfilzomib (cycle 1: 20 mg/m2 IV on days 1 and 2 and then 56 mg/m2 on days 8, 9, 15, and 16; cycle 2 and beyond: 56 mg/m2 IV on days 1, 2, 8, 9, 15, and 16). Repeat treatment cycles every 28 days until disease progression. Give IV dexamethasone prior to isatuximab and/or carfilzomib on days these agents are given on the same day and then give dexamethasone orally for other scheduled doses. At a median follow-up time of 20.7 months, the median progression-free survival was significantly improved in patients with relapsed or refractory multiple myeloma who received isatuximab, carfilzomib, and dexamethasone compared with carfilzomib and dexamethasone alone (median time not calculated vs. 19.15 months; hazard ratio = 0.53; 95% CI, 0.32 to 0.79; p = 0.0007) in a prespecified interim analysis of a multinational, randomized, phase 3 trial (the IKEMA trial; n = 302). Patients (median age, 64 years) in this study had received a median of 2 prior therapies; 61% of patients had previously received a stem-cell transplantation.
NOTE: Ixazomib is FDA approved in combination with lenalidomide and dexamethasone for the treatment of multiple myeloma in patients who have received at least 1 prior therapy.
Oral dosage Adults
40 mg orally on days 1, 8, 15, and 22 in combination with ixazomib 4 mg orally on days 1, 8, and 15 and lenalidomide 25 mg orally daily on days 1 through 21. Repeat treatment cycles every 28 days until disease progression. The median progression-free survival time was significantly improved with ixazomib plus lenalidomide and dexamethasone compared with placebo plus lenalidomide and dexamethasone (20.6 months vs. 14.7 months; hazard ratio (HR) = 0.74; 95% CI, 0.59 to 0.94; p = 0.01) in patients with relapsed and/or refractory multiple myeloma who had received 1 to 3 prior therapies in a multinational, randomized, double-blind, phase 3 trial (n = 722; TOURMALINE-MM1 trial). At a median follow-up time of 85 months, the median overall survival time was not significantly improved in the ixazomib-containing arm (53.6 months vs. 51.6 months; HR = 0.939; 95%CI, 0.784 to 1.125). In this trial, subsequent lines of therapy were given in 71.7% and 69.9% of patients who received ixazomib plus lenalidomide and dexamethasone (median, 2 subsequent therapies; range, 1 to 9) and lenalidomide and dexamethasone (median, 3 subsequent therapies; range, 1 to 12), respectively. The median age of patients in this study was 66 years (range, 30 to 91 years); prior therapy included a stem-cell transplant in 57% of patients, proteasome inhibitor therapy in 70% of patients, and immunomodulatory drug therapy in 55% of patients. Thromboprophylaxis was recommended for all patients.
NOTE: Daratumumab/hyaluronidase is FDA approved in combination with pomalidomide and dexamethasone for this indication.
Oral dosage Adults and Geriatric patients younger than 75 years
40 mg orally once weekly (on days 1, 8, 15, and 22) repeated every 28 days until disease progression; give in combination with daratumumab/hyaluronidase (1,800 mg daratumumab and 30,000 units hyaluronidase subcutaneously weekly on weeks 1 to 8 (8 doses), every other week on weeks 9 to 24 (8 doses), and then every 4 weeks starting on week 25 until disease progression) and pomalidomide (4 mg PO daily on days 1 to 21 repeated every 28 days). At a median follow-up of 16.9 months, the median progression-free survival was significantly improved (12.4 months vs. 6.9 months; hazard ratio, 0.63; 95%CI, 0.47 to 0.85) in patients with relapsed or refractory multiple myeloma who received daratumumab/hyaluronidase plus pomalidomide and dexamethasone compared with pomalidomide and dexamethasone alone in a randomized, phase 3 trial (n = 304; the APOLLO trial). Overall survival data were not mature at the time of this analysis. In this trial, eligible patients had received at least 1 previous line of therapy with both lenalidomide and a proteasome inhibitor, had a partial response or better to one or more previous lines of antimyeloma therapy, and were refractory to lenalidomide if they had received only 1 previous line of treatment. Patients (median age, 67 years; range, 42 to 86 years) in the daratumumab/hyaluronidase arm had received a median of 2 (range, 1 to 5) prior therapies; 60% of patients had received a prior autologous stem-cell transplantation.
20 mg orally once weekly (on days 1, 8, 15, and 22) repeated every 28 days until disease progression; give in combination with daratumumab/hyaluronidase (1,800 mg daratumumab and 30,000 units hyaluronidase subcutaneously weekly on weeks 1 to 8 (8 doses), every other week on weeks 9 to 24 (8 doses), and then every 4 weeks starting on week 25 until disease progression) and pomalidomide (4 mg PO daily on days 1 to 21 repeated every 28 days). At a median follow-up of 16.9 months, the median progression-free survival was significantly improved (12.4 months vs. 6.9 months; hazard ratio, 0.63; 95%CI, 0.47 to 0.85) in patients with relapsed or refractory multiple myeloma who received daratumumab/hyaluronidase plus pomalidomide and dexamethasone compared with pomalidomide and dexamethasone alone in a randomized, phase 3 trial (n = 304; the APOLLO trial). Overall survival data were not mature at the time of this analysis. In this trial, eligible patients had received at least 1 previous line of therapy with both lenalidomide and a proteasome inhibitor, had a partial response or better to one or more previous lines of antimyeloma therapy, and were refractory to lenalidomide if they had received only 1 previous line of treatment. Patients (median age, 67 years; range, 42 to 86 years) in the daratumumab/hyaluronidase arm had received a median of 2 (range, 1 to 5) prior therapies; 60% of patients had received a prior autologous stem-cell transplantation.
NOTE: Carfilzomib and daratumumab/hyaluronidase are both FDA approved in combination with dexamethasone for this indication.
Oral and Intravenous dosage Adults 75 years or younger
40 mg PO or IV per week in combination with carfilzomib and daratumumab/hyaluronidase; treatment cycles are repeated every 28 days until disease progression or unacceptable toxicity. Dexamethasone dosing day(s)/schedule differ with twice weekly or once weekly carfilzomib regimens. Give dexamethasone 30 minutes to 4 hours prior to the carfilzomib. Give the treatment dexamethasone dose as the premedication steroid when these drugs are scheduled on the same day as daratumumab; hyaluronidase. With carfilzomib 20 mg/m2 and 56 mg/m2 twice weekly regimen, give dexamethasone 20 mg PO/IV on days 1, 2, 8, 9, 15, 16, 22 and 23 on cycles 1 and 2 and then 20 mg PO/IV on days 1, 2, 8, 9, 15, and 16 and 40 mg PO/IV on day 22 on subsequent cycles. With carfilzomib 20 mg/m2 and 70 mg/m2 once weekly regimen, give dexamethasone 20 mg PO/IV on days 1, 2, 8, 9, 15, 16, 22, and 23 on cycles 1 and 2; 20 mg PO/IV on days 1, 2, 15, and 16 and 40 mg PO/IV on days 8 and 22 on cycles 3, 4, 5, and 6; and 20 mg PO/IV on days 1 and 2 and 40 mg PO/IV on days 8, 15, and 22 on cycles 7 and beyond. In patients with a BMI of less than 18.5 who received the carfilzomib once weekly regimen, give a reduced dexamethasone dosage of 20 mg PO/IV on days 1 and 2 of cycle 1 then 20 mg PO/IV weekly. Daratumumab; hyaluronidase is administered as follows: 1,800 mg daratumumab and 30,000 units hyaluronidase subcutaneously weekly on weeks 1 to 8 (8 doses), 1,800 mg daratumumab and 30,000 units hyaluronidase every 2 weeks on weeks 9 to 24 (8 doses), and then 1,800 mg daratumumab and 30,000 units hyaluronidase every 4 weeks starting on week 25 until disease progression. The overall response rate was 84.8% in 66 patients with relapsed or refractory multiple myeloma who received carfilzomib (20 mg/m2 and 70 mg/m2 once weekly regimen), daratumumab/hyaluronidase, and dexamethasone in a multicohort, phase 2 trial (the PLEIADES trial). The stringent complete response rate was 16.7% and the complete response rate was 21.2%. At a median follow-up time of 9.2 months, the median duration of response was not reached. Patients (median age, 61 years; range, 42 to 84 years) in this trial had received at least 1 previous therapy line that contained lenalidomide; 79% of patients had a prior stem-cell transplant.
20 mg PO/IV on days 1 and 2 of week 1 and then 20 mg PO/IV once weekly in combination with carfilzomib and daratumumab/hyaluronidase; treatment cycles are repeated every 28 days until disease progression or unacceptable toxicity. Give dexamethasone 30 minutes to 4 hours prior to the carfilzomib. Carfilzomib is administered as either a 20 mg/m2 and 56 mg/m2 twice weekly or a 20 mg/m2 and 70 mg/m2 once weekly regimen. Give the treatment dexamethasone dose as the premedication steroid when these scheduled on the same day as daratumumab; hyaluronidase. Daratumumab; hyaluronidase is administered as follows: 1,800 mg daratumumab and 30,000 units hyaluronidase subcutaneously weekly on weeks 1 to 8 (8 doses), 1,800 mg daratumumab and 30,000 units hyaluronidase every 2 weeks on weeks 9 to 24 (8 doses), and then 1,800 mg daratumumab and 30,000 units hyaluronidase every 4 weeks starting on week 25 until disease progression. The overall response rate was 84.8% in 66 patients with relapsed or refractory multiple myeloma who received carfilzomib (20 mg/m2 and 70 mg/m2 once weekly regimen), daratumumab/hyaluronidase, and dexamethasone in a multicohort, phase 2 trial (the PLEIADES trial). The stringent complete response rate was 16.7% and the complete response rate was 21.2%. At a median follow-up time of 9.2 months, the median duration of response was not reached. Patients (median age, 61 years; range, 42 to 84 years) in this trial had received at least 1 previous therapy line that contained lenalidomide; 79% of patients had a prior stem-cell transplant.
Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Adjust according to patient response. Because of the potential complications of steroid use, steroids should be used selectively and in the lowest dose possible for the shortest duration as possible.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response. Because of the potential complications of steroid use, steroids should be used selectively and in the lowest dose possible for the shortest duration as possible.
Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust according to patient response. Because of the potential complications of steroid use, steroids should be used selectively and in the lowest dose possible for the shortest duration as possible.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response. Because of the potential complications of steroid use, steroids should be used selectively and in the lowest dose possible for the shortest duration as possible.
0.7 mg implant by intravitreal injection in the affected eye(s). Guidelines recommend intravitreous steroids as a second-line alternative treatment for central-involved diabetic macular edema (CIDME). Steroid therapies are associated with inferior visual acuity outcomes and increased rate of cataracts and glaucoma when compared against intravitreal injections of anti-vascular endothelial growth factor (anti-VEGF) agents.
0.7 mg implant by intravitreal injection in the affected eye(s). Retreatment will generally be performed after 3 to 4 months with a mean of approximately 2 to 3 injections/year. Guidelines suggest switching to a steroid in nonresponders who have already been treated with anti-vascular endothelial growth factor (VEGF) (after 3 to 6 injections, depending on the specific response of each patient) is reasonable. Steroids may be considered as a first-line therapy for patients who have a recent history of a major cardiovascular event or those who are unwilling to come for monthly injections (and/or monitoring) in the first 6 months of therapy; however, intraocular pressure still needs to be monitored every 2 to 8 weeks after dexamethasone implant injection.
Place the insert containing 0.4 mg of dexamethasone into the lower lacrimal canaliculus, just below the punctal opening. A single insert releases a 0.4 mg dose for up to 30 days following insertion.
0.005 mL of dexamethasone 9% (equivalent to 517 mcg) as a single dose as directed, intraocularly in the posterior chamber at the end of surgery.
0.4 mg/kg/dose PO once daily or every other day as needed for symptom control. Consider add-on low dose oral corticosteroids (7.5 mg/day or less of prednisone equivalent) only for those with poor symptom control and/or frequent exacerbation despite good inhaler technique and treatment adherence. Add corticosteroids only after exclusion of other contributory factors and consideration of other add-on treatments. Guidelines suggest dexamethasone syrup as an alternative in persons unable to tolerate liquid prednisone or prednisolone.
6 mg PO once daily for up to 10 days or until hospital discharge (whichever comes first) is recommended by the National Institutes of Health (NIH) COVID-19 treatment guidelines for use in hospitalized patients who require supplemental oxygen, including those on high-flow oxygen, noninvasive ventilation, mechanical ventilation, or extracorporeal membrane oxygenation (ECMO). This recommendation also applies to pregnant women, as the potential benefit of decreased maternal mortality justifies the low risk of fetal adverse effects with the short course of therapy. The NIH advises clinicians to review the patient's medical history and assess the potential risks and benefits before starting dexamethasone. The World Health Organization (WHO) strongly recommends the use of systemic corticosteroids for 7 to 10 days in patients with severe or critical COVID-19.
0.15 mg/kg/dose (Max: 6 mg/dose) PO once daily for up to 10 days, although data are limited. The National Institutes of Health (NIH) COVID-19 treatment guidelines recommend dexamethasone (with or without remdesivir) for hospitalized pediatric patients who require high-flow oxygen or noninvasive ventilation. Dexamethasone (without remdesivir) is also recommended for pediatric patients requiring mechanical ventilation or extracorporeal membrane oxygenation (ECMO). The addition of baricitinib or tocilizumab may be considered for patients who do not have rapid (e.g., within 24 hours) improvement in oxygenation after initiation of dexamethasone. Corticosteroids are not routinely recommended for pediatric patients who require only conventional oxygen, but corticosteroids can be considered in combination with remdesivir for patients with increasing oxygen needs, particularly adolescents. The use of dexamethasone for treatment of severe COVID-19 in pediatric patients who are profoundly immunocompromised has not been evaluated and may be harmful; in such cases, treatment should be considered on a case-by-case basis.[65314]
6 mg IV once daily for up to 10 days or until hospital discharge (whichever comes first) is recommended by the National Institutes of Health (NIH) COVID-19 treatment guidelines for use in hospitalized patients who require supplemental oxygen, including those on high-flow oxygen, noninvasive ventilation, mechanical ventilation, or extracorporeal membrane oxygenation (ECMO). This recommendation also applies to pregnant women, as the potential benefit of decreased maternal mortality justifies the low risk of fetal adverse effects with the short course of therapy. The NIH advises clinicians to review the patient's medical history and assess the potential risks and benefits before starting dexamethasone. The World Health Organization (WHO) strongly recommends the use of systemic corticosteroids for 7 to 10 days in patients with severe or critical COVID-19.
0.15 mg/kg/dose (Max: 6 mg/dose) IV once daily for up to 10 days, although data are limited. The National Institutes of Health (NIH) COVID-19 treatment guidelines recommend dexamethasone (with or without remdesivir) for hospitalized pediatric patients who require high-flow oxygen or noninvasive ventilation. Dexamethasone (without remdesivir) is also recommended for pediatric patients requiring mechanical ventilation or extracorporeal membrane oxygenation (ECMO). The addition of baricitinib or tocilizumab may be considered for patients who do not have rapid (e.g., within 24 hours) improvement in oxygenation after initiation of dexamethasone. Corticosteroids are not routinely recommended for pediatric patients who require only conventional oxygen, but corticosteroids can be considered in combination with remdesivir for patients with increasing oxygen needs, particularly adolescents. The use of dexamethasone for treatment of severe COVID-19 in pediatric patients who are profoundly immunocompromised has not been evaluated and may be harmful; in such cases, treatment should be considered on a case-by-case basis.
0.15 to 0.3 mg/kg/dose (Max: 6 mg/dose) PO once daily for up to 10 days is recommended as first-line immunomodulatory treatment in patients with persistent oxygen requirements due to COVID-19.
0.15 to 0.3 mg/kg/dose (Max: 6 mg/dose) IV once daily for up to 10 days is recommended as first-line immunomodulatory treatment in patients with persistent oxygen requirements due to COVID-19.
0.5 mg/kg/dose (Max: 10 mg/dose) IV every 6 hours for 6 doses with the first dose given 6 to 12 hours prior to extubation. One prospective, randomized study (n = 153) found no significant difference in the risk of postextubation stridor, the average number of racemic epinephrine treatments, or the number of patients requiring reintubation in patients receiving dexamethasone compared to those receiving placebo. Another prospective, randomized study (n = 66) found that dexamethasone-treated patients had a significantly lower rate of postextubation stridor at 10 minutes, 6 hours, and 12 hours but not 24 hours and fewer patients requiring epinephrine or reintubation compared to placebo-treated patients. A systematic review of clinical trials of dexamethasone for the prevention of postextubation stridor concluded that therapy may be beneficial in high-risk patients, such as those with underlying airway anomalies or multiple airway manipulations.
Various regimens have been used. 0.25 mg/kg/dose IV every 8 hours for 3 doses with the first dose given approximately 4 hours prior to scheduled extubation was studied in a prospective, randomized trial in 50 premature neonates (mean gestational age, 27.7 to 28.7 weeks) who were at high risk for airway edema. The rate of postextubation stridor and reintubation was significantly lower in the dexamethasone group compared to the placebo group. A systematic review of clinical trials of dexamethasone for the prevention of extubation failure recommends therapy be reserved for use in high risk neonates, such as those with repeated or prolonged intubations, due to a lack of benefit in low risk neonates and the risk of adverse effects. Use preservative-free products for administration to neonates when possible.
1 to 2 mg/kg IV load followed by 0.25 to 0.5 mg/kg/dose IV every 6 hours. Max: 16 mg/dose.
A bolus of 8 to 10 mg dexamethasone (or equivalent) PO or IV, followed by 16 mg/day PO (usually in twice-daily to four-times-daily doses for tolerance) is a typical dose; doses are adjusted to patient condition and are either maintained or tapered over a few weeks dependent on radiation therapy cycles and/or anticipated surgery. A broad dosage range of 16 to 100 mg/day has been used depending on the presence of paraparesis, etc. Higher quality data are needed to establish the benefits vs. risks and optimal dose and duration of therapy. Experts generally agree that patients who have neurologic deficits should receive dexamethasone; many patients with MSCC require corticosteroids to help preserve neurologic function, such as ambulation.
NOTE: For CNS infections related to tuberculosis, see tuberculosis.
