PREDNISONE

Prednisone is the most commonly-prescribed oral corticosteroid. The drug is metabolized in the liver to its active form, prednisolone. Relative to hydrocortisone, prednisone is roughly 4 times as potent as a glucocorticoid. Prednisone is used in many conditions in adult and pediatric patients, including allograft rejection, asthma, chronic obstructive pulmonary disease (COPD), systemic lupus erythematosus (SLE), rheumatoid and psoriatic arthritis, and many other allergic, dermatologic, and inflammatory states. Prednisone has very little mineralocorticoid activity, so it is not used in the management of adrenal insufficiency unless a more potent mineralocorticoid is administered concomitantly. Systemic corticosteroids may be added to other long-term maintenance medications in the management of uncontrolled severe persistent asthma. Once stabilization of asthma is achieved, regular attempts should be made to reduce or eliminate the use of systemic corticosteroids due to the side effects associated with chronic administration. Short courses of treatment may be used in moderate to severe exacerbations of asthma. Short courses of systemic corticosteroids such as prednisone have particular benefits in treating acute exacerbations of COPD. If long-term therapy with prednisone is required for any indication, the lowest possible effective dose should be used.

Updates for coronavirus disease 2019 (COVID-19):
The World Health Organization strongly recommends the use of systemic corticosteroids, including prednisone, in patients with severe or critical COVID-19; but suggests against use in patients with non-severe COVID-19. The National Institutes of Health (NIH) COVID-19 treatment guidelines recommend using another corticosteroid, dexamethasone, in hospitalized patients with COVID-19 who require supplemental oxygen, including those on high-flow oxygen, noninvasive ventilation, mechanical ventilation, or extracorporeal membrane oxygenation (ECMO); however, prednisone may be used as an alternative corticosteroid if dexamethasone is unavailable. The NIH recommends against the use of corticosteroids in patients with mild to moderate COVID-19 (i.e., non-hospitalized patients or hospitalized patients that do not require supplemental oxygen).

General Administration Information
For storage information, see the specific product information within the How Supplied section.

Route-Specific Administration

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

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

Prolonged administration of physiologic replacement dosages of glucocorticoids does not usually cause adverse effects. The severity of the adverse effects associated with prolonged administration of pharmacological dosages of corticosteroids, such as prednisone, increases with duration of therapy. Short term administration of large doses typically does not cause adverse effects, but long term administration can lead to adrenocortical atrophy and generalized protein depletion.

Glucocorticoids, such as prednisone, are responsible for protein metabolism, and prolonged therapy can result in various musculoskeletal manifestations, including: myopathy (myalgia, muscle wasting, muscle weakness, and quadriparesis), arthralgia, impaired wound healing, tendon rupture (particularly affecting the Achilles tendon), bone matrix atrophy (osteoporosis and osteopenia), bone fractures such as vertebral compression fractures or fractures of long bones, and avascular necrosis of femoral or humoral heads. These effects are more likely to occur in older or debilitated patients. Of note, abrupt cessation of corticosteroids can cause arthralgia and myalgia. Glucocorticoids interact with calcium metabolism at many sites, including: decreasing the synthesis by osteoblasts of the principle proteins of bone matrix, malabsorption of calcium in both the nephron and the gut, and reduction of sex hormone concentrations. Although all of these actions probably contribute to glucocorticoid-induced osteoporosis, the actions on osteoblasts is most important. Glucocorticoids do not modify vitamin D metabolism. Postmenopausal women, in particular, should be monitored for signs of osteoporosis during corticosteroid therapy. Because of retardation of bone growth, children receiving prolonged corticosteroid therapy may have growth inhibition.

Corticosteroid therapy, including prednisone therapy, can mask the symptoms of infection and should be avoided during an acute viral, fungal, or bacterial infection. Leukocytosis is a common physiologic effect of systemic corticosteroid therapy and may need to be differentiated from the leukocytosis that occurs with inflammatory or infectious processes. Neutropenia, including febrile neutropenia, has been reported by recipients of corticosteroids. Immunosuppression is most likely to occur in patients receiving high-dose (e.g., equivalent to 1 mg/kg or more of prednisone daily), systemic corticosteroid therapy for any period of time, particularly in conjunction with corticosteroid-sparing drugs (e.g., troleandomycin) and/or concomitant immunosuppressant agents; however, patients receiving moderate dosages of systemic corticosteroids for short periods or low dosages for prolonged periods also may be at risk. Corticosteroids can reactivate tuberculosis and should not be used in patients with a history of active tuberculosis except when chemoprophylaxis is instituted concomitantly. Patients receiving immunosuppressive doses of corticosteroids should be advised to avoid exposure to measles or varicella (chickenpox) and, if exposed to these diseases, to seek medical advice immediately. Additionally, health care providers should monitor prednisone recipients for signs of an opportunistic fungal infection as cases of oropharyngeal candidiasis have been reported with the use of corticosteroids. The development of Kaposi's sarcoma has been associated with prolonged administration of corticosteroids, such as prednisone. Discontinuation of prednisone may result in clinical improvement.