Intravenous dosage Adults
0.15 mg/kg/dose IV every 6 hours for 2 to 4 days for pneumococcal meningitis; administer the first dose 10 to 20 minutes before or concomitantly with the first dose of antimicrobial agent. Do not administer to patients who have already received antimicrobial therapy as this is unlikely to improve patient outcome.[32690]
0.15 mg/kg/dose IV every 6 hours for 2 to 4 days for H. influenzae type b; administer the first dose 10 to 20 minutes before or concomitantly with the first dose of antimicrobial agent. Do not administer to patients who have already received antimicrobial therapy as this is unlikely to improve patient outcome. Use in pneumococcal meningitis is controversial and may be considered in those older than 6 weeks of age after weighing the possible benefits and risks.[32690]
0.15 mg/kg/dose PO every 6 hours for 2 to 4 days for pneumococcal meningitis; administer the first dose 10 to 20 minutes before or concomitantly with the first dose of antimicrobial agent. Do not administer to patients who have already received antimicrobial therapy as this is unlikely to improve patient outcome.[32690]
0.15 mg/kg/dose PO every 6 hours for 2 to 4 days for H. influenzae type b; administer the first dose 10 to 20 minutes before or concomitantly with the first dose of antimicrobial agent. Do not administer to patients who have already received antimicrobial therapy as this is unlikely to improve patient outcome. Use in pneumococcal meningitis is controversial and may be considered in those older than 6 weeks of age after weighing the possible benefits and risks.[32690]
American Society of Clinical Oncology (ASCO) guideline-based dosage regimens are stratified according to patient risk. HIGHLY EMETOGENIC CHEMOTHERAPY: 12 mg PO or IV prior to chemotherapy, then 8 mg PO or IV on days 2 to 3 or days 2 to 4. If an NK1 receptor antagonist is not included in the anti-emetic regimen, increase to dexamethasone 20 mg PO or IV prior to chemotherapy, then 16 mg PO or IV on days 2 to 3 or days 2 to 4. MODERATELY EMETOGENIC CHEMOTHERAPY: 8 mg PO or IV prior to chemotherapy, then 8 mg PO or IV on days 2 and 3. LOW EMOTOGENIC RISK CHEMOTHERAPY: 8 mg PO or IV as a single dose prior to chemotherapy. (NOTE: Other regimens have been used historically during chemotherapy - e.g., 10 to 20 mg IV before administration of chemotherapy, with additional, lower doses given for 24 to 72 hours, as needed).
10
to 14 mg/m2/dose IV is usually used prior to chemotherapy. A 5-HT3 antagonist is usually given along with dexamethasone for highly-emetogenic chemotherapy. An example regimen: dexamethasone 10 mg/m2/dose IV once daily, along with ondansetron. Some patients receive repeat dexamethasone every 12 hours, either IV or PO, but optimal regimens for repeat dosing are not established. For chemotherapy that is less emetogenic, doses as low as 6 mg/m2/dose PO have been given. The optimal dose of steroids for chemotherapy-induced nausea/vomiting (CINV) in children is not determined, and there are safety considerations.For the treatment of pruritus and inflammatory effects of corticosteroid-responsive dermatoses and dermatologic disorders, including alopecia areata, atopic dermatitis, bullous dermatitis herpetiformis, contact dermatitis, cutaneous T-cell lymphoma (CTCL) or mycosis fungoides, discoid lupus erythematosus, exfoliative dermatitis, granuloma annulare, keloids, lichen planus, lichen simplex chronicus or neurodermatitis, necrobiosis lipoidica diabeticorum, pemphigus, plaque psoriasis, severe seborrheic dermatitis, severe erythema multiforme, Stevens-Johnson syndrome (SJS), and toxic epidermal necrolysis† (TEN). For the treatment of atopic dermatitis, bullous dermatitis herpetiformis, contact dermatitis, cutaneous T-cell lymphoma (CTCL) or mycosis fungoides, exfoliative dermatitis, pemphigus, severe seborrheic dermatitis, and severe erythema multiforme. Oral dosage (dexamethasone) Adults
0.75 to 9 mg/day PO in 2 to 4 divided doses. Adjust dose according to response.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO in 3 to 4 divided doses, initially. Adjust dose according to response.
0.5 to 9 mg/day IV or IM in 2 to 4 divided doses. Adjust dose according to response.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM in 3 to 4 divided doses. Adjust dose according to response.
2 to 6 mg by intralesional injection; may repeat dose every 3 to 5 days to every 2 to 3 weeks. Dosage dependent upon degree of inflammation, size, disease state, and location of affected area. Usually employed when condition to be treated is limited to 1 or 2 sites.
8 to 16 mg or 0.1 to 0.3 mg/kg/dose IV or IM once daily, then taper dose over 7 to 10 days.
0.1 to 0.3 mg/kg/dose IV or IM once daily, then taper dose over 7 to 10 days.
100 mg or 1 to 1.5 mg/kg/dose IV or IM once daily for 3 days.
1 to 1.5 mg/kg/dose IV or IM once daily for 3 days.
Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust according to patient response.
0.06 to 0.3 mg/kg/day or 1.2 to 10 mg/m2/day IV or IM, in divided doses every 6 to 12 hours.
0.15 to 0.6 mg/kg/dose (Usual Max: 16 mg/dose) PO as a single dose.
0.15 to 0.6 mg/kg/dose (Usual Max: 16 mg/dose) IV or IM as a single dose.
Numerous dosing schedules have been studied. The Dexamethasone: A Randomized Trial (DART) study (n = 70, median gestational age 25 weeks) used the following tapering dose schedule over 10 days: 0.075 mg/kg/dose IV twice daily for 3 days, 0.05 mg/kg/dose IV twice daily for 3 days, 0.025 mg/kg/dose IV twice daily for 2 days, and 0.01 mg/kg/dose IV twice daily for 2 days. This dosing regimen facilitated extubation by day 10 but did not significantly improve mortality or oxygen dependence at 36 weeks; follow-up at 2 years of age did not indicate any significant adverse neurodevelopmental outcomes in patients treated with dexamethasone. Use is somewhat controversial, and most experts suggest using low doses and careful patient selection. The American Academy of Pediatrics (AAP) recommends against the use of high-dose dexamethasone (greater than 0.5 mg/kg/day) due to the risk of short- and long-term adverse effects, including neurodevelopmental effects. Late corticosteroid therapy (initiated after 7 days of age) may be preferred over early therapy (initiated at less than 7 days of age). Late therapy may reduce neonatal mortality without significantly increasing potential adverse long-term neurodevelopmental outcomes.
6 mg IM every 12 hours for 4 doses between 24 and 34 weeks gestation with risk for preterm delivery within 7 days. Use may also be considered starting at 22 weeks gestation if neonatal resuscitation is planned and after appropriate counseling. If labor is impending and further doses are unlikely, the first dose of dexamethasone should still be given because treatment with corticosteroids for less than 24 hours is still associated with a significant reduction in neonatal morbidity/mortality. However, no additional benefit has been demonstrated for courses of antenatal steroids with shorter dosage intervals than those recommended, often referred to as accelerated dosing, even when delivery is imminent. A repeat or rescue course of corticosteroids may be considered when less than 34 weeks gestation, with risk of preterm delivery within the next 7 days, and whose prior course of antenatal corticosteroids was administered more than 14 days previously. Rescue course corticosteroids could be provided as early as 7 days from the prior dose if indicated by clinical situation.[64435]
6 mg IM every 12 hours for 4 doses between 24 and 34 weeks gestation with risk for preterm delivery within 7 days. Use may also be considered starting at 22 weeks gestation if neonatal resuscitation is planned and after appropriate counseling. If labor is impending and further doses are unlikely, the first dose of dexamethasone should still be given because treatment with corticosteroids for less than 24 hours is still associated with a significant reduction in neonatal morbidity/mortality. However, no additional benefit has been demonstrated for courses of antenatal steroids with shorter dosage intervals than those recommended, often referred to as accelerated dosing, even when delivery is imminent. A repeat or rescue course of corticosteroids may be considered when less than 34 weeks gestation, with risk of preterm delivery within the next 7 days, and whose prior course of antenatal corticosteroids was administered more than 14 days previously. Rescue course corticosteroids could be provided as early as 7 days from the prior dose if indicated by clinical situation.[64435]
Initially, 0.75 to 9 mg/day PO, given in 2 to 4 divided doses. Dosing can be quite variable, depending on the patient's condition. Adjust according to patient response.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.
Initially, 0.5 to 9 mg/day IV or IM, in 2 to 4 divided doses. Adjust according to patient response.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM given in 3 to 4 divided doses is the FDA-approved general dosage range. Adjust according to patient response.
0.7 mg implant by intravitreal injection.
0.4 mg in the lower lacrimal punctum into the canaliculus as a single dose. A single insert releases a 0.4 mg dose od dexamethasone for up to 30 days after insertion.
1 to 2 drops in the affected eye(s) every hour during the day and every 2 hours during the night, initially. Reduce dose to 1 drop in the affected eye(s) every 4 hours when a favorable response occurs, and then 1 drop in the affected eye(s) 3 to 4 times daily as warranted.
1 to 2 drops in the affected eye(s) every hour for severe disease and every 4 to 6 hours for mild disease. Taper dose to discontinuation as inflammation subsides.
1 to 2 drops in the affected eye(s) every hour for severe disease and every 4 to 6 hours for mild disease. Taper dose to discontinuation as inflammation subsides.
0.75 to 9 mg/day PO in 2 to 4 divided doses, initially. Adjust according to patient response.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day PO in 3 to 4 divided doses, initially. Adjust according to patient response.
0.5 to 9 mg/day IV or IM in 2 to 4 divided doses, initially. Adjust according to patient response.
0.02 to 0.3 mg/kg/day or 0.6 to 9 mg/m2/day IV or IM in 3 to 4 divided doses. Adjust according to patient response.
1 to 2 drops in each eye 4 times daily, initially. Reduce dose to 1 to 2 drops in each eye twice daily after 1 to 2 weeks if positive response in signs and/or symptoms and start cyclosporine, then taper or discontinue steroid therapy after 2 to 4 weeks. Consider extending duration to 4 weeks if no response at 2 weeks, especially in patients with moderate to severe disease.
0.5 mg PO once daily at bedtime, administered on cycle days 3 to 12, days 5 to 9, or starting on day 5 and continuing through conception, in combination with clomiphene (doses ranging from 50 to 200 mg/day) has been studied. Alternatively, dexamethasone 2 mg PO once daily on cycle days 5 to 14 in combination with clomiphene 200 mg/day or dexamethasone 1 mg PO twice daily on cycle days 3 to 12 in combination with clomiphene 100 mg/day PO has also been studied; HCG was administered to augment ovulation. Optimal timing and dose of dexamethasone is not clear and has varied from study to study. Combination therapy has been shown to increase ovulation rates (range, 75% to 100%) and pregnancy rates (range, 38% to 74%) in women with both normal and elevated DHEA-S concentrations and in those women with or without polycystic ovary syndrome (PCOS). A Cochrane's review indicates that dexamethasone-clomiphene combination is one of the few adjunctive therapies for infertility that has been shown to improve pregnancy rates (fixed OR 11.3, 95% CI 5.3 to 24; NNT 2.7, 95% CI 2.1 to 3.6) ; the 2 studies in this review used differing doses of 0.5 mg PO at bedtime on days 5 to 9 or 2 mg PO/day on days 5 to 14. Several theories on the mechanism of dexamethasone in infertility exist. One theory is that dexamethasone enhances folliculogenesis by suppressing adrenal androgen hypersecretion, which should augment the actions of clomiphene. Dexamethasone may increase FSH concentrations thereby facilitating folliculogenesis. Finally, dexamethasone may decrease the elevated LH concentrations in patients with PCOS.
4 mg PO every 6 hours until symptoms resolve.
0.15 mg/kg/dose (Max: 4 mg/dose) PO every 6 hours until symptoms resolve.
4 mg IV or IM every 6 hours until symptoms resolve.
0.15 mg/kg/dose (Max: 4 mg/dose) IV or IM every 6 hours until symptoms resolve.
8 mg PO once, then 4 mg PO every 6 hours until symptoms resolve. May add acetazolamide.
0.15 mg/kg/dose (Max: 4 mg/dose) PO every 6 hours until symptoms resolve. May add acetazolamide.
8 mg IV or IM once, then 4 mg IV or IM every 6 hours until symptoms resolve. May add acetazolamide.
0.15 mg/kg/dose (Max: 4 mg/dose) IV or IM every 6 hours until symptoms resolve. May add acetazolamide.
2 to 4 mg IV once for established post-operative nausea/vomiting (PONV), per treatment guidelines; readministration of longer-acting drugs, such as dexamethasone, is not recommended. If PONV prophylaxis was either inadequate or not initially given, dexamethasone is an appropriate rescue treatment option if not initially used for PONV prophylaxis. Of note, the 5-HT3 antagonists are the only class of drugs that have been adequately studied for the treatment of established PONV.
2 mg PO every 6 hours or 4 mg PO every 12 hours starting the day of ascent and continuing for 2 to 3 days after reaching the target altitude or until descent is initiated. Do not exceed 10 days to prevent glucocorticoid toxicity or adrenal suppression. May consider 4 mg PO every 6 hours for very high risk situations (e.g., military or search and rescue personnel being airlifted to altitudes higher than 3,500 meters with immediate performance of physical activity). Prophylactic medications should be considered in addition to slow ascent for moderate- to high-risk situations. Dexamethasone is suggested as an alternative in individuals with a history of intolerance or allergy to acetazolamide or as an adjunct to acetazolamide in rare, emergency circumstances requiring rapid ascent and immediate performance of physical activity.
4 to 5 mg IV at anesthesia induction is recommended by treatment guidelines for patients at an increased risk for post-operative nausea and vomiting (PONV); administration at induction rather than at the end of surgery is preferred. Some studies suggest that 8 mg IV is associated with a dose-dependent increase in quality of recovery, including reduced fatigue, postoperative pain, and need for opioid analgesia; however, further confirmation is necessary before larger doses are universally recommend. Safety data regarding the perioperative use of dexamethasone point to a possible increased risk of wound infection and/or increased blood glucose in some patients. A single dexamethasone dose (4 to 8 mg IV) is, however, considered safe for PONV prophylaxis. For patients with labile glucose control, dexamethasone use is relatively contraindicated.
0.15 to 1 mg/kg/dose IV (Max: 8 to 25 mg/dose IV) given as a single intraoperative dose reduces the incidence of postoperative nausea/vomiting in the first 24 hours, improves postoperative pain control, and decreases the time to resumption of soft/solid diet without adverse effects and is recommended in patients undergoing tonsillectomy. A lower dose of 0.015 mg/kg/dose (Max: 5 mg/dose) in combination with ondansetron 0.1 mg/kg/dose (Max: 4 mg) is recommended first-line for postoperative vomiting prophylaxis in children by the Society for Ambulatory Anesthesiology.
Due to the lack of consistent efficacy data and the high risk of adverse effects, the American Academy of Pediatrics does not recommend systemic corticosteroids for the management of bronchiolitis in any setting. However, other authors state corticosteroids may be beneficial in severely ill or mechanically ventilated patients. One randomized trial of 800 infants seen in the emergency department used 1 mg/kg PO once (Max: 10 mg/dose) followed by 0.6 mg/kg/dose PO once daily (Max: 10 mg/dose) for 5 days. Dexamethasone in combination with nebulized epinephrine was effective in reducing hospital admissions by day 7 of illness compared to treatment with dexamethasone alone, epinephrine alone, or placebo. In a study of 200 infants (median age 3.5 months) with an asthma risk, as determined by eczema or a family history of asthma in a first-degree relative, dexamethasone 1 mg/kg (single dose) PO then 0.6 mg/kg/dose PO once daily for 4 more days was administered with salbutamol. In infants receiving dexamethasone with salbutamol, the time to readiness for discharge was 18.6 hours vs. 27.1 hours in patients not receiving dexamethasone (p = 0.015). In contrast, 1 mg/kg/dose PO (Max: 12 mg/dose) given as a single dose did not reduce hospitalization rates, Respiratory Assessment Change Scores (RACS), length of hospitalization for those patients who required admission, or subsequent hospitalizations within 7 days compared to placebo in another large, randomized trial (n = 600).
Due to the lack of consistent efficacy data and the high risk of adverse effects, the American Academy of Pediatrics does not recommend systemic corticosteroids for the management of bronchiolitis in any setting. However, other authors state corticosteroids may be beneficial in severely ill or mechanically ventilated patients. 0.15 mg/kg/dose IV every 6 hours for 48 hours with the first dose administered within 24 hours of mechanical ventilation was used in patients with respiratory syncytial virus. In a post hoc analysis of patients with bronchiolitis (n = 39), the mean duration of mechanical ventilation and of supplemental oxygen were significantly shorter in patients receiving dexamethasone compared to those receiving placebo (4.9 and 7.7 days vs. 9.2 and 11.3 days, respectively); no differences were seen in the length of intensive care unit or hospital stay.
20 mg IV on day 1 in combination with rituximab 375 mg/m2 IV on day 1 and cyclophosphamide 100 mg/m2 orally twice daily on days 1 to 5 (total dose of 1,000 mg/m2/cycle) repeated every 21 days for 6 cycles was evaluated in a single-arm, phase II trial.
40 mg IV on days 1, 8, 15, and 22 in cycles 2 and 5 in combination with bortezomib and rituximab was evaluated in a nonrandomized phase II trial. Bortezomib was given as follows: 1.3 mg/m2 IV on days 1, 4, 8, and 11 for the first 21-day cycle (cycle 1) then 1.6 mg/m2 IV on days 1, 8, 15, and 22 repeated every 35 days for 4 additional cycles (cycles 2, 3, 4, and 5). Rituximab was given as 375 mg/m2 IV on days 1, 8, 15, and 22 in cycles 2 and 5 (for 8 total doses). All patients received premedication with acetaminophen 1,000 mg PO and diphenhydramine 50 mg IV prior to rituximab and herpes zoster prophylaxis with valacyclovir or acyclovir.