Corticosteroids are divided into two classes: mineralocorticoids and glucocorticoids. Prednisone is a glucocorticoid with minimal mineralocorticoid activity. Mineralocorticoids alter electrolyte and fluid balance by facilitating sodium retention and hydrogen and potassium excretion at the level of the distal renal tubule, resulting in increased plasma volume. Although the incidence may vary by study design and population, mineralocorticoid properties of prednisone can cause fluid retention; electrolyte disturbances (hypokalemia, hypokalemic metabolic alkalosis, hypernatremia, hypocalcemia); and edema. In a review of 93 studies of corticosteroid use, hypertension was found to develop approximately 4 times as often in steroid recipients compared to control groups. Congestive heart failure can occur in susceptible patients. In a study, an increased risk of heart failure was observed for medium-dose glucocorticoid use as compared with nonuse. At the beginning of the study, patients were at least 40 years of age and had not been hospitalized for cardiovascular disease. Medium exposure was defined as less than 7.5 mg daily of prednisolone or the equivalent given orally, rectally, or parenterally.

Adverse neurologic effects have been reported during prolonged administration of corticosteroids like prednisone and include amnesia and memory impairment, headache, insomnia, vertigo, restlessness, increased motor activity, impaired cognition, ischemic peripheral neuropathy, neuritis, paresthesias, seizures or convulsions, and EEG changes. Mental disturbances, including depression, anxiety, euphoria, delirium, dementia, hallucinations, irritability, malaise, mania, mood swings, personality changes, schizophrenic reactions, psychosis, and withdrawn behavior, have also been reported; emotional lability and psychotic problems can be exacerbated by corticosteroid therapy.

Although corticosteroids like prednisone are used to treat Graves' ophthalmopathy, ocular effects, such as corneal perforation, exophthalmos, posterior subcapsular cataracts, retinopathy, or ocular hypertension, can result from prolonged use of glucocorticoids and could result in glaucoma or ocular nerve damage including optic neuritis. Temporary or permanent visual impairment, including blurred vision and blindness, has been reported with glucocorticoid administration by several routes of administration including intranasal and ophthalmic administration. Secondary fungal and viral ocular infection can be exacerbated by corticosteroid therapy.

Prolonged corticosteroid therapy with prednisone may adversely affect the endocrine system, resulting in hypercorticism (Cushing's syndrome including fat abnormalities such as buffalo hump and moon face), menstrual irregularity, or decreased carbohydrate and glucose tolerance. Systemic corticosteroids are a common cause of drug-induced hyperglycemia. In the hospital setting, there is evidence that more than 50% of the patients receiving high-dose systemic steroids develop hyperglycemia, with many more having at least 1 episode of hyperglycemia or a mean blood glucose of 140 mg/dL or greater. Long-term use produces metabolic and endocrine effects that include insulin resistance that may lead to new diagnoses of diabetes mellitus (DM) in patients without a history of hyperglycemia or DM prior to corticosteroid use. Glucosuria (glycosuria) and aggravation of existing DM may also occur.

Adverse GI effects associated with corticosteroid administration such as prednisone include nausea, vomiting, and anorexia with subsequent weight loss. Of note, abrupt cessation of corticosteroids can cause anorexia, nausea, vomiting, and weight loss. Appetite stimulation with weight gain, diarrhea, constipation, abdominal pain and/or distention, hiccups, esophageal ulceration, gastritis, GI perforation, GI bleeding, GI irritation, and pancreatitis have also been reported. Although it was once believed that corticosteroids contributed to the development of peptic ulcer disease, in a review of 93 studies of corticosteroid use, the incidence of peptic ulcer disease was not found to be higher in steroid recipients compared to control groups. While most of these studies did not utilize endoscopy, it is unlikely that corticosteroids contribute to the development of peptic ulcer disease.