Dexamethasone in combination with lenalidomide (15 mg PO daily on days 1 to 21) and cyclophosphamide repeated every 28 days has been evaluated in nonrandomized, phase II studies. Treatment duration, drug dosages of cyclophosphamide and dexamethasone, and thromboprophylaxis agents/recommendations varied in these studies. In one study, 12 cycles of dexamethasone (20 mg PO on days 1, 2, 3, 4, 9, 10, 11, and 12 for 6 cycles; then 20 mg PO on days 1, 2, 3, and 4 for an additional 6 cycles), lenalidomide, and cyclophosphamide (300 mg/m2 IV on days 1 and 8 for 6 cycles; then 300 mg/m2 IV on day 1 for an additional 6 cycles) were given and then maintenance therapy with lenalidomide and dexamethasone was administered for 3 additional years or until disease progression. Patients with cardiac stage III had an upfront dose modification of dexamethasone. In another study, dexamethasone (40 mg PO on days 1, 8, 15, and 22), lenalidomide, and cyclophosphamide (500 mg PO on days 1, 8, and 15) therapy was given for a maximum of 9 cycles; treatment was discontinued after cycle 6 if a complete response or partial response/very good partial response plus organ response was obtained. In this study, patients with fluid retention over 3% of body weight despite optimal diuretic use received a lower dose of dexamethasone (20 mg once weekly). In a third study, cycles of dexamethasone (40 mg PO on days 1, 8, 15, and 22), lenalidomide, and cyclophosphamide (300 mg/m2 PO on days 1, 8, and 15) were continued until disease progression, unacceptable toxicity, or up to 2 years; however, cyclophosphamide was given for up to a maximum of 12 cycles only.
40 mg orally on days 1, 8, 15, and 22 in combination with lenalidomide (10 mg PO daily on days 1 to 21) and melphalan repeated every 28 days has been evaluated in nonrandomized studies. Treatment duration, the melphalan dosage, and thromboprophylaxis agents/recommendations varied in these studies. In one study, melphalan (0.18 mg/kg PO daily on days 1, 2, 3, and 4), lenalidomide, and dexamethasone therapy was given for a maximum of 9 cycles; single-agent lenalidomide was continued in responding patients. In another study, lenalidomide, melphalan (5 mg/m2 PO daily on days 1, 2, 3, and 4), and dexamethasone were continued until disease progression, unacceptable toxicity, or up to 12 cycles.
40 mg orally daily on days 1, 2, 3, and 4 repeated every 28 days on cycles 1 and 2 and then 40 mg orally daily on days 1, 2, 3, and 4 repeated every 35 days up to a maximum of 8 cycles in combination with bortezomib and melphalan (BMdex regimen) was evaluated in a multicenter, randomized, open-label, phase 3 trial (n = 109). Patients were evaluated for response after 3 and 6 cycles of therapy; patients with a partial response (PR) or better after cycle 3 received an additional 3 cycles of therapy. Patients with a complete response (CR) or a PR and organ response stopped treatment after cycle 6.
NOTE: Daratumumab; hyaluronidase is FDA approved in combination with bortezomib, cyclophosphamide, and dexamethasone for the treatment of newly diagnosed light-chain amyloidosis.
Intravenous and Oral dosage Adults
40 mg IV or PO in combination with bortezomib 1.3 mg/m2 subcutaneously and cyclophosphamide 300 mg/m2 (Max dose of 500 mg) IV or PO each given weekly on days 1, 8, 15, and 22 repeated every 28 days for a maximum of 6 cycles (VCd) plus up to 2 years of subcutaneous daratumumab; hyaluronidase (D-VCd) was evaluated in transplant eligible, newly diagnosed light-chain amyloidosis patients in a randomized, phase 3 trial (n = 388; the ANDROMEDA trial). The dose of dexamethasone was reduced to 20 mg in patients older than 70 years or who had a body mass index less than 18.5, hypervolemia, poorly controlled diabetes mellitus, or prior intolerance to steroid therapy. Daratumumab; hyaluronidase was administered as follows: 1,800 mg daratumumab and 30,000 units hyaluronidase subcutaneously weekly on weeks 1 to 8 (8 doses), 1,800 mg daratumumab and 30,000 units hyaluronidase every 2 weeks on weeks 9 to 24 (8 doses), and then 1,800 mg daratumumab and 30,000 units hyaluronidase every 4 weeks starting on week 25 until disease progression or for a maximum of 2 years. At a median follow-up time of 11.4 (range, 0.03 to 21.3) months, the hematologic complete response rate was significantly improved (53.3% vs. 18.1%; relative risk ratio = 2.9; 95% CI, 2.1 to 4.1; p less than 0.001) in patients who received D-VCd compared with VCd in the ANDROMEDA trial. The median time to hemCR was 60 and 85 days in the D-VCd and VCd arms, respectively.
10 mg PO once daily for 1 to 2 days.
0.6 mg/kg/dose (Max: 10 mg/dose) PO once daily for 1 to 2 days.
10 mg IM once daily for 1 to 2 days.
0.6 mg/kg/dose (Max: 10 mg/dose) IM once daily for 1 to 2 days.
2 mg PO every 6 hours. Taper dose based on clinical response and the duration of steroid therapy.
2 mg IV every 6 hours. Taper dose based on clinical response and the duration of steroid therapy.
6 to 8 mg PO divided into 3 daily doses starting 3 days before antiparasitics and continuing for the duration of therapy. Titrate based on clinical response. Taper over 6 to 8 weeks to avoid rebound symptoms.
0.1 to 0.2 mg/kg/day PO starting 3 days before antiparasitics and continuing for the duration of therapy. Titrate based on clinical response. Taper over 6 to 8 weeks after antiparasitic therapy is complete to avoid rebound symptoms.
†Indicates off-label use
Dosing Considerations
Specific guidelines for systemic dosage adjustments in hepatic impairment are not available; it appears that no dosage adjustments are needed.
Renal ImpairmentSpecific guidelines for dosage adjustments in renal impairment are not available; it appears that no dosage adjustments are needed.
Drug Interactions
Abatacept: (Moderate) Concomitant use of immunosuppressives, as well as long-term corticosteroids, may potentially increase the risk of serious infection in abatacept treated patients. Advise patients taking abatacept to seek immediate medical advice if they develop signs and symptoms suggestive of infection.
Acetaminophen; Aspirin, ASA; Caffeine: (Moderate) 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; 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) Monitor for reduced efficacy of codeine and signs of opioid withdrawal in patients who have developed physical dependence if coadministration with dexamethasone is necessary; consider increasing the dose of codeine as needed. It is recommended to avoid this combination when codeine is being used for cough. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs of respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a weak CYP3A inducer. Concomitant use with dexamethasone can increase norcodeine levels via increased CYP3A metabolism, resulting in decreased metabolism via CYP2D6 resulting in lower morphine levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
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) Monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal if coadministration with dexamethasone is necessary; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs of respiratory depression and sedation. Hydrocodone is a CYP3A substrate and dexamethasone is a weak CYP3A inducer. Concomitant use with CYP3A inducers can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
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 CYP3A substrate and dexamethasone is a weak CYP3A inducer. Concomitant use with CYP3A inducers can decrease oxycodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
Acetaminophen; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
Acetazolamide: (Moderate) Corticosteroids may increase the risk of hypokalemia if used concurrently with acetazolamide. Hypokalemia may be especially severe with prolonged use of corticotropin, ACTH. Monitor serum potassium levels to determine the need for potassium supplementation and/or alteration in drug therapy.
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. Dexamethasone is primarily metabolized by CYP3A and adagrasib is a strong CYP3A inhibitor. 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: (Moderate) Monitor for an increase in albendazole-related adverse reactions if concomitant use with dexamethasone is necessary. Concomitant use increased the steady-state trough concentrations of albendazole sulfoxide by about 56%.
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.
Alfentanil: (Moderate) Consider an increased dose of alfentanil and monitor for evidence of opioid withdrawal if coadministration with dexamethasone is necessary. If dexamethasone is discontinued, consider reducing the alfentanil dosage and monitor for evidence of respiratory depression. Coadministration of a weak CYP3A inducer like dexamethasone with alfentanil, a CYP3A substrate, may decrease exposure to alfentanil resulting in decreased efficacy or onset of withdrawal symptoms in a patient who has developed physical dependence to alfentanil. Alfentanil plasma concentrations will increase once the inducer is stopped, which may increase or prolong the therapeutic and adverse effects, including serious respiratory depression.
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.
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.
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.
Amobarbital: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with barbiturates is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A substrate and barbiturates are strong CYP3A inducers.
Amoxicillin; Clarithromycin; Omeprazole: (Moderate) Monitor for steroid-related adverse reactions if coadministration of clarithromycin 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. Dexamethasone is primarily metabolized by CYP3A and clarithromycin is a strong CYP3A inhibitor. 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.
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 CYP3A substrate and apalutamide is a strong CYP3A 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.
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.
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) Monitor for decreased efficacy of dexamethasone if coadministration with barbiturates is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A substrate and barbiturates are strong CYP3A inducers. (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) 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 codeine and signs of opioid withdrawal in patients who have developed physical dependence if coadministration with dexamethasone is necessary; consider increasing the dose of codeine as needed. It is recommended to avoid this combination when codeine is being used for cough. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs of respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a weak CYP3A inducer. Concomitant use with dexamethasone can increase norcodeine levels via increased CYP3A metabolism, resulting in decreased metabolism via CYP2D6 resulting in lower morphine levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
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 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 CYP3A substrate and dexamethasone is a weak CYP3A inducer. Concomitant use with CYP3A inducers can decrease oxycodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
Atazanavir: (Moderate) Monitor for steroid-related adverse reactions and a decrease in atazanavir efficacy if concomitant use of dexamethasone and atazanavir is necessary. If long term coadministration is required, consider using an alternative corticosteroid, such as prednisone or prednisolone. Concomitant use may increase dexamethasone concentrations and decrease atazanavir exposure. Dexamethasone is a CYP3A substrate and CYP3A inducer; atazanavir is a CYP3A substrate and strong CYP3A inhibitor. 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.
Atazanavir; Cobicistat: (Major) Avoid concurrent use of dexamethasone with cobicistat-containing regimens due to the risk of decreased 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. Consider an alternative corticosteroid (i.e., beclomethasone, prednisone, prednisolone) for long-term use. If concomitant use is necessary, monitor virologic response and for corticosteroid-related adverse effects. Dexamethasone is a CYP3A4 substrate and weak CYP3A inducer; cobicistat is a CYP3A4 substrate and strong CYP3A inhibitor. 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. (Moderate) Monitor for steroid-related adverse reactions and a decrease in atazanavir efficacy if concomitant use of dexamethasone and atazanavir is necessary. If long term coadministration is required, consider using an alternative corticosteroid, such as prednisone or prednisolone. Concomitant use may increase dexamethasone concentrations and decrease atazanavir exposure. Dexamethasone is a CYP3A substrate and CYP3A inducer; atazanavir is a CYP3A substrate and strong CYP3A inhibitor. 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.
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 weak CYP3A inducer. Coadministration with a weak CYP3A inducer resulted in a 25% reduction in atogepant overall exposure and a 24% reduction in atogepant peak concentration.
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.
Avanafil: (Major) Coadministration of avanafil with dexamethasone is not recommended by the manufacturer of avanafil due to the potential for decreased avanafil efficacy. Avanafil is a CYP3A substrate and dexamethasone is a CYP3A inducer. Although the potential effect of CYP inducers on the pharmacokinetics of avanafil has not been evaluated, plasma concentrations may decrease.
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.
Barbiturates: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with barbiturates is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A substrate and barbiturates are strong CYP3A inducers.
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.
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.
Benzhydrocodone; Acetaminophen: (Moderate) Monitor for reduced efficacy of benzhydrocodone and signs of opioid withdrawal if coadministration with dexamethasone is necessary; consider increasing the dose of benzhydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of benzhydrocodone and frequently monitor for signs of respiratory depression and sedation. Benzhydrocodone is a prodrug for hydrocodone. Hydrocodone is a CYP3A substrate and dexamethasone is a weak CYP3A inducer. Concomitant use with CYP3A inducers can decrease hydrocodone concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
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.
Bictegravir; Emtricitabine; Tenofovir Alafenamide: (Moderate) Monitor for a decrease in bictegravir efficacy during concurrent use of bictegravir and dexamethasone. If long term coadministration is required, consider using an alternative corticosteroid, such as prednisone or prednisolone. Concomitant use may decrease bictegravir exposure leading to potential loss of virologic control. Bictegravir is a CYP3A substrate and dexamethasone is a weak CYP3A inducer.
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.
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.
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.
Buprenorphine: (Moderate) Monitor for decreased efficacy of buprenorphine, and potentially the onset of a withdrawal syndrome in patients who have developed physical dependence to buprenorphine, if coadministration with dexamethasone is necessary; consider increasing the dose of buprenorphine until stable drug effects are achieved. If dexamethasone is discontinued, consider a buprenorphine dose reduction and monitor for signs of respiratory depression. Buprenorphine is a CYP3A substrate and dexamethasone is a CYP3A inducer.
Buprenorphine; Naloxone: (Moderate) Monitor for decreased efficacy of buprenorphine, and potentially the onset of a withdrawal syndrome in patients who have developed physical dependence to buprenorphine, if coadministration with dexamethasone is necessary; consider increasing the dose of buprenorphine until stable drug effects are achieved. If dexamethasone is discontinued, consider a buprenorphine dose reduction and monitor for signs of respiratory depression. Buprenorphine is a CYP3A substrate and dexamethasone is a CYP3A inducer.
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) Monitor for decreased efficacy of buspirone if dexamethasone is added to a patient on a stable dosage of buspirone; a dose increase of buspirone may be needed to maintain anxiolytic activity. Buspirone is a sensitive CYP3A substrate and dexamethasone is a CYP3A inducer.
Butabarbital: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with barbiturates is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A substrate and barbiturates are strong CYP3A inducers.
Butalbital; Acetaminophen: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with barbiturates is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A substrate and barbiturates are strong CYP3A inducers.
Butalbital; Acetaminophen; Caffeine: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with barbiturates is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A substrate and barbiturates are strong CYP3A inducers.
Butalbital; Acetaminophen; Caffeine; Codeine: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with barbiturates is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A substrate and barbiturates are strong CYP3A inducers. (Moderate) Monitor for reduced efficacy of codeine and signs of opioid withdrawal in patients who have developed physical dependence if coadministration with dexamethasone is necessary; consider increasing the dose of codeine as needed. It is recommended to avoid this combination when codeine is being used for cough. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs of respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a weak CYP3A inducer. Concomitant use with dexamethasone can increase norcodeine levels via increased CYP3A metabolism, resulting in decreased metabolism via CYP2D6 resulting in lower morphine levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
Butalbital; Aspirin; Caffeine; Codeine: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with barbiturates is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A substrate and barbiturates are strong CYP3A inducers. (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 codeine and signs of opioid withdrawal in patients who have developed physical dependence if coadministration with dexamethasone is necessary; consider increasing the dose of codeine as needed. It is recommended to avoid this combination when codeine is being used for cough. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs of respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a weak CYP3A inducer. Concomitant use with dexamethasone can increase norcodeine levels via increased CYP3A metabolism, resulting in decreased metabolism via CYP2D6 resulting in lower morphine levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
Cabotegravir; Rilpivirine: (Contraindicated) Concurrent use of dexamethasone (more than 1 dose) and rilpivirine is contraindicated. Concomitant use may decrease the exposure and efficacy of rilpivirine leading to potential development of viral resistance. Rilpivirine is a CYP3A substrate and dexamethasone is an inducer of CYP3A4.
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.
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.
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) Monitor for decreased efficacy of both drugs if dexamethasone is coadministered with carbamazepine; dosage adjustments of either drug may be needed. Concomitant use may decrease the exposure of both drugs. Dexamethasone is a CYP3A substrate and weak CYP3A inducer; carbamazepine is a CYP3A substrate and strong CYP3A inducer.
Cariprazine: (Major) Coadministration of cariprazine with dexamethasone is not recommended as the net effect of CYP3A induction on cariprazine and its metabolites is unclear. Cariprazine is a CYP3A substrate and dexamethasone is a weak CYP3A inducer. Coadministration of cariprazine with CYP3A inducers has not been evaluated.
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.
Caspofungin: (Major) Consider a caspofungin dosage increase if concomitant use with dexamethasone is necessary. Increase the caspofungin dose to 70 mg/day in adults and 70 mg/m2/day (up to 70 mg/day) in pediatric patients. Concomitant use may decrease caspofungin exposure which may reduce its efficacy. Caspofungin is a CYP3A substrate and dexamethasone is a CYP3A inducer.
Celecoxib; Tramadol: (Moderate) Monitor for reduced efficacy of tramadol and signs of opioid withdrawal if coadministration with dexamethasone is necessary; consider increasing the dose of tramadol as needed. If dexamethasone is discontinued, consider a dose reduction of tramadol and frequently monitor for seizures, serotonin syndrome, and signs of respiratory depression and sedation. Tramadol is a CYP3A substrate and dexamethasone is a weak CYP3A inducer. Concomitant use with CYP3A inducers can decrease tramadol levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
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 CYP3A inhibitors, especially for long-term use. Ceritinib is a strong CYP3A4 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.
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.
Chloramphenicol: (Moderate) Monitor for steroid-related adverse reactions if coadministration of chloramphenicol 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. Dexamethasone is primarily metabolized by CYP3A and chloramphenicol is a strong CYP3A inhibitor. 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.
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) Monitor for reduced efficacy of codeine and signs of opioid withdrawal in patients who have developed physical dependence if coadministration with dexamethasone is necessary; consider increasing the dose of codeine as needed. It is recommended to avoid this combination when codeine is being used for cough. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs of respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a weak CYP3A inducer. Concomitant use with dexamethasone can increase norcodeine levels via increased CYP3A metabolism, resulting in decreased metabolism via CYP2D6 resulting in lower morphine levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
Chlorpheniramine; Dextromethorphan; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
Chlorpheniramine; Dihydrocodeine; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.
Chlorpheniramine; Hydrocodone: (Moderate) Monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal if coadministration with dexamethasone is necessary; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs of respiratory depression and sedation. Hydrocodone is a CYP3A substrate and dexamethasone is a weak CYP3A inducer. Concomitant use with CYP3A inducers can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
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) Monitor for a decrease in dexamethasone efficacy during concurrent use of dexamethasone and cholestyramine. 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.
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: (Moderate) Monitor for steroid-related adverse reactions if coadministration of clarithromycin 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. Dexamethasone is primarily metabolized by CYP3A and clarithromycin is a strong CYP3A inhibitor. 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.
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) Monitor for loss of clozapine effectiveness if coadministered with dexamethasone. Consideration should be given to increasing the clozapine dose if necessary. When dexamethasone is discontinued, reduce the clozapine dose based on clinical response. Clozapine is a CYP3A substrate and dexamethasone is a weak CYP3A inducer.
Cobicistat: (Major) Avoid concurrent use of dexamethasone with cobicistat-containing regimens due to the risk of decreased 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. Consider an alternative corticosteroid (i.e., beclomethasone, prednisone, prednisolone) for long-term use. If concomitant use is necessary, monitor virologic response and for corticosteroid-related adverse effects. Dexamethasone is a CYP3A4 substrate and weak CYP3A inducer; cobicistat is a CYP3A4 substrate and strong CYP3A inhibitor. 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.
Codeine: (Moderate) Monitor for reduced efficacy of codeine and signs of opioid withdrawal in patients who have developed physical dependence if coadministration with dexamethasone is necessary; consider increasing the dose of codeine as needed. It is recommended to avoid this combination when codeine is being used for cough. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs of respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a weak CYP3A inducer. Concomitant use with dexamethasone can increase norcodeine levels via increased CYP3A metabolism, resulting in decreased metabolism via CYP2D6 resulting in lower morphine levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
Codeine; Guaifenesin: (Moderate) Monitor for reduced efficacy of codeine and signs of opioid withdrawal in patients who have developed physical dependence if coadministration with dexamethasone is necessary; consider increasing the dose of codeine as needed. It is recommended to avoid this combination when codeine is being used for cough. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs of respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a weak CYP3A inducer. Concomitant use with dexamethasone can increase norcodeine levels via increased CYP3A metabolism, resulting in decreased metabolism via CYP2D6 resulting in lower morphine levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
Codeine; Guaifenesin; Pseudoephedrine: (Moderate) Monitor for reduced efficacy of codeine and signs of opioid withdrawal in patients who have developed physical dependence if coadministration with dexamethasone is necessary; consider increasing the dose of codeine as needed. It is recommended to avoid this combination when codeine is being used for cough. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs of respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a weak CYP3A inducer. Concomitant use with dexamethasone can increase norcodeine levels via increased CYP3A metabolism, resulting in decreased metabolism via CYP2D6 resulting in lower morphine levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
Codeine; Phenylephrine; Promethazine: (Moderate) Monitor for reduced efficacy of codeine and signs of opioid withdrawal in patients who have developed physical dependence if coadministration with dexamethasone is necessary; consider increasing the dose of codeine as needed. It is recommended to avoid this combination when codeine is being used for cough. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs of respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a weak CYP3A inducer. Concomitant use with dexamethasone can increase norcodeine levels via increased CYP3A metabolism, resulting in decreased metabolism via CYP2D6 resulting in lower morphine levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence. (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) Monitor for reduced efficacy of codeine and signs of opioid withdrawal in patients who have developed physical dependence if coadministration with dexamethasone is necessary; consider increasing the dose of codeine as needed. It is recommended to avoid this combination when codeine is being used for cough. If dexamethasone is discontinued, consider a dose reduction of codeine and frequently monitor for signs of respiratory depression and sedation. Codeine is primarily metabolized by CYP2D6 to morphine, and by CYP3A to norcodeine; norcodeine does not have analgesic properties. Dexamethasone is a weak CYP3A inducer. Concomitant use with dexamethasone can increase norcodeine levels via increased CYP3A metabolism, resulting in decreased metabolism via CYP2D6 resulting in lower morphine levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
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) Closely monitor cyclosporine concentrations and adjust the dose of cyclosporine as appropriate if coadministration with dexamethasone is necessary. Concurrent use may decrease cyclosporine exposure resulting in decreased efficacy. Cyclosporine is extensively metabolized by CYP3A and has a narrow therapeutic index; dexamethasone is a weak CYP3A inducer.
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.
Darunavir: (Moderate) Monitor for steroid-related adverse reactions and a decrease in darunavir efficacy if concomitant use of dexamethasone and darunavir is necessary. If long term coadministration is required, consider using an alternative corticosteroid, such as prednisone or prednisolone. Concomitant use may increase dexamethasone concentrations and decrease darunavir exposure. Dexamethasone is a CYP3A substrate and CYP3A inducer; darunavir is a CYP3A substrate and strong CYP3A inhibitor. 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.
Darunavir; Cobicistat: (Major) Avoid concurrent use of dexamethasone with cobicistat-containing regimens due to the risk of decreased 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. Consider an alternative corticosteroid (i.e., beclomethasone, prednisone, prednisolone) for long-term use. If concomitant use is necessary, monitor virologic response and for corticosteroid-related adverse effects. Dexamethasone is a CYP3A4 substrate and weak CYP3A inducer; cobicistat is a CYP3A4 substrate and strong CYP3A inhibitor. 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. (Moderate) Monitor for steroid-related adverse reactions and a decrease in darunavir efficacy if concomitant use of dexamethasone and darunavir is necessary. If long term coadministration is required, consider using an alternative corticosteroid, such as prednisone or prednisolone. Concomitant use may increase dexamethasone concentrations and decrease darunavir exposure. Dexamethasone is a CYP3A substrate and CYP3A inducer; darunavir is a CYP3A substrate and strong CYP3A inhibitor. 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.
Darunavir; Cobicistat; Emtricitabine; Tenofovir alafenamide: (Major) Avoid concurrent use of dexamethasone with cobicistat-containing regimens due to the risk of decreased 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
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.
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.
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.
Diazepam: (Moderate) Monitor patients for decreased efficacy of diazepam if coadministration with dexamethasone is necessary. Concurrent use may decrease diazepam exposure. Diazepam is a CYP3A substrate and dexamethasone is a CYP3A inducer.
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. Concomitant use may decrease the exposure and efficacy of rilpivirine leading to potential development of viral resistance. Rilpivirine is a CYP3A substrate and dexamethasone is an inducer of CYP3A4.
Doravirine: (Moderate) Monitor for a decrease in doravirine efficacy during concurrent use of doravirine and dexamethasone. If long term coadministration is required, consider using an alternative corticosteroid, such as prednisone or prednisolone. Concomitant use may decrease doravirine exposure leading to potential loss of virologic control. Doravirine is a CYP3A substrate and dexamethasone is a weak CYP3A inducer.
Doravirine; Lamivudine; Tenofovir disoproxil fumarate: (Moderate) Monitor for a decrease in doravirine efficacy during concurrent use of doravirine and dexamethasone. If long term coadministration is required, consider using an alternative corticosteroid, such as prednisone or prednisolone. Concomitant use may decrease doravirine exposure leading to potential loss of virologic control. Doravirine is a CYP3A substrate and dexamethasone is a weak CYP3A inducer.
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.
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.
Efavirenz: (Moderate) Monitor for a decrease in efavirenz efficacy during concurrent use of efavirenz and dexamethasone. If long term coadministration is required, consider using an alternative corticosteroid, such as prednisone or prednisolone. Concomitant use may decrease efavirenz exposure leading to potential loss of virologic control. Efavirenz is a CYP3A substrate and dexamethasone is a weak CYP3A inducer.
Efavirenz; Emtricitabine; Tenofovir Disoproxil Fumarate: (Moderate) Monitor for a decrease in efavirenz efficacy during concurrent use of efavirenz and dexamethasone. If long term coadministration is required, consider using an alternative corticosteroid, such as prednisone or prednisolone. Concomitant use may decrease efavirenz exposure leading to potential loss of virologic control. Efavirenz is a CYP3A substrate and dexamethasone is a weak CYP3A inducer.
Efavirenz; Lamivudine; Tenofovir Disoproxil Fumarate: (Moderate) Monitor for a decrease in efavirenz efficacy during concurrent use of efavirenz and dexamethasone. If long term coadministration is required, consider using an alternative corticosteroid, such as prednisone or prednisolone. Concomitant use may decrease efavirenz exposure leading to potential loss of virologic control. Efavirenz is a CYP3A substrate and dexamethasone is a weak CYP3A inducer.
Elvitegravir; Cobicistat; Emtricitabine; Tenofovir Alafenamide: (Major) Avoid concurrent use of dexamethasone with cobicistat-containing regimens due to the risk of decreased 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. Consider an alternative corticosteroid (i.e., beclomethasone, prednisone, prednisolone) for long-term use. If concomitant use is necessary, monitor virologic response and for corticosteroid-related adverse effects. Dexamethasone is a CYP3A4 substrate and weak CYP3A inducer; cobicistat is a CYP3A4 substrate and strong CYP3A inhibitor. 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. (Moderate) Monitor for a decrease in elvitegravir efficacy during concurrent use of elvitegravir and dexamethasone. If long term coadministration is required, consider using an alternative corticosteroid, such as prednisone or prednisolone. Concomitant use may decrease elvitegravir exposure leading to potential loss of virologic control. Elvitegravir is a CYP3A substrate and dexamethasone is a weak CYP3A inducer.
Elvitegravir; Cobicistat; Emtricitabine; Tenofovir Disoproxil Fumarate: (Major) Avoid concurrent use of dexamethasone with cobicistat-containing regimens due to the risk of decreased 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. Consider an alternative corticosteroid (i.e., beclomethasone, prednisone, prednisolone) for long-term use. If concomitant use is necessary, monitor virologic response and for corticosteroid-related adverse effects. Dexamethasone is a CYP3A4 substrate and weak CYP3A inducer; cobicistat is a CYP3A4 substrate and strong CYP3A inhibitor. 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. (Moderate) Monitor for a decrease in elvitegravir efficacy during concurrent use of elvitegravir and dexamethasone. If long term coadministration is required, consider using an alternative corticosteroid, such as prednisone or prednisolone. Concomitant use may decrease elvitegravir exposure leading to potential loss of virologic control. Elvitegravir is a CYP3A substrate and dexamethasone is a weak CYP3A inducer.
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. Concomitant use may decrease the exposure and efficacy of rilpivirine leading to potential development of viral resistance. Rilpivirine is a CYP3A substrate and dexamethasone is an inducer of CYP3A4.
Emtricitabine; Rilpivirine; Tenofovir Disoproxil Fumarate: (Contraindicated) Concurrent use of dexamethasone (more than 1 dose) and rilpivirine is contraindicated. Concomitant use may decrease the exposure and efficacy of rilpivirine leading to potential development of viral resistance. Rilpivirine is a CYP3A substrate and dexamethasone is an inducer of CYP3A4.
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.
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 CYP3A substrate and enzalutamide is a strong CYP3A 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.
Erlotinib: (Major) Avoid the coadministration of erlotinib with dexamethasone if possible due to the risk of decreased erlotinib efficacy. If concomitant use is unavoidable, increase the dose of erlotinib by 50 mg increments at 2-week intervals as tolerated, to a maximum of 450 mg. Also, monitor for symptoms of gastrointestinal (GI) perforation (e.g., severe abdominal pain, fever, nausea, and vomiting); permanently discontinue erlotinib in patients who develop GI perforation. Erlotinib is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Coadministration may decrease plasma concentrations of erlotinib. The pooled incidence of GI perforation clinical trials of erlotinib ranged from 0.1% to 0.4%, including fatal cases; patients receiving concomitant dexamethasone may be at increased risk.
Ertugliflozin: (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.
Ertugliflozin; 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.
Ertugliflozin; Sitagliptin: (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.
Erythromycin: (Moderate) Monitor for steroid-related adverse reactions if concomitant use of erythromycin with dexamethasone is necessary. Concomitant use may increase dexamethasone exposure. Dexamethasone is a CYP3A substrate and erythromycin is a moderate CYP3A inhibitor.
Estramustine: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
Estrogens: (Moderate) Monitor for corticosteroid-related adverse events if corticosteroids are used with estrogens. Concurrent use may increase the exposure of corticosteroids. Estrogens may decrease the hepatic clearance of corticosteroids thereby increasing their effect.
Etravirine: (Moderate) Monitor for a decrease in etravirine efficacy during concurrent use of etravirine and dexamethasone. If long term coadministration is required, consider using an alternative corticosteroid, such as prednisone or prednisolone. Concomitant use may decrease etravirine exposure leading to potential loss of virologic control. Etravirine is a CYP3A substrate and dexamethasone is a weak CYP3A inducer.
Exenatide: (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.
Fentanyl: (Moderate) Consider an increased dose of fentanyl and monitor for evidence of opioid withdrawal if concurrent use of dexamethasone is necessary. If dexamethasone is discontinued, consider reducing the fentanyl dosage and monitor for evidence of respiratory depression. Coadministration of a CYP3A4 inducer like dexamethasone with fentanyl, a CYP3A4 substrate, may decrease exposure to fentanyl resulting in decreased efficacy or onset of withdrawal symptoms in a patient who has developed physical dependence to fentanyl. Fentanyl plasma concentrations will increase once the inducer is stopped, which may increase or prolong the therapeutic and adverse effects, including serious respiratory depression.
Fosamprenavir: (Moderate) Monitor for a decrease in fosamprenavir efficacy during concurrent use of fosamprenavir and dexamethasone. If long term coadministration is required, consider using an alternative corticosteroid, such as prednisone or prednisolone. Concomitant use may decrease fosamprenavir exposure leading to potential loss of virologic control. Fosamprenavir is a CYP3A4 substrate and dexamethasone is a weak CYP3A inducer.
Fosinopril; 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.
Gallium Ga 68 Dotatate: (Moderate) Repeated administration of high corticosteroid doses prior to gallium Ga 68 dotatate may result in false negative imaging. High-dose corticosteroid therapy is generally defined as at least 20 mg/day of prednisone or equivalent (or 2 mg/kg/day for patients weighing less than 10 kg) for at least 14 consecutive days. Corticosteroids can down-regulate somatostatin subtype 2 receptors: thereby, interfering with binding of gallium Ga 68 dotatate to malignant cells that overexpress these receptors.
Glimepiride: (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.
Glipizide: (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.
Glipizide; 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 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.
Glyburide: (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.
Glyburide; 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 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.
Glycerol Phenylbutyrate: (Moderate) Corticosteroids may induce elevated blood ammonia concentrations. Corticosteroids should be used with caution in patients receiving glycerol phenylbutyrate. Monitor ammonia concentrations closely.
Guaifenesin; Hydrocodone: (Moderate) Monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal if coadministration with dexamethasone is necessary; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs of respiratory depression and sedation. Hydrocodone is a CYP3A substrate and dexamethasone is a weak CYP3A inducer. Concomitant use with CYP3A inducers can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
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.
Haloperidol: (Moderate) Caution is advisable during concurrent use of haloperidol and corticosteroids as electrolyte imbalance caused by corticosteroids may increase the risk of QT prolongation with haloperidol.
Hemin: (Moderate) Hemin works by inhibiting aminolevulinic acid synthetase. Corticosteroids increase the activity of this enzyme should not be used with hemin.
Homatropine; Hydrocodone: (Moderate) Monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal if coadministration with dexamethasone is necessary; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs of respiratory depression and sedation. Hydrocodone is a CYP3A substrate and dexamethasone is a weak CYP3A inducer. Concomitant use with CYP3A inducers can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
Hydantoins: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with phenytoin/fosphenytoin is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A substrate and phenytoin is a strong CYP3A inducer.
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.
Hydrochlorothiazide, HCTZ; Methyldopa: (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.
Hydrochlorothiazide, HCTZ; Moexipril: (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.
Hydrocodone: (Moderate) Monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal if coadministration with dexamethasone is necessary; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs of respiratory depression and sedation. Hydrocodone is a CYP3A substrate and dexamethasone is a weak CYP3A inducer. Concomitant use with CYP3A inducers can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
Hydrocodone; Ibuprofen: (Moderate) Monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal if coadministration with dexamethasone is necessary; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs of respiratory depression and sedation. Hydrocodone is a CYP3A substrate and dexamethasone is a weak CYP3A inducer. Concomitant use with CYP3A inducers can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
Hydrocodone; Pseudoephedrine: (Moderate) Monitor for reduced efficacy of hydrocodone and signs of opioid withdrawal if coadministration with dexamethasone is necessary; consider increasing the dose of hydrocodone as needed. If dexamethasone is discontinued, consider a dose reduction of hydrocodone and frequently monitor for signs of respiratory depression and sedation. Hydrocodone is a CYP3A substrate and dexamethasone is a weak CYP3A inducer. Concomitant use with CYP3A inducers can decrease hydrocodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
Hydroxyurea: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
Hylan G-F 20: (Major) The safety and efficacy of hylan G-F 20 given concomitantly with other intra-articular injectables have not been established. Other intra-articular injections may include intra-articular steroids (betamethasone, dexamethasone, hydrocortisone, prednisolone, methylprednisolone, and triamcinolone).
Hyoscyamine; Methenamine; Methylene Blue; Phenyl Salicylate; Sodium Biphosphate: (Moderate) 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) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia.
Ibritumomab Tiuxetan: (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia. (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
Ibuprofen; 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 CYP3A substrate and dexamethasone is a weak CYP3A inducer. Concomitant use with CYP3A inducers can decrease oxycodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
Idelalisib: (Moderate) Monitor for steroid-related adverse reactions if coadministration of idelalisib 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. Dexamethasone is primarily metabolized by CYP3A and idelalisib is a strong CYP3A inhibitor. 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.
Incretin Mimetics: (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.
Indapamide: (Moderate) Additive hypokalemia may occur when indapamide is coadministered with other drugs with a significant risk of hypokalemia such as systemic corticosteroids. Coadminister with caution and careful monitoring.
Indinavir: (Moderate) Monitor for steroid-related adverse reactions and a decrease in indinavir efficacy if concomitant use of dexamethasone and indinavir is necessary. If long term coadministration is required, consider using an alternative corticosteroid, such as beclomethasone or prednisolone. Concomitant use may increase dexamethasone concentrations and decrease indinavir exposure. Dexamethasone is a CYP3A substrate and CYP3A inducer; indinavir is a CYP3A substrate and strong CYP3A inhibitor. 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.
Inebilizumab: (Moderate) Concomitant usage of inebilizumab with immunosuppressant drugs, including systemic corticosteroids, may increase the risk of infection. Consider the risk of additive immune system effects when coadministering therapies that cause immunosuppression with inebilizumab.
Infliximab: (Moderate) Many serious infections during infliximab therapy have occurred in patients who received concurrent immunosuppressives that, in addition to their underlying Crohn's disease or rheumatoid arthritis, predisposed patients to infections. The impact of concurrent infliximab therapy and immunosuppression on the development of malignancies is unknown. In clinical trials, the use of concomitant immunosuppressant agents appeared to reduce the frequency of antibodies to infliximab and appeared to reduce infusion reactions.
Insulin Degludec; Liraglutide: (Moderate) 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.
Insulin Glargine; Lixisenatide: (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.
Insulins: (Moderate) Monitor blood glucose during concomitant corticosteroid and insulin use; an insulin 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.
Interferon Alfa-2b: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
Iohexol: (Major) Serious adverse events, including death, have been observed during intrathecal administration of both corticosteroids (i.e., dexamethasone) and radiopaque contrast agents (i.e., iohexol); therefore, concurrent use of these medications via the intrathecal route is contraindicated. Cases of cortical blindness, stroke, spinal cord infarction, paralysis, seizures, nerve injury, brain edema, and death have been temporally associated (i.e., within minutes to 48 hours after injection) with epidural administration of injectable corticosteroids. In addition, patients inadvertently administered iohexol formulations not indicated for intrathecal use have experienced seizures, convulsions, cerebral hemorrhages, brain edema, and death. Administering these medications together via the intrathecal route may increase the risk for serious adverse events.
Iopamidol: (Contraindicated) Because both intrathecal corticosteroids (i.e., dexamethasone) and intrathecal radiopaque contrast agents (i.e., iopamidoll) can increase the risk of seizures, the intrathecal administration of corticosteroids with intrathecal radiopaque contrast agents is contraindicated.
Irbesartan; 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.
Isoniazid, INH; Pyrazinamide, PZA; Rifampin: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with rifampin is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A4 substrate and rifampin is a strong CYP3A4 inducer.
Isoniazid, INH; Rifampin: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with rifampin is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A4 substrate and rifampin is a strong CYP3A4 inducer.
Isoproterenol: (Moderate) The risk of cardiac toxicity with isoproterenol in asthma patients appears to be increased with the coadministration of corticosteroids. Intravenous infusions of isoproterenol in refractory asthmatic children at rates of 0.05 to 2.7 mcg/kg/min have caused clinical deterioration, myocardial infarction (necrosis), congestive heart failure and death.
Isotretinoin: (Minor) Both isotretinoin and corticosteroids can cause osteoporosis during chronic use. Patients receiving systemic corticosteroids should receive isotretinoin therapy with caution.
Isradipine: (Minor) Monitor for decreased efficacy of isradipine if coadministration with dexamethasone is necessary. Concomitant use may decrease isradipine exposure. Isradipine is a CYP3A substrate and dexamethasone is a weak CYP3A inducer.
Itraconazole: (Moderate) Monitor for steroid-related adverse reactions if coadministration of itraconazole 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. Dexamethasone is primarily metabolized by CYP3A and itraconazole is a strong CYP3A inhibitor. 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.
Ketoconazole: (Moderate) Monitor for steroid-related adverse reactions if coadministration of ketoconazole 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. Dexamethasone is primarily metabolized by CYP3A and ketoconazole is a strong CYP3A inhibitor. Ketoconazole has been reported to decrease the metabolism of certain corticosteroids by up to 60%, leading to increased risk of corticosteroid side effects.
Lansoprazole; Amoxicillin; Clarithromycin: (Moderate) Monitor for steroid-related adverse reactions if coadministration of clarithromycin 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. Dexamethasone is primarily metabolized by CYP3A and clarithromycin is a strong CYP3A inhibitor. 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.
Lapatinib: (Major) Avoid coadministration of lapatinib with dexamethasone due to decreased plasma concentrations of lapatinib. If concomitant use is unavoidable, gradually titrate the dose of lapatinib from 1,250 mg per day to 4,500 mg per day in patients receiving concomitant capecitabine (HER2-positive metastatic breast cancer), and from 1,500 mg per day to 5,500 mg per day in patients receiving concomitant aromatase inhibitor therapy (HR-positive, HER2-positive breast cancer) based on tolerability. If dexamethasone is discontinued, reduce lapatinib to the indicated dose. Lapatinib is a CYP3A4 substrate and dexamethasone is a CYP3A4 inducer.
L-Asparaginase Escherichia coli: (Moderate) Concomitant use of L-asparaginase with corticosteroids can result in additive hyperglycemia. L-Asparaginase transiently inhibits insulin production contributing to hyperglycemia seen during concurrent corticosteroid therapy. Insulin therapy may be required in some cases. Administration of L-asparaginase after rather than before corticosteroids reportedly has produced fewer hypersensitivity reactions.
Lenacapavir: (Moderate) Monitor for steroid-related adverse reactions if coadministration of lenacapavir with dexamethasone is necessary, due to increased dexamethasone exposure; Cushing's syndrome and adrenal suppression could potentially occur with long-term use. If concomitant use is necessary, initiate dexamethasone at the lowest starting dose and titrate carefully. Alternatively, consider the use of corticosteroids such as beclomethasone and prednisolone, whose concentrations are less affected by CYP3A inhibitors, especially for long-term use. Dexamethasone is primarily metabolized by CYP3A and lenacapavir is a CYP3A inhibitor.
Levoketoconazole: (Moderate) Monitor for steroid-related adverse reactions if coadministration of ketoconazole 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. Dexamethasone is primarily metabolized by CYP3A and ketoconazole is a strong CYP3A inhibitor. Ketoconazole has been reported to decrease the metabolism of certain corticosteroids by up to 60%, leading to increased risk of corticosteroid side effects.
Lidocaine; 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.
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.
Liraglutide: (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.
Lisinopril; 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.
Live Vaccines: (Contraindicated) Live vaccines should generally not be administered to an immunosuppressed patient. Live vaccines may induce the illness they are intended to prevent and are generally contraindicated for use during immunosuppressive treatment. The immune response of the immunocompromised patient to vaccines may be decreased, even despite alternate vaccination schedules or more frequent booster doses. If immunization is necessary, choose an alternative to live vaccination, or, consider a delay or change in the immunization schedule. Practitioners should refer to the most recent CDC guidelines regarding vaccination of patients who are receiving drugs that adversely affect the immune system. The immunosuppressive effects of steroid treatment differ, but many clinicians consider a dose equivalent to either 2 mg/kg/day or 20 mg/day of prednisone as sufficiently immunosuppressive to raise concern about the safety of immunization with live vaccines. Patients on corticosteroid treatment for 2 weeks or more may be vaccinated after steroid therapy has been discontinued for at least 3 months in accordance with general recommendations for the use of live vaccines. The CDC has stated that discontinuation of steroids for 1 month prior to live vaccine administration may be sufficient. Live vaccines should not be given to individuals who are considered to be immunocompromised until more information is available.
Lixisenatide: (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.
Lomustine, CCNU: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
Lonafarnib: (Moderate) Monitor for steroid-related adverse reactions if coadministration of lonafarnib 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. Dexamethasone is primarily metabolized by CYP3A and lonafarnib is a strong CYP3A inhibitor. 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.
Lonapegsomatropin: (Moderate) Corticosteroids can retard bone growth and therefore, can inhibit the growth-promoting effects of somatropin. If corticosteroid therapy is required, the corticosteroid dose should be carefully adjusted.
Loop diuretics: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and loop diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and loop diuretics cause increased renal potassium loss.
Lopinavir; Ritonavir: (Moderate) Monitor for a decrease in lopinavir efficacy during concurrent use of lopinavir and dexamethasone. If long term coadministration is required, consider using an alternative corticosteroid, such as prednisone or prednisolone. Concomitant use may decrease lopinavir exposure leading to potential loss of virologic control. Lopinavir is a CYP3A4 substrate and dexamethasone is a weak CYP3A inducer. (Moderate) Monitor for steroid-related adverse reactions and a decrease in ritonavir efficacy if concomitant use of dexamethasone and ritonavir is necessary. If long term coadministration is required, consider using an alternative corticosteroid, such as prednisone or prednisolone. Concomitant use may increase dexamethasone concentrations and decrease ritonavir exposure. Dexamethasone is a CYP3A substrate and CYP3A inducer; ritonavir is a CYP3A substrate and strong CYP3A inhibitor. 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.
Losartan; 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.
Lumacaftor; Ivacaftor: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with combination lumacaftor; ivacaftor is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A substrate and combination lumacaftor; ivacaftor is a strong CYP3A inducer.
Lumateperone: (Major) Avoid coadministration of lumateperone and dexamethasone as concurrent use may decrease lumateperone exposure which may reduce efficacy. Lumateperone is a CYP3A substrate; dexamethasone is a weak CYP3A inducer. Although data are unavailable for weak CYP3A inducers, coadministration with a strong CYP3A inducer significantly decreased lumateperone exposure.
Lutetium Lu 177 dotatate: (Major) Avoid repeated administration of high doses of glucocorticoids during treatment with lutetium Lu 177 dotatate due to the risk of decreased efficacy of lutetium Lu 177 dotatate. Lutetium Lu 177 dotatate binds to somatostatin receptors, with the highest affinity for subtype 2 somatostatin receptors (SSTR2); glucocorticoids can induce down-regulation of SSTR2.
Macimorelin: (Major) Avoid use of macimorelin with drugs that directly affect pituitary growth hormone secretion, such as corticosteroids. Healthcare providers are advised to discontinue corticosteroid therapy and observe a sufficient washout period before administering macimorelin. Use of these medications together may impact the accuracy of the macimorelin growth hormone test.
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.
Mannitol: (Moderate) Corticosteroids may accentuate the electrolyte loss associated with diuretic therapy resulting in hypokalemia. Also, corticotropin may cause calcium loss and sodium and fluid retention. Mannitol itself can cause hypernatremia. Close monitoring of electrolytes should occur in patients receiving these drugs concomitantly.
Mecasermin, Recombinant, rh-IGF-1: (Moderate) Additional monitoring may be required when coadministering systemic or inhaled corticosteroids and mecasermin, recombinant, rh-IGF-1. In animal studies, corticosteroids impair the growth-stimulating effects of growth hormone (GH) through interference with the physiological stimulation of epiphyseal chondrocyte proliferation exerted by GH and IGF-1. Dexamethasone administration on long bone tissue in vitro resulted in a decrease of local synthesis of IGF-1. Similar counteractive effects are expected in humans. If systemic or inhaled glucocorticoid therapy is required, the steroid dose should be carefully adjusted and growth rate monitored.
Mefloquine: (Moderate) Use mefloquine with caution if coadministration with dexamethasone is necessary as concurrent use may decrease mefloquine exposure and efficacy. Mefloquine is a CYP3A substrate and dexamethasone is a weak CYP3A inducer.
Meglitinides: (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.
Meperidine: (Moderate) Monitor for reduced efficacy of meperidine and signs of opioid withdrawal if coadministration with dexamethasone is necessary. Consider increasing the dose of meperidine as needed. If dexamethasone is discontinued, consider a dose reduction of meperidine and frequently monitor for signs of respiratory depression and sedation. Meperidine is a substrate of CYP3A; dexamethasone is a weak CYP3A inducer. Concomitant use can decrease meperidine exposure resulting in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
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.
Metformin; Repaglinide: (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 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.
Metformin; Rosiglitazone: (Moderate) Monitor blood glucose during concomitant corticosteroid and metformin use; a metformin dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Ri sk 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.
Metformin; Saxagliptin: (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.
Metformin; Sitagliptin: (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.
Methadone: (Moderate) Monitor for reduced efficacy of methadone and signs of opioid withdrawal if coadministration with dexamethasone is necessary. Consider increasing the dose of methadone as needed. If dexamethasone is discontinued, consider a dose reduction of methadone and frequently monitor for signs of respiratory depression and sedation. Methadone is a substrate of CYP3A, CYP2B6, CYP2C19, CYP2C9, and CYP2D6; dexamethasone is a weak CYP3A inducer. Concomitant use can decrease methadone exposure resulting in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
Methazolamide: (Moderate) Corticosteroids may increase the risk of hypokalemia if used concurrently with methazolamide. Hypokalemia may be especially severe with prolonged use of corticotropin, ACTH. Monitor serum potassium levels to determine the need for potassium supplementation and/or alteration in drug therapy. The chronic use of corticosteroids may augment calcium excretion with methazolamide leading to increased risk for hypocalcemia and/or osteoporosis.
Methenamine; Sodium Acid Phosphate: (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia.
Methenamine; Sodium Acid Phosphate; Methylene Blue; Hyoscyamine: (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia.
Methenamine; Sodium 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.
Methohexital: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with barbiturates is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A substrate and barbiturates are strong CYP3A inducers.
Methoxsalen: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
Methyclothiazide: (Moderate) 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.
Metolazone: (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.
Metoprolol; 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.
Metyrapone: (Contraindicated) Medications which affect pituitary or adrenocortical function, including all corticosteroid therapy, should be discontinued prior to and during testing with metyrapone. Patients taking inadvertent doses of corticosteroids on the test day may exhibit abnormally high basal plasma cortisol levels and a decreased response to the test. Although systemic absorption of ocular, inhaled and topical corticosteroids is minimal, temporary discontinuation of these products should be considered if possible to reduce the potential for interference with the test results.
Micafungin: (Moderate) Leukopenia, neutropenia, anemia, and thrombocytopenia have been associated with micafungin. Patients who are taking immunosuppressives such as the corticosteroids with micafungin concomitantly may have additive risks for infection or other side effects. In a pharmacokinetic trial, micafungin had no effect on the pharmacokinetics of prednisolone. Acute intravascular hemolysis and hemoglobinuria was seen in a healthy volunteer during infusion of micafungin (200 mg) and oral prednisolone (20 mg). This reaction was transient, and the subject did not develop significant anemia.
Mifepristone: (Major) Mifepristone for termination of pregnancy is contraindicated in patients on long-term corticosteroid therapy and mifepristone for Cushing's disease or other chronic conditions is contraindicated in patients who require concomitant treatment with systemic corticosteroids for life-saving purposes, such as serious medical conditions or illnesses (e.g., immunosuppression after organ transplantation). For other situations where corticosteroids are used for treating non-life threatening conditions, mifepristone may lead to reduced corticosteroid efficacy and exacerbation or deterioration of such conditions. This is because mifepristone exhibits antiglucocorticoid activity that may antagonize corticosteroid therapy and the stabilization of the underlying corticosteroid-treated illness. Mifepristone may also cause adrenal insufficiency, so patients receiving corticosteroids for non life-threatening illness require close monitoring. Because serum cortisol levels remain elevated and may even increase during treatment with mifepristone, serum cortisol levels do not provide an accurate assessment of hypoadrenalism. Patients should be closely monitored for signs and symptoms of adrenal insufficiency, If adrenal insufficiency occurs, stop mifepristone treatment and administer systemic glucocorticoids without delay; high doses may be needed to treat these events. Factors considered in deciding on the duration of glucocorticoid treatment should include the long half-life of mifepristone (85 hours).
Mitotane: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with mitotane is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A substrate and mitotane is a strong CYP3A inducer.
Mitoxantrone: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
Mivacurium: (Moderate) 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.
Nanoparticle Albumin-Bound Paclitaxel: (Moderate) Monitor for decreased efficacy of nab-paclitaxel if coadministration with dexamethasone is necessary due to the risk of decreased plasma concentrations of paclitaxel. Nab-paclitaxel is a CYP3A substrate and dexamethasone is a weak CYP3A inducer.
Nanoparticle Albumin-Bound Sirolimus: (Moderate) Monitor for reduced sirolimus efficacy if sirolimus is coadministered with dexamethasone. Concomitant use may decrease sirolimus exposure. Sirolimus is a CYP3A substrate and dexamethasone is a weak CYP3A inducer.
Natalizumab: (Major) Ordinarily, patients receiving chronic immunosuppressant therapy should not be treated with natalizumab. Treatment recommendations for combined corticosteroid therapy are dependent on the underlying indication for natalizumab therapy. Corticosteroids should be tapered in those patients with Crohn's disease who are on chronic corticosteroids when they start natalizumab therapy, as soon as a therapeutic benefit has occurred. If the patient cannot discontinue systemic corticosteroids within 6 months, discontinue natalizumab. The concomitant use of natalizumab and corticosteroids may further increase the risk of serious infections, including progressive multifocal leukoencephalopathy, over the risk observed with use of natalizumab alone. In multiple sclerosis (MS) clinical trials, an increase in infections was seen in patients concurrently receiving short courses of corticosteroids. However, the increase in infections in natalizumab-treated patients who received steroids was similar to the increase in placebo-treated patients who received steroids. Short courses of steroid use during natalizumab, such as when they are needed for MS relapse treatment, appear to be acceptable for use concurrently.
Nateglinide: (Moderate) 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.
Nefazodone: (Moderate) Monitor for steroid-related adverse reactions if coadministration of nefazodone 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. Dexamethasone is primarily metabolized by CYP3A and nefazodone is a strong CYP3A inhibitor. 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.
Nelarabine: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
Nelfinavir: (Moderate) Monitor for steroid-related adverse reactions and a decrease in nelfinavir efficacy if concomitant use of dexamethasone and nelfinavir is necessary. If long term coadministration is required, consider using an alternative corticosteroid, such as prednisone or prednisolone. Concomitant use may increase dexamethasone concentrations and decrease nelfinavir exposure. Dexamethasone is a CYP3A substrate and CYP3A inducer; nelfinavir is a CYP3A substrate and strong CYP3A inhibitor. 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.
Neostigmine: (Moderate) Concomitant use of anticholinesterase agents, such as neostigmine, and systemic corticosteroids may produce severe weakness in patients with myasthenia gravis. If possible, anticholinesterase agents should be withdrawn at least 24 hours before initiating systemic corticosteroid therapy.
Neostigmine; Glycopyrrolate: (Moderate) Concomitant use of anticholinesterase agents, such as neostigmine, and systemic corticosteroids may produce severe weakness in patients with myasthenia gravis. If possible, anticholinesterase agents should be withdrawn at least 24 hours before initiating systemic corticosteroid therapy.
Netupitant, Fosnetupitant; Palonosetron: (Minor) When dexamethasone is used with netupitant; palonosetron, follow the approved dexamethasone dosage reduction: 12 mg on day 1 followed by 8 mg per day on days 2 to 4, if needed based on the emetogenic potential of the chemotherapy regimen. Dexamethasone is a CYP3A substrate and netupitant is a moderate CYP3A inhibitor. Concomitant use of dexamethasone and netupitant increases the systemic exposure of dexamethasone by more than 2-fold.
Neuromuscular blockers: (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.
Nevirapine: (Moderate) Monitor for a decrease in nevirapine efficacy during concurrent use of nevirapine and dexamethasone. If long term coadministration is required, consider using an alternative corticosteroid, such as prednisone or prednisolone. Concomitant use may decrease nevirapine exposure leading to potential loss of virologic control. Nevirapine is a CYP3A substrate and dexamethasone is a weak CYP3A inducer.
Nimodipine: (Moderate) Monitor for decreased efficacy of nimodipine if coadministration with dexamethasone is necessary as concomitant use may decrease plasma concentrations of nimodipine. Nimodipine is a CYP3A substrate and dexamethasone is a weak CYP3A inducer.
Nirmatrelvir; Ritonavir: (Moderate) Monitor for a diminished response to nirmatrelvir if concomitant use of dexamethasone is necessary. Concomitant use of nirmatrelvir and dexamethasone may reduce the therapeutic effect of nirmatrelvir. Nirmatrelvir is a CYP3A substrate and dexamethasone is a CYP3A inducer. (Moderate) Monitor for steroid-related adverse reactions and a decrease in ritonavir efficacy if concomitant use of dexamethasone and ritonavir is necessary. If long term coadministration is required, consider using an alternative corticosteroid, such as prednisone or prednisolone. Concomitant use may increase dexamethasone concentrations and decrease ritonavir exposure. Dexamethasone is a CYP3A substrate and CYP3A inducer; ritonavir is a CYP3A substrate and strong CYP3A inhibitor. 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.
Nisoldipine: (Major) Avoid coadministration of nisoldipine with dexamethasone as concurrent use may decrease nisoldipine exposure and efficacy. Alternative antihypertensive therapy should be considered. Nisoldipine is a CYP3A substrate and dexamethasone is a CYP3A inducer. Coadministration with a strong CYP3A inducer lowered nisoldipine plasma concentrations to undetectable levels.
Nonsteroidal antiinflammatory drugs: (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and nonsteroidal antiinflammatory drug (NSAID) use. Concomitant use increases the risk of GI bleeding. The Beers criteria recommends that this drug combination be avoided in older adults; if coadministration cannot be avoided, provide gastrointestinal protection.
Ocrelizumab: (Moderate) Ocrelizumab has not been studied in combination with other immunosuppressive or immune modulating therapies used for the treatment of multiple sclerosis, including immunosuppressant doses of corticosteroids. Concomitant use of ocrelizumab with any of these therapies may increase the risk of immunosuppression. Monitor patients carefully for signs and symptoms of infection.
Ofatumumab: (Moderate) Concomitant use of ofatumumab with corticosteroids may increase the risk of immunosuppression. Monitor patients carefully for signs and symptoms of infection. Ofatumumab has not been studied in combination with other immunosuppressive or immune modulating therapies used for the treatment of multiple sclerosis, including immunosuppressant doses of corticosteroids.
Olmesartan; Amlodipine; 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.
Olmesartan; 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.
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 CYP3A substrate and dexamethasone is a weak CYP3A inducer. Concomitant use with CYP3A inducers can decrease oxycodone levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
Oxymetholone: (Moderate) Concomitant use of oxymetholone with corticosteroids or corticotropin, ACTH may cause increased edema. Manage edema with diuretic and/or digitalis therapy.
Paclitaxel: (Moderate) Monitor for decreased efficacy of paclitaxel if coadministration with dexamethasone is necessary due to the risk of decreased plasma concentrations of paclitaxel. Paclitaxel is a CYP3A substrate and dexamethasone is a weak CYP3A inducer.
Pancuronium: (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.
Pegaspargase: (Moderate) Monitor for an increase in glucocorticoid-related adverse reactions such as hyperglycemia and osteonecrosis during concomitant use of pegaspargase and glucocorticoids.
Penicillamine: (Major) Agents such as immunosuppressives have adverse reactions similar to those of penicillamine. Concomitant use of penicillamine with these agents is contraindicated because of the increased risk of developing severe hematologic and renal toxicity.
Pentobarbital: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with barbiturates is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A substrate and barbiturates are strong CYP3A inducers.
Phenobarbital: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with barbiturates is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A substrate and barbiturates are strong CYP3A inducers.
Phenobarbital; Hyoscyamine; Atropine; Scopolamine: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with barbiturates is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A substrate and barbiturates are strong CYP3A inducers.
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.
Photosensitizing agents (topical): (Minor) Corticosteroids administered prior to or concomitantly with photosensitizing agents used in photodynamic therapy may decrease the efficacy of the treatment.
Physostigmine: (Moderate) Concomitant use of anticholinesterase agents, such as physostigmine, and systemic corticosteroids may produce severe weakness in patients with myasthenia gravis. If possible, withdraw anticholinesterase inhibitors at least 24 hours before initiating corticosteroid therapy.
Pimozide: (Moderate) According to the manufacturer of pimozide, the drug should not be coadministered with drugs known to cause electrolyte imbalances, such as high-dose, systemic corticosteroid therapy. Pimozide is associated with a well-established risk of QT prolongation and torsade de pointes (TdP), and electrolyte imbalances (e.g., hypokalemia, hypocalcemia, hypomagnesemia) may increase the risk of life-threatening arrhythmias. Pimozide is contraindicated in patients with known hypokalemia or hypomagnesemia. Topical corticosteroids are less likely to interact.
Pioglitazone; Glimepiride: (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.
Pioglitazone; 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.
Ponesimod: (Moderate) Monitor for signs and symptoms of infection. Additive immune suppression may result from concomitant use of ponesimod and high-dose corticosteroid therapy which may extend the duration or severity of immune suppression. High-dose corticosteroid therapy is generally defined as a dose of at least 20 mg/day of prednisone or equivalent (or 2 mg/kg/day for patients weighing less than 10 kg) for at least 14 consecutive days.
Posaconazole: (Moderate) Monitor for steroid-related adverse reactions if coadministration of posaconazole 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. Dexamethasone is primarily metabolized by CYP3A and posaconazole is a strong CYP3A inhibitor. 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.
Potassium Phosphate; Sodium Phosphate: (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia.
Potassium-sparing diuretics: (Minor) The manufacturer of spironolactone lists corticosteroids as a potential drug that interacts with spironolactone. Intensified electrolyte depletion, particularly hypokalemia, may occur. However, potassium-sparing diuretics such as spironolactone do not induce hypokalemia. In fact, hypokalemia is one of the indications for potassium-sparing diuretic therapy. Therefore, drugs that induce potassium loss, such as corticosteroids, could counter the hyperkalemic effects of potassium-sparing diuretics.
Pramlintide: (Moderate) 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.
Prasterone, Dehydroepiandrosterone, DHEA (Dietary Supplements): (Moderate) Corticosteroids blunt the adrenal secretion of endogenous DHEA and DHEAS, resulting in reduced DHEA and DHEAS serum concentrations.
Prasterone, Dehydroepiandrosterone, DHEA (FDA-approved): (Moderate) Corticosteroids blunt the adrenal secretion of endogenous DHEA and DHEAS, resulting in reduced DHEA and DHEAS serum concentrations.
Praziquantel: (Moderate) Monitor for reduced response to praziquantel if coadministered with dexamethasone. Concomitant use may produce therapeutically ineffective concentrations of praziquantel. In vitro and drug interactions studies suggest that the CYP3A isoenzyme is the major enzyme involved in praziquantel metabolism; dexamethasone is a weak CYP3A inducer.
Prilocaine; 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.
Primidone: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with barbiturates is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A substrate and barbiturates are strong CYP3A inducers.
Promethazine; 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.
Propranolol: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Propranolol; Hydrochlorothiazide, HCTZ: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response. (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.
Purine analogs: (Minor) Concurrent use of purine analogs with other agents which cause bone marrow or immune suppression such as other antineoplastic agents or immunosuppressives may result in additive effects.
Pyridostigmine: (Moderate) Concomitant use of anticholinesterase agents, such as pyridostigmine, and corticosteroids may produce severe weakness in patients with myasthenia gravis. If possible, anticholinesterase agents should be withdrawn at least 24 hours before initiating corticosteroid therapy.
Quinapril; 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.
Quinolones: (Moderate) Quinolones have been associated with an increased risk of tendon rupture requiring surgical repair or resulting in prolonged disability; this risk is further increased in those receiving concomitant corticosteroids. Discontinue quinolone therapy at the first sign of tendon inflammation or tendon pain, as these are symptoms that may precede rupture of the tendon.
Repaglinide: (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.
Ribociclib: (Moderate) Monitor for steroid-related adverse reactions if coadministration of ribociclib 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. Dexamethasone is primarily metabolized by CYP3A and ribociclib is a strong CYP3A inhibitor. 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.
Ribociclib; Letrozole: (Moderate) Monitor for steroid-related adverse reactions if coadministration of ribociclib 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. Dexamethasone is primarily metabolized by CYP3A and ribociclib is a strong CYP3A inhibitor. 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.
Rifampin: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with rifampin is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A4 substrate and rifampin is a strong CYP3A4 inducer.
Rifapentine: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with rifapentine is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A4 substrate and rifapentine is a strong CYP3A4 inducer.
Rilpivirine: (Contraindicated) Concurrent use of dexamethasone (more than 1 dose) and rilpivirine is contraindicated. Concomitant use may decrease the exposure and efficacy of rilpivirine leading to potential development of viral resistance. Rilpivirine is a CYP3A substrate and dexamethasone is an inducer of CYP3A4.
Ritonavir: (Moderate) Monitor for steroid-related adverse reactions and a decrease in ritonavir efficacy if concomitant use of dexamethasone and ritonavir is necessary. If long term coadministration is required, consider using an alternative corticosteroid, such as prednisone or prednisolone. Concomitant use may increase dexamethasone concentrations and decrease ritonavir exposure. Dexamethasone is a CYP3A substrate and CYP3A inducer; ritonavir is a CYP3A substrate and strong CYP3A inhibitor. 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.
Rituximab: (Moderate) Rituximab and corticosteroids are commonly used together; however, monitor the patient for immunosuppression and signs and symptoms of infection during combined chronic therapy.
Rituximab; Hyaluronidase: (Moderate) Rituximab and corticosteroids are commonly used together; however, monitor the patient for immunosuppression and signs and symptoms of infection during combined chronic therapy.
Rocuronium: (Moderate) 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.
Salicylates: (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.
Salsalate: (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.
Saquinavir: (Moderate) Monitor for steroid-related adverse reactions and a decrease in saquinavir efficacy if concomitant use of dexamethasone and saquinavir is necessary. If long term coadministration is required, consider using an alternative corticosteroid, such as prednisone or prednisolone. Concomitant use may increase dexamethasone concentrations and decrease saquinavir exposure. Dexamethasone is a CYP3A substrate and CYP3A inducer; saquinavir is a CYP3A substrate and strong CYP3A inhibitor. 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.
Sargramostim, GM-CSF: (Major) Avoid the concomitant use of sargramostim and systemic corticosteroid agents due to the risk of additive myeloproliferative effects. If coadministration of these drugs is required, frequently monitor patients for clinical and laboratory signs of excess myeloproliferative effects (e.g., leukocytosis). Sargramostim is a recombinant human granulocyte-macrophage colony-stimulating factor that works by promoting proliferation and differentiation of hematopoietic progenitor cells.
SARS-CoV-2 (COVID-19) vaccines: (Moderate) Patients receiving corticosteroids in greater than physiologic doses may have a diminished response to the SARS-CoV-2 virus vaccine. Counsel patients receiving corticosteroids about the possibility of a diminished vaccine response and to continue to follow precautions to avoid exposure to SARS-CoV-2 virus after receiving the vaccine.
Secobarbital: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with barbiturates is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A substrate and barbiturates are strong CYP3A inducers.
Semaglutide: (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.
SGLT2 Inhibitors: (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.
Sildenafil: (Moderate) Monitor for decreased efficacy of sildenafil if coadministration with dexamethasone is necessary as concurrent use may decrease sildenafil exposure. Sildenafil is a sensitive CYP3A substrate and dexamethasone is a weak CYP3A inducer. Population pharmacokinetic analysis indicates an approximately 3-fold increase in sildenafil clearance with concomitant use of weak CYP3A inducers.
Sipuleucel-T: (Major) Concomitant use of sipuleucel-T and immunosuppressives should be avoided. Concurrent administration of immunosuppressives with the leukapheresis procedure that occurs prior to sipuleucel-T infusion has not been studied. Sipuleucel-T stimulates the immune system and patients receiving immunosuppressives may have a diminished response to sipuleucel-T. When appropriate, consider discontinuing or reducing the dose of immunosuppressives prior to initiating therapy with sipuleucel-T.
Sirolimus: (Moderate) Monitor sirolimus concentrations and adjust sirolimus dosage as appropriate during concomitant use of dexamethasone. Concomitant use may decrease sirolimus exposure and efficacy. Sirolimus is a CYP3A substrate and dexamethasone is a weak CYP3A inducer.
Sodium Benzoate; Sodium Phenylacetate: (Moderate) Corticosteroids may cause protein breakdown, which could lead to elevated blood ammonia concentrations, especially in patients with an impaired ability to form urea. Corticosteroids should be used with caution in patients receiving treatment for hyperammonemia.
Sodium Phenylbutyrate: (Moderate) The concurrent use of corticosteroids with sodium phenylbutyrate may increase plasma ammonia levels (hyperammonemia) by causing the breakdown of body protein. Patients with urea cycle disorders being treated with sodium phenylbutyrate usually should not receive regular treatment with corticosteroids.
Sodium Phenylbutyrate; Taurursodiol: (Moderate) The concurrent use of corticosteroids with sodium phenylbutyrate may increase plasma ammonia levels (hyperammonemia) by causing the breakdown of body protein. Patients with urea cycle disorders being treated with sodium phenylbutyrate usually should not receive regular treatment with corticosteroids.
Sodium Phosphate Monobasic Monohydrate; Sodium Phosphate Dibasic Anhydrous: (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia.
Somapacitan: (Moderate) Patients treated with glucocorticoid replacement for hypoadrenalism may require an increase in their maintenance or stress steroid doses following initiation of somapacitan. Monitor for signs/symptoms of reduced serum cortisol concentrations. Growth hormone (GH) inhibits 11betaHSD-1. Consequently, patients with untreated GH deficiency have relative increases in 11betaHSD-1 and serum cortisol. The initiation of somapacitan may result in inhibition of 11betaHSD-1 and reduced serum cortisol concentrations.
Somatrogon: (Moderate) Monitor for a decrease in serum cortisol concentrations and corticosteroid efficacy during concurrent use of corticosteroids and somatrogon. Patients treated with glucocorticoid replacement for hypoadrenalism may require an increase in their maintenance or stress steroid doses following initiation of somatrogon. Additionally, supraphysiologic glucocorticoid treatment may attenuate the growth promoting effects of somatrogon. Carefully adjust glucocorticoid replacement dosing to avoid hypoadrenalism and an inhibitory effect on growth.
Somatropin, rh-GH: (Moderate) Corticosteroids can retard bone growth and therefore, can inhibit the growth-promoting effects of somatropin. If corticosteroid therapy is required, the corticosteroid dose should be carefully adjusted.
Sotagliflozin: (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.
Spironolactone; 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.
St. John's Wort, Hypericum perforatum: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with St. John's wort is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A substrate and St. John's wort is a strong CYP3A inducer.
Succinylcholine: (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.
Sufentanil: (Moderate) Because the dose of the sufentanil sublingual tablets cannot be titrated, consider an alternate opiate if dexamethasone must be administered. Monitor for reduced efficacy of sufentanil injection and signs of opioid withdrawal if coadministration with dexamethasone is necessary; consider increasing the dose of sufentanil injection as needed. If dexamethasone is discontinued, consider a dose reduction of sufentanil injection and frequently monitor for signs of respiratory depression and sedation. Sufentanil is a CYP3A substrate and dexamethasone is a weak CYP3A inducer. Concomitant use with CYP3A inducers can decrease sufentanil concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
Sulfonylureas: (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.
Tacrolimus: (Moderate) Monitor tacrolimus serum concentrations as appropriate if coadministration with dexamethasone is necessary; a tacrolimus dose adjustment may be needed. Concurrent administration may decrease tacrolimus concentrations. Tacrolimus is a sensitive CYP3A substrate with a narrow therapeutic range; dexamethasone is a weak CYP3A inducer.
Telmisartan; 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.
Temsirolimus: (Major) Avoid coadministration of temsirolimus with dexamethasone due to the risk of decreased plasma concentrations of the primary active metabolite of temsirolimus (sirolimus). If concomitant use is unavoidable, consider increasing the dose of temsirolimus from 25 mg per week up to 50 mg per week. If dexamethasone is discontinued, decrease the dose of temsirolimus to the dose used before initiation of dexamethasone. Temsirolimus is a CYP3A4 substrate and dexamethasone is a CYP3A4 inducer.
Testosterone: (Moderate) Monitor for fluid retention during concurrent corticosteroid and testosterone use. Concurrent use may result in increased fluid retention.
Thalidomide: (Moderate) Coadministration of dexamethasone with thalidomide should be employed cautiously, as toxic epidermal necrolysis has been reported with concomitant use.
Thiazide diuretics: (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.
Thiazolidinediones: (Moderate) Monitor blood glucose during concomitant corticosteroid and thiazolidinedione use; a thiazolidinedione 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.
Tipranavir: (Moderate) Monitor for steroid-related adverse reactions and a decrease in tipranavir efficacy if concomitant use of dexamethasone and tipranavir is necessary. If long term coadministration is required, consider using an alternative corticosteroid, such as prednisone or prednisolone. Concomitant use may increase dexamethasone concentrations and decrease tipranavir exposure. Dexamethasone is a CYP3A substrate and CYP3A inducer; tipranavir is a CYP3A substrate and strong CYP3A inhibitor. 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.
Tirzepatide: (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.
Tolazamide: (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.
Tolbutamide: (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.
Toremifene: (Moderate) Monitor for a decrease in toremifene efficacy during concurrent use of toremifene and dexamethasone. Concomitant use may decrease toremifene exposure. Toremifene is a CYP3A substrate and dexamethasone is a CYP3A inducer.
Tositumomab: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
Tramadol: (Moderate) Monitor for reduced efficacy of tramadol and signs of opioid withdrawal if coadministration with dexamethasone is necessary; consider increasing the dose of tramadol as needed. If dexamethasone is discontinued, consider a dose reduction of tramadol and frequently monitor for seizures, serotonin syndrome, and signs of respiratory depression and sedation. Tramadol is a CYP3A substrate and dexamethasone is a weak CYP3A inducer. Concomitant use with CYP3A inducers can decrease tramadol levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
Tramadol; Acetaminophen: (Moderate) Monitor for reduced efficacy of tramadol and signs of opioid withdrawal if coadministration with dexamethasone is necessary; consider increasing the dose of tramadol as needed. If dexamethasone is discontinued, consider a dose reduction of tramadol and frequently monitor for seizures, serotonin syndrome, and signs of respiratory depression and sedation. Tramadol is a CYP3A substrate and dexamethasone is a weak CYP3A inducer. Concomitant use with CYP3A inducers can decrease tramadol levels; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
Tretinoin, ATRA: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
Triamterene; 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.
Tuberculin Purified Protein Derivative, PPD: (Moderate) Immunosuppressives may decrease the immunological response to tuberculin purified protein derivative, PPD. This suppressed reactivity can persist for up to 6 weeks after treatment discontinuation. Consider deferring the skin test until completion of the immunosuppressive therapy.
Tucatinib: (Moderate) Monitor for steroid-related adverse reactions if coadministration of tucatinib 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 CYP3A4 inhibitors, especially for long-term use. Tucatinib 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.
Ubrogepant: (Major) Increase the initial and second dose of ubrogepant to 100 mg if coadministered with dexamethasone as concurrent use may decrease ubrogepant exposure and reduce its efficacy. Ubrogepant is a CYP3A4 substrate; dexamethasone is a moderate CYP3A4 inducer.
Ulipristal: (Major) Avoid coadministration of ulipristal with dexamethasone. Concomitant use may decrease the plasma concentration and effectiveness of ulipristal. Ulipristal is a substrate of CYP3A and dexamethasone is a CYP3A inducer.
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.
Vecuronium: (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.
Vigabatrin: (Major) Vigabatrin should not be used with corticosteroids, which are associated with serious ophthalmic effects (e.g., retinopathy or glaucoma) unless the benefit of treatment clearly outweighs the risks.
Vincristine Liposomal: (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia.
Vonoprazan; Amoxicillin; Clarithromycin: (Moderate) Monitor for steroid-related adverse reactions if coadministration of clarithromycin 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. Dexamethasone is primarily metabolized by CYP3A and clarithromycin is a strong CYP3A inhibitor. 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.
Voriconazole: (Moderate) Monitor for steroid-related adverse reactions if coadministration of voriconazole 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. Dexamethasone is primarily metabolized by CYP3A and voriconazole is a strong CYP3A inhibitor. 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.
Vorinostat: (Moderate) Use vorinostat and corticosteroids together with caution; the risk of QT prolongation and arrhythmias may be increased if electrolyte abnormalities occur. Corticosteroids may cause electrolyte imbalances; hypomagnesemia, hypokalemia, or hypocalcemia and may increase the risk of QT prolongation with vorinostat. Frequently monitor serum electrolytes if concomitant use of these drugs is necessary.
Warfarin: (Moderate) Monitor the INR if warfarin is administered with corticosteroids. The effect of corticosteroids on warfarin is variable. There are reports of enhanced as well as diminished effects of anticoagulants when given concurrently with corticosteroids; however, limited published data exist, and the mechanism of the interaction is not well described. High-dose corticosteroids appear to pose a greater risk for increased anticoagulant effect. In addition, corticosteroids have been associated with a risk of peptic ulcer and gastrointestinal bleeding.
Zafirlukast: (Minor) Zafirlukast inhibits the CYP3A4 isoenzymes and should be used cautiously in patients stabilized on drugs metabolized by CYP3A4, such as corticosteroids.
ng to the manufacturer of pimozide, the drug should not be coadministered with drugs known to cause electrolyte imbalances, such as high-dose, systemic corticosteroid therapy. Pimozide is associated with a well-established risk of QT prolongation and torsade de pointes (TdP), and electrolyte imbalances (e.g., hypokalemia, hypocalcemia, hypomagnesemia) may increase the risk of life-threatening arrhythmias. Pimozide is contraindicated in patients with known hypokalemia or hypomagnesemia. Topical corticosteroids are less likely to interact.
Pioglitazone; Glimepiride: (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.
Pioglitazone; 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.
Pirtobrutinib: (Major) Avoid concurrent use of pirtobrutinib and dexamethasone due to the risk of decreased pirtobrutinib exposure which may reduce its efficacy. If concomitant use is necessary, an empiric pirtobrutinib dosage increase is required. If the current dosage is 200 mg once daily, increase the dose to 300 mg; if the current dosage is 50 mg or 100 mg once daily, increase the dose by 50 mg. Pirtobrutinib is a CYP3A substrate and dexamethasone is a moderate CYP3A inducer. Concomitant use with other moderate CYP3A inducers reduced pirtobrutinib overall exposure by 27% and 49%.
Ponesimod: (Moderate) Monitor for signs and symptoms of infection. Additive immune suppression may result from concomitant use of ponesimod and high-dose corticosteroid therapy which may extend the duration or severity of immune suppression. High-dose corticosteroid therapy is generally defined as a dose of at least 20 mg/day of prednisone or equivalent (or 2 mg/kg/day for patients weighing less than 10 kg) for at least 14 consecutive days.
Posaconazole: (Moderate) Posaconazole and dexamethasone should be coadministered with caution due to an increased potential for adverse events. Posaconazole is a potent inhibitor of CYP3A4, an isoenzyme partially responsible for the metabolism of dexamethasone. Further, both dexamethasone and posaconazole are substrates of the drug efflux protein, P-glycoprotein, which when administered together may increase the absorption or decrease the clearance of the other drug. This complex interaction may cause alterations in the plasma concentrations of both posaconazole and dexamethasone, ultimately resulting in an increased risk of adverse events.
Potassium Phosphate; Sodium Phosphate: (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia.
Potassium-sparing diuretics: (Minor) The manufacturer of spironolactone lists corticosteroids as a potential drug that interacts with spironolactone. Intensified electrolyte depletion, particularly hypokalemia, may occur. However, potassium-sparing diuretics such as spironolactone do not induce hypokalemia. In fact, hypokalemia is one of the indications for potassium-sparing diuretic therapy. Therefore, drugs that induce potassium loss, such as corticosteroids, could counter the hyperkalemic effects of potassium-sparing diuretics.
Pramlintide: (Moderate) 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.
Prasterone, Dehydroepiandrosterone, DHEA (Dietary Supplements): (Moderate) Corticosteroids blunt the adrenal secretion of endogenous DHEA and DHEAS, resulting in reduced DHEA and DHEAS serum concentrations.
Prasterone, Dehydroepiandrosterone, DHEA (FDA-approved): (Moderate) Corticosteroids blunt the adrenal secretion of endogenous DHEA and DHEAS, resulting in reduced DHEA and DHEAS serum concentrations.
Praziquantel: (Moderate) Drugs that induce hepatic metabolism via the microsomal CYP450 enzyme system decrease the bioavailability of praziquantel. Plasma levels of praziquantel have been reported to be 50% lower when dexamethasone was given simultaneously, presumably due to CYP induction by dexamethasone.
Pretomanid: (Major) Avoid coadministration of pretomanid with dexamethasone as concurrent use may decrease pretomanid exposure which may lead to decreased efficacy. Pretomanid is a CYP3A4 substrate; dexamethasone is a moderate CYP3A4 inducer. Coadministration with another moderate CYP3A4 inducer decreased pretomanid exposure by 35%.
Prilocaine; 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.
Primidone: (Moderate) Coadministration may result in decreased exposure to dexamethasone. Primidone is a CYP3A4 inducer; dexamethasone is a CYP3A4 substrate. Monitor for decreased response to dexamethasone during concurrent use.
Promethazine; 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.
Propranolol: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response.
Propranolol; Hydrochlorothiazide, HCTZ: (Moderate) Monitor blood sugar during concomitant corticosteroid and propranolol use due to risk for hypoglycemia. Concurrent use may increase risk of hypoglycemia because of loss of the counter-regulatory cortisol response. (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.
Purine analogs: (Minor) Concurrent use of purine analogs with other agents which cause bone marrow or immune suppression such as other antineoplastic agents or immunosuppressives may result in additive effects.
Pyridostigmine: (Moderate) Concomitant use of anticholinesterase agents, such as pyridostigmine, and corticosteroids may produce severe weakness in patients with myasthenia gravis. If possible, anticholinesterase agents should be withdrawn at least 24 hours before initiating corticosteroid therapy.
Quinapril; 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.
Quinidine: (Moderate) Quinidine is a substrate of the CYP3A4 isoenzyme. Inducers of CYP3A4 such as dexamethasone may increase hepatic elimination of quinidine with the potential for reduced efficacy of quinidine.
Quinolones: (Moderate) Quinolones have been associated with an increased risk of tendon rupture requiring surgical repair or resulting in prolonged disability; this risk is further increased in those receiving concomitant corticosteroids. Discontinue quinolone therapy at the first sign of tendon inflammation or tendon pain, as these are symptoms that may precede rupture of the tendon.
Rapacuronium: (Moderate) 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.
Repaglinide: (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.
Ribociclib: (Moderate) Monitor for an increase in dexamethasone-related adverse reactions if coadministration with ribociclib is necessary. Dexamethasone is a CYP3A4 substrate and ribociclib is a strong CYP3A4 inhibitor.
Ribociclib; Letrozole: (Moderate) Monitor for an increase in dexamethasone-related adverse reactions if coadministration with ribociclib is necessary. Dexamethasone is a CYP3A4 substrate and ribociclib is a strong CYP3A4 inhibitor.
Rifampin: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with rifampin is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A4 substrate and rifampin is a strong CYP3A4 inducer.
Rifapentine: (Moderate) Monitor for decreased efficacy of dexamethasone if coadministration with rifapentine is necessary; consider increasing the dose of dexamethasone if clinically appropriate. Dexamethasone is a CYP3A4 substrate and rifapentine is a strong CYP3A4 inducer.
Rilonacept: (Moderate) Patients receiving immunosuppressives along with rilonacept may be at a greater risk of developing an infection.
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.
Rimegepant: (Major) Avoid coadministration of rimegepant with dexamethasone; concurrent use may significantly decrease rimegepant exposure which may result in loss of efficacy. Rimegepant is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer.
Ripretinib: (Major) Avoid coadministration of ripretinib with dexamethasone. If concomitant use is unavoidable, increase the frequency of ripretinib dosing from 150 mg once daily to 150 mg twice daily; monitor for clinical response and tolerability. Resume once daily dosing of ripretinib 14 days after discontinuation of dexamethasone. Coadministration is predicted to decrease the exposure of ripretinib and its active metabolite (DP-5439), which may decrease ripretinib anti-tumor activity. Ripretinib and DP-5439 are metabolized by CYP3A and dexamethasone is a moderate CYP3A inducer. Drug interaction modeling studies suggest coadministration with a moderate CYP3A inducer may decrease ripretinib exposure by 56%.
Ritonavir: (Moderate) Close monitoring of therapeutic and adverse effects is required when dexamethasone is coadministered with ritonavir. Ritonavir inhibits CYP3A4 and dexamethasone is a CYP3A4 substrate.
Rituximab: (Moderate) Rituximab and corticosteroids are commonly used together; however, monitor the patient for immunosuppression and signs and symptoms of infection during combined chronic therapy.
Rituximab; Hyaluronidase: (Moderate) Rituximab and corticosteroids are commonly used together; however, monitor the patient for immunosuppression and signs and symptoms of infection during combined chronic therapy.
Rivaroxaban: (Minor) Coadministration of rivaroxaban and dexamethasone may result in decreased rivaroxaban exposure and may decrease the efficacy of rivaroxaban. Dexamethasone is an inducer of CYP3A4, and rivaroxaban is a substrate of CYP3A4. If these drugs are administered concurrently, monitor the patient for signs of lack of efficacy of rivaroxaban.
Rocuronium: (Moderate) 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.
Roflumilast: (Major) Coadminister dexamethasone and roflumilast cautiously as this may lead to reduced systemic exposure to roflumilast. Dexamethasone induces CYP3A4 and roflumilast is a CYP3A4 substrate. In pharmacokinetic study, administration of a single dose of roflumilast in patients receiving another CYP3A4 inducer, rifampin, resulted in decreased roflumilast Cmax and AUC, as well as increased Cmax and decreased AUC of the active metabolite roflumilast N-oxide.
Romidepsin: (Major) The concomitant use of romidepsin, a CYP3A4 substrate, and dexamethasone, a strong CYP3A4 inducer, may result in significantly altered romidepsin plasma exposure. Therefore, avoid using romidepsin with potent CYP3A4 inducers if possible.
Ruxolitinib: (Moderate) Ruxolitinib is a CYP3A4 substrate. When used with drugs that are CYP3A4 inducers such as dexamethasone, a dose adjustment is not necessary, but closely monitor patients and titrate the ruxolitinib dose based on safety and efficacy. The Cmax and AUC of a single 50 mg dose of ruxolitinib was decreased by 32% and 61%, respectively, after rifampin 600 mg once daily was administered for 10 days. The relative exposure to ruxolitinib's active metabolites increased by about 100%, which may partially explain the reported disproportionate 10% reduction in the pharmacodynamic marker pSTAT3 inhibition.
Salicylates: (Moderate) 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.
Salsalate: (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.
Saquinavir: (Major) Avoid concurrent administration of dexamethasone and saquinavir boosted with ritonavir. Dexamethasone is may induce the CYP3A4 metabolism of saquinavir, resulting in reduced saquinavir plasma concentrations. Decreased saquinavir plasma concentrations could lead to HIV treatment failures or the development of viral-resistance. If used concomitantly, the patient should be observed for changes in the clinical efficacy and concentrations of the antiretroviral regimen.
Sargramostim, GM-CSF: (Major) Avoid the concomitant use of sargramostim and systemic corticosteroid agents due to the risk of additive myeloproliferative effects. If coadministration of these drugs is required, frequently monitor patients for clinical and laboratory signs of excess myeloproliferative effects (e.g., leukocytosis). Sargramostim is a recombinant human granulocyte-macrophage colony-stimulating factor that works by promoting proliferation and differentiation of hematopoietic progenitor cells.
SARS-CoV-2 (COVID-19) vaccines: (Moderate) Patients receiving corticosteroids in greater than physiologic doses may have a diminished response to the SARS-CoV-2 virus vaccine. Counsel patients receiving corticosteroids about the possibility of a diminished vaccine response and to continue to follow precautions to avoid exposure to SARS-CoV-2 virus after receiving the vaccine.
Selpercatinib: (Major) Avoid coadministration of selpercatinib and dexamethasone due to the risk of decreased selpercatinib exposure which may reduce its efficacy. Selpercatinib is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Coadministration with other moderate CYP3A4 inducers is predicted to decrease selpercatinib exposure by 40% to 70%.
Selumetinib: (Major) Avoid coadministration of selumetinib and dexamethasone due to the risk of decreased selumetinib exposure which may reduce its efficacy. Selumetinib is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Coadministration with a moderate CYP3A4 inducer is predicted to decrease selumetinib exposure by 38%.
Semaglutide: (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.
SGLT2 Inhibitors: (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.
Sildenafil: (Minor) Sildenafil is metabolized principally by CYP3A4. It can be expected that concomitant administration of sildenafil with CYP3A4 enzyme inducers like dexamethasone will decrease plasma concentrations of sildenafil.
Siponimod: (Moderate) Concomitant use of siponimod and dexamethasone is not recommended for patients with CYP2C9*1/*3 and *2/*3 genotypes due to a significant decrease in siponimod exposure. Siponimod is a CYP2C9 and CYP3A4 substrate; dexamethasone is a moderate CYP3A4 inducer. Across different CYP2C9 genotypes, a moderate CYP3A4 inducer decreased the exposure of siponimod by up to 52% according to in silico evaluation. Additonally, monitor patients carefully for signs and symptoms of infection if coadministration is necessary, as concomitant use may increase the risk of immunosuppression. Siponimod has not been studied in combination with other immunosuppressive therapies used for the treatment of multiple sclerosis, including immunosuppressant doses of corticosteroids.
Sipuleucel-T: (Major) Concomitant use of sipuleucel-T and immunosuppressives should be avoided. Concurrent administration of immunosuppressives with the leukapheresis procedure that occurs prior to sipuleucel-T infusion has not been studied. Sipuleucel-T stimulates the immune system and patients receiving immunosuppressives may have a diminished response to sipuleucel-T. When appropriate, consider discontinuing or reducing the dose of immunosuppressives prior to initiating therapy with sipuleucel-T.
Sirolimus: (Moderate) Monitor sirolimus concentrations and adjust sirolimus dosage as appropriate during concomitant use of dexamethasone. Concomitant use may decrease sirolimus exposure and efficacy. Sirolimus is a CYP3A substrate and dexamethasone is a moderate CYP3A inducer.
Sodium Benzoate; Sodium Phenylacetate: (Moderate) Corticosteroids may cause protein breakdown, which could lead to elevated blood ammonia concentrations, especially in patients with an impaired ability to form urea. Corticosteroids should be used with caution in patients receiving treatment for hyperammonemia.
Sodium Phenylbutyrate: (Moderate) The concurrent use of corticosteroids with sodium phenylbutyrate may increase plasma ammonia levels (hyperammonemia) by causing the breakdown of body protein. Patients with urea cycle disorders being treated with sodium phenylbutyrate usually should not receive regular treatment with corticosteroids.
Sodium Phenylbutyrate; Taurursodiol: (Moderate) The concurrent use of corticosteroids with sodium phenylbutyrate may increase plasma ammonia levels (hyperammonemia) by causing the breakdown of body protein. Patients with urea cycle disorders being treated with sodium phenylbutyrate usually should not receive regular treatment with corticosteroids.
Sodium Phosphate Monobasic Monohydrate; Sodium Phosphate Dibasic Anhydrous: (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia.
Sofosbuvir; Velpatasvir: (Major) Avoid coadministration of velpatasvir with dexamethasone. Taking these drugs together may significantly decrease velpatasvir plasma concentrations, potentially resulting in loss of antiviral efficacy. Velpatasvir is a CYP3A4 substrate; dexamethasone a moderate inducer of CYP3A4. Additionally, velpatasvir is an inhibitor of the drug transporter P-glycoprotein (P-gp). Coadministration with substrates of this transporter, such as dexamethasone, may increase their exposure.
Sofosbuvir; Velpatasvir; Voxilaprevir: (Major) Avoid coadministration of velpatasvir with dexamethasone. Taking these drugs together may significantly decrease velpatasvir plasma concentrations, potentially resulting in loss of antiviral efficacy. Velpatasvir is a CYP3A4 substrate; dexamethasone a moderate inducer of CYP3A4. Additionally, velpatasvir is an inhibitor of the drug transporter P-glycoprotein (P-gp). Coadministration with substrates of this transporter, such as dexamethasone, may increase their exposure. (Major) Avoid coadministration of voxilaprevir (a CYP3A4 substrate) with moderate to strong inducers of CYP3A4, such as dexamethasone. Taking these drugs together may significantly decrease voxilaprevir plasma concentrations, potentially resulting in loss of antiviral efficacy. In addition, voxilaprevir, a P-glycoprotein (P-gp) inhibitor, may alter concentrations of dexamethasone, a P-gp substrate.
Somapacitan: (Moderate) Patients treated with glucocorticoid replacement for hypoadrenalism may require an increase in their maintenance or stress steroid doses following initiation of somapacitan. Monitor for signs/symptoms of reduced serum cortisol concentrations. Growth hormone (GH) inhibits 11betaHSD-1. Consequently, patients with untreated GH deficiency have relative increases in 11betaHSD-1 and serum cortisol. The initiation of somapacitan may result in inhibition of 11betaHSD-1 and reduced serum cortisol concentrations.
Somatropin, rh-GH: (Moderate) Corticosteroids can retard bone growth and therefore, can inhibit the growth-promoting effects of somatropin. If corticosteroid therapy is required, the corticosteroid dose should be carefully adjusted.
Sonidegib: (Major) Avoid the concomitant use of sonidegib and dexamethasone; sonidegib levels may be significantly decreased and its efficacy reduced. Sonidegib is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Physiologic-based pharmacokinetics (PBPK) simulations indicate that a moderate CYP3A4 inducer would decrease the sonidegib AUC by 56% if administered for 14 days and by 69% if the moderate CYP3A inducer is administered for more than 14 days.
Sorafenib: (Major) Avoid coadministration of sorafenib with dexamethasone due to decreased plasma concentrations of sorafenib. Sorafenib is a CYP3A4 substrate and dexamethasone is a CYP3A4 inducer. Concomitant use with another strong CYP3A4 inducer decreased sorafenib exposure by 37%.
Sotagliflozin: (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.
Spironolactone; 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.
Succinylcholine: (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.
Sufentanil: (Moderate) Because the dose of the sufentanil sublingual tablets cannot be titrated, consider an alternate opiate if dexamethasone must be administered. Monitor for reduced efficacy of sufentanil injection and signs of opioid withdrawal if coadministration with dexamethasone is necessary; consider increasing the dose of sufentanil injection as needed. If dexamethasone is discontinued, consider a dose reduction of sufentanil injection and frequently monitor for signs or respiratory depression and sedation. Sufentanil is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Concomitant use with CYP3A4 inducers can decrease sufentanil concentrations; this may result in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence.
Sulfonylureas: (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.
Tadalafil: (Minor) Tadalafil is metabolized principally by cytochrome P450 3A4. Studies have shown that concomitant administration of CYP3A4 enzyme-inducers, such as dexamethasone, will decrease plasma levels of tadalafil.
Tasimelteon: (Moderate) Caution is recommended during concurrent use of tasimelteon and dexamethasone. Because tasimelteon is partially metabolized via CYP3A4, use with CYP3A4 inducers, such as dexamethasone, may reduce the efficacy of tasimelteon.
Tazemetostat: (Major) Avoid coadministration of tazemetostat with dexamethasone as concurrent use may decrease tazemetostat exposure, which may reduce its efficacy. Tazemetostat is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer.
Telbivudine: (Moderate) The risk of myopathy may be increased if corticosteroids are coadministered with telbivudine. Monitor patients for any signs or symptoms of unexplained muscle pain, tenderness, or weakness, particularly during periods of upward dosage titration.
Telmisartan; 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.
Telmisartan; 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.
Temsirolimus: (Major) Avoid coadministration of temsirolimus with dexamethasone due to the risk of decreased plasma concentrations of the primary active metabolite of temsirolimus (sirolimus). If concomitant use is unavoidable, consider increasing the dose of temsirolimus from 25 mg per week up to 50 mg per week. If dexamethasone is discontinued, decrease the dose of temsirolimus to the dose used before initiation of dexamethasone. Temsirolimus is a CYP3A4 substrate and dexamethasone is a CYP3A4 inducer. Coadministration with another strong CYP3A4 inducer had no significant effect on the AUC or Cmax of temsirolimus, but decreased the AUC and Cmax of the active metabolite, sirolimus, by 56% and 65%, respectively.
Terbinafine: (Moderate) Due to the risk for breakthrough fungal infections, caution is advised when administering terbinafine with dexamethasone. Although this interaction has not been studied by the manufacturer, and published literature suggests the potential for interactions to be low, taking these drugs together may decrease the systemic exposure of terbinafine. Predictions about the interaction can be made based on the metabolic pathways of both drugs. Terbinafine is metabolized by at least 7 CYP isoenyzmes, with major contributions coming from CYP3A4; dexamethasone induces this enzyme. Monitor patients for breakthrough fungal infections.
Testosterone: (Moderate) Monitor for fluid retention during concurrent corticosteroid and testosterone use. Concurrent use may result in increased fluid retention.
Thalidomide: (Moderate) Coadministration of dexamethasone with thalidomide should be employed cautiously, as toxic epidermal necrolysis has been reported with concomitant use.
Thiazide diuretics: (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.
Thiazolidinediones: (Moderate) Monitor blood glucose during concomitant corticosteroid and thiazolidinedione use; a thiazolidinedione 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.
Ticagrelor: (Moderate) Coadministration of ticagrelor with dexamethasone may result in decreased concentrations of ticagrelor. Use combination with caution and monitor for decreased efficacy of ticagrelor. Ticagrelor is a substrate of CYP3A4/5 and dexamethasone is a moderate CYP3A4 inducer.
Tirzepatide: (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.
Tolazamide: (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.
Tolbutamide: (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.
Toremifene: (Major) Avoid coadministration of dexamethasone with toremifene due to decreased plasma concentrations of toremifene which may result in decreased efficacy. Toremifene is a CYP3A4 substrate and dexamethasone is a CYP3A4 inducer. Coadministration with strong CYP3A4 inducers lowers steady-state serum concentrations of toremifene.
Tositumomab: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
Tretinoin, ATRA: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.
Triamterene; 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.
Tuberculin Purified Protein Derivative, PPD: (Moderate) Immunosuppressives may decrease the immunological response to tuberculin purified protein derivative, PPD. This suppressed reactivity can persist for up to 6 weeks after treatment discontinuation. Consider deferring the skin test until completion of the immunosuppressive therapy.
Tucatinib: (Moderate) Monitor for steroid-related adverse reactions if coadministration of tucatinib 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 CYP3A4 inhibitors, especially for long-term use. Tucatinib 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.
Ubrogepant: (Major) Increase the initial and second dose of ubrogepant to 100 mg if coadministered with dexamethasone as concurrent use may decrease ubrogepant exposure and reduce its efficacy. Ubrogepant is a CYP3A4 substrate; dexamethasone is a moderate CYP3A4 inducer.
Ulipristal: (Major) Avoid administration of ulipristal with drugs that induce CYP3A4. Ulipristal is a substrate of CYP3A4 and dexamethasone is a CYP3A4 inducer. Concomitant use may decrease the plasma concentration and effectiveness of ulipristal.
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.
Vecuronium: (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.
Vemurafenib: (Major) Concomitant use of vemurafenib and dexamethasone may result in altered concentrations of dexamethasone and decreased concentrations vemurafenib. Vemurafenib is a substrate/inducer of CYP3A4 and a substrate/inhibitor of P-glycoprotein (P-gp). Dexamethasone is a substrate/inducer of CYP3A4 and a substrate of P-gp. Avoid using these agents together if possible.
Venetoclax: (Major) Avoid the concomitant use of venetoclax and dexamethasone; venetoclax levels may be decreased and its efficacy reduced. Venetoclax is a CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Consider alternative agents. In a drug interaction study (n = 11), the venetoclax Cmax and AUC values were decreased by 42% and 71%, respectively, following the co-administration of multiple doses of a strong CYP3A4 inducer. Use of venetoclax with a moderate CYP3A4 inducer has not been evaluated.
Vigabatrin: (Major) Vigabatrin should not be used with corticosteroids, which are associated with serious ophthalmic effects (e.g., retinopathy or glaucoma) unless the benefit of treatment clearly outweighs the risks.
Vincristine Liposomal: (Moderate) Avoid the concomitant use of dexamethasone and vincristine. Vincristine is a substrate for cytochrome P450 (CYP) 3A4. Agents that induce CYP 3A4 such as dexamethasone may increase the metabolism of vincristine and decrease the efficacy of drug. (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia.
Vincristine: (Moderate) Avoid the concomitant use of dexamethasone and vincristine. Vincristine is a substrate for cytochrome P450 (CYP) 3A4. Agents that induce CYP 3A4 such as dexamethasone may increase the metabolism of vincristine and decrease the efficacy of drug.
Voclosporin: (Major) Avoid coadministration of voclosporin with dexamethasone. Coadministration may decrease voclosporin exposure resulting in decreased efficacy. Voclosporin is a sensitive CYP3A4 substrate and dexamethasone is a moderate CYP3A4 inducer. Coadministration with moderate CYP3A4 inducers is predicted to decrease voclosporin exposure by 70%.
Vonoprazan; Amoxicillin: (Major) Avoid concomitant use of vonoprazan and dexamethasone due to decreased plasma concentrations of vonoprazan, which may reduce its efficacy. Vonoprazan is a CYP3A substrate and dexamethasone is a moderate CYP3A inducer. Vonoprazan exposures are predicted to be 50% lower when coadministered with a moderate CYP3A4 inducer.
Vonoprazan; Amoxicillin; Clarithromycin: (Major) Avoid concomitant use of vonoprazan and dexamethasone due to decreased plasma concentrations of vonoprazan, which may reduce its efficacy. Vonoprazan is a CYP3A substrate and dexamethasone is a moderate CYP3A inducer. Vonoprazan exposures are predicted to be 50% lower when coadministered with a moderate CYP3A4 inducer. (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.
Vorapaxar: (Moderate) Use caution during concurrent use of vorapaxar and dexamethasone. Decreased serum concentrations of vorapaxar and thus decreased efficacy are possible when vorapaxar, a CYP3A4 substrate, is coadministered with dexamethasone, a CYP3A inducer.
Voriconazole: (Moderate) Monitor for potential adrenal dysfunction with concomitant use of voriconazole and dexamethasone. In patients taking corticosteroids, voriconazole-associated CYP3A4 inhibition of their metabolism may lead to corticosteroid excess and adrenal suppression. Corticosteroid exposure is likely to be increased. Voriconazole is a strong CYP3A4 inhibitor, and dexamethasone is a CYP3A4 substrate.
Vorinostat: (Moderate) Use vorinostat and corticosteroids together with caution; the risk of QT prolongation and arrhythmias may be increased if electrolyte abnormalities occur. Corticosteroids may cause electrolyte imbalances; hypomagnesemia, hypokalemia, or hypocalcemia and may increase the risk of QT prolongation with vorinostat. Frequently monitor serum electrolytes if concomitant use of these drugs is necessary.
Voxelotor: (Major) Avoid coadministration of voxelotor and dexamethasone as concurrent use may decrease voxelotor exposure and lead to reduced efficacy. If coadministration is unavoidable, increase voxelotor dosage to 2,000 mg PO once daily in patients 12 years and older. In patients 4 to 11 years old, weight-based dosage adjustments are recommended; consult product labeling for specific recommendations. Voxelotor is a substrate of CYP3A; dexamethasone is a moderate CYP3A inducer. Coadministration of voxelotor with a moderate CYP3A inducer is predicted to decrease voxelotor exposure by up to 24%.
Warfarin: (Moderate) Monitor the INR if warfarin is administered with corticosteroids. The effect of corticosteroids on warfarin is variable. There are reports of enhanced as well as diminished effects of anticoagulants when given concurrently with corticosteroids; however, limited published data exist, and the mechanism of the interaction is not well described. High-dose corticosteroids appear to pose a greater risk for increased anticoagulant effect. In addition, corticosteroids have been associated with a risk of peptic ulcer and gastrointestinal bleeding.
Zafirlukast: (Minor) Zafirlukast inhibits the CYP3A4 isoenzymes and should be used cautiously in patients stabilized on drugs metabolized by CYP3A4, such as corticosteroids.
Zanubrutinib: (Major) Avoid concurrent use of zanubrutinib and dexamethasone due to the risk of decreased zanubrutinib exposure which may reduce its efficacy. If concomitant use is necessary, increase the zanubrutinib dose to 320 mg twice daily and monitor response. Resume the previous dose of zanubrutinib if dexamethasone is discontinued. Zanubrutinib is a CYP3A substrate and dexamethasone is a moderate CYP3A inducer. Concomitant use with another moderate CYP3A inducer decreased zanubrutinib exposure by 44%.
Zolpidem: (Moderate) It is advisable to closely monitor for reductions in zolpidem efficacy during co-administration of moderate CYP3A4 inducers, such as dexamethasone. CYP3A4 is the primary isoenzyme responsible for zolpidem metabolism, and there is evidence of significant decreases in systemic exposure and pharmacodynamic effects of zolpidem during co-administration of rifampin, a potent CYP3A4 inducer.
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
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.
Mechanism Of Action
Glucocorticoids are naturally occurring hormones that prevent or suppress inflammation and immune responses when administered at pharmacological doses. At the molecular level, unbound glucocorticoids readily cross cell membranes and bind with high affinity to specific cytoplasmic receptors. This binding induces a response by modifying transcription and, ultimately, protein synthesis to achieve the steroid's intended action. Such actions can include: inhibition of leukocyte infiltration at the site of inflammation, interference in the function of mediators of the inflammatory response, and suppression of humoral immune responses. Some of the net effects include reduction in edema or scar tissue and a general suppression in an immune response. The degree of clinical effect is normally related to the dose administered. The anti-inflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, collectively called lipocortins. Lipocortins, in turn, control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of the precursor molecule arachidonic acid. Likewise, the numerous adverse effects related to corticosteroid use usually depend on the dose administered and the duration of therapy.
Pharmacokinetics
Dexamethasone is administered via oral, intravenous, intramuscular, intraarticular, intravitreal, ophthalmic, and otic routes. Certain dosage forms, like inhalational products, have been removed from marketing. Circulating drug binds weakly to plasma proteins, with only the unbound portion of a dose being active. Systemic dexamethasone is quickly distributed into the kidneys, intestines, skin, liver, and muscle. Corticosteroids distribute into breast milk and cross the placenta. Systemic dexamethasone is metabolized by the liver to inactive metabolites. These inactive metabolites, as well as a small portion of unchanged drug, are excreted in the urine. The plasma elimination half-life of dexamethasone is approximately 1.8 to 3.5 hours whereas the biological half-life is 36 to 54 hours.
Affected cytochrome P450 (CYP450) isoenzymes and drug transporters: CYP3A4, P-glycoprotein (P-gp)
Dexamethasone is a weak inducer of CYP3A4 and is a substrate for both P-glycoprotein (P-gp) and CYP3A4.
Dexamethasone is rapidly and well absorbed after oral administration. In adults, bioavailability has been reported to be in the range of approximately 60% to 100%, with no significant differences between the elixir and tablet formulations. Peak concentrations occur 1 to 2 hours after oral administration. However, 1 study of 13 patients (aged 14 to 28 years) with congenital adrenal hyperplasia reported a mean time to peak concentrations for oral dexamethasone of 45 minutes (range 30 to 120 minutes).
Intravenous RoutePeak concentrations were reached approximately 60 minutes after single-dose administration of IV dexamethasone in neonates.
Intramuscular RouteThe onset and duration of action of dexamethasone injection ranges from 2 days to 3 weeks and is dependent on whether the drug is administered by intra-articular or IM injection and by the extent of the local blood supply.
Other Route(s)Intra-articular Route
The onset and duration of action of dexamethasone injection ranges from 2 days to 3 weeks and is dependent on whether the drug is administered by intra-articular or IM injection and by the extent of the local blood supply.
Ophthalmic Route
Following ophthalmic administration, dexamethasone is absorbed through the aqueous humor and distribute into the local tissues, with only minimal systemic absorption occurring. Ophthalmic doses are metabolized locally.
Intravitreal Implant Route
After the insertion of the dexamethasone intravitreal implant (0.35 mg or 0.7 mg) in 21 patients, plasma concentrations were obtained on days 1, 7, 30, 60, and 90. Overall, the majority of dexamethasone plasma concentration measurements were below the lower limit of quantitation (LLOQ = 50 pg/mL). Ten of the 73 samples in the patients receiving the 0.7 mg dose and 2 of the 42 samples in the patients receiving the 0.35 mg dose were above the LLOQ (range, 52 to 94 pg/mL). The highest plasma concentration (94 pg/mL) was observed in one patient who had received the 0.7 mg dose. Age, body weight, and gender did not affect the plasma dexamethasone concentrations. In vitro metabolism studies of the intravitreal implant showed no metabolites.
Intraocular Route
Systemic exposure to dexamethasone was evaluated in a subgroup of patients enrolled in 2 studies (n = 25 for the first study and n = 13 for the second study). The patients received a single intraocular injection of dexamethasone containing 342 mcg or 517 mcg of dexamethasone at the end of cataract surgery and blood samples were collected prior to surgery and at the several time points post-surgery between Day 1 and up to Day 30. In the first study, the dexamethasone plasma concentrations on post-surgery Day 1 ranged from 0.09 to 0.86 ng/mL and from 0.07 to 1.16 ng/mL following administration of dexamethasone 342 mcg and 517 mcg, respectively. In the second study, dexamethasone plasma concentrations on post-surgery Day 1 ranged from 0.349 to 2.79 ng/mL following administration of dexamethasone 517 mcg. In both the studies, dexamethasone plasma concentrations declined over time and very few patients had quantifiable dexamethasone plasma concentrations at the final time point of sampling (Day 15 or Day 30).
Intracanalicular Route
Systemic exposure to dexamthasone was evaluated in 16 healthy volunteers. Plasma samples were obtained prior to and at several time points on Days 1 to 29. Dexamethasone plasma concentrations were detectable (above 50 pg/mL, the lower limit of quantification of the assay) in 11% of samples (21 of 189), and ranged from 0.05 ng/mL to 0.81 ng/mL.
Pregnancy And Lactation
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.