Various adverse dermatologic effects reported during corticosteroid therapy include skin atrophy or thin, fragile skin, acne vulgaris, acneiform rash, alopecia or thinning scalp hair, skin hyperpigmentation, skin hypopigmentation, sterile abscess, suppressed reactions to skin tests, diaphoresis, xerosis, facial erythema, striae, petechiae, hirsutism, lupus-like symptoms, ecchymosis and easy bruising, perineal pain and irritation, purpura, rash (unspecified), and telangiectasia. Hypersensitivity reactions of corticosteroid like prednisone may manifest as allergic dermatitis, urticaria, anaphylactoid reactions, and/or angioedema.

Pharmacologic doses of corticosteroids like prednisone administered for prolonged periods may result in physiological dependence due to hypothalamic-pituitary-adrenal (HPA) suppression. Exogenous corticosteroids exert negative feedback on the pituitary, inhibiting the secretion of adrenocorticotropin (ACTH) and a decrease in ACTH-mediated synthesis of endogenous corticosteroids and androgens by the adrenal cortex results. The severity of glucocorticoid-induced secondary adrenocortical insufficiency varies among individuals and is dependent upon the dose, frequency, time of administration, and duration of therapy. Administering the drug on alternate days may help to alleviate this adverse effect. Patients with HPA suppression will require increased doses of corticosteroid therapy during periods of physiologic stress. Acute adrenal insufficiency and even death may occur if the sudden withdrawal of the drugs is undertaken. Withdrawal from prolonged oral corticosteroid therapy should be gradual; HPA suppression can last for up to 12 months following cessation of therapy, and patients may need supplemental corticosteroid treatment during periods of physiologic stress, such as surgery, acute blood loss, or infection, even after the drug has been discontinued. Also, a withdrawal syndrome may occur following abrupt discontinuance of corticosteroid therapy and is unrelated to adrenocortical insufficiency. This syndrome includes symptoms such as anorexia, lethargy, nausea/vomiting, headache, fever, arthralgia, myalgia, exfoliative dermatitis, weight loss, and hypotension. These effects are thought to be due to the sudden change in glucocorticoid concentration rather than to low corticosteroid levels. Increased intracranial pressure with papilledema (i.e., pseudotumor cerebri) has also been reported with glucocorticoids usually after treatment.

Hypercholesterolemia, atherosclerosis, fat (lipid) embolism, sinus tachycardia, palpitations, bradycardia, syncope, vasculitis, necrotizing angiitis, thrombosis, thromboembolism, and thrombo-phlebitis have been associated with corticosteroid therapy, including prednisone. Glucocorticoid use appears to increase the risk of cardiovascular events such as myocardial infarction, left ventricular rupture (in persons who recently experienced a myocardial infarction), angina, angioplasty, coronary revascularization, stroke, transient ischemic attack, cardiomegaly, arrhythmia exacerbation and ECG changes, hypertrophic cardiomyopathy (in premature infants), and pulmonary edema, cardiac arrest or cardiovascular death. As determined from observational data, the rate of cardiovascular events was 17 per 1,000 person-years among 82,202 non-users of glucocorticoids. In contrast, the rate was 23.9 per 1,000 person-years among 68,781 glucocorticoid users. Furthermore, the rate of cardiovascular events was 76.5 per 1,000 person-years for high exposure patients. After adjustment for known covariates by multivariate analysis, high-dose glucocorticoid use was associated with a 2.56-fold increased risk of cardiovascular events as compared with nonuse. At the beginning of the study, patients were at least 40 years of age and had not been hospitalized for cardiovascular disease. High glucocorticoid exposure was defined as at least 7.5 mg daily of prednisolone, or an equivalent (oral rectal, or parenteral) whereas medium exposure was defined as less than the listed dosage by any of the 3 routes. Low-dose exposure was defined as inhaled, topical, or nasal usage only.

Dizziness and anemia have been reported with corticosteroid use such as prednisone. Corticosteroids may decrease serum concentrations of vitamin C (ascorbic acid) and vitamin A, which may rarely produce symptoms of vitamin A deficiency or vitamin C deficiency. Some loss of folic acid may also be caused by corticosteroid use; glossitis may be noted.

Cases of elevated hepatic enzymes (usually reversible upon discontinuation) and hepatomegaly have been associated with prednisone treatment.

Prednisone is contraindicated in patients with a hypersensitivity to prednisone or to any components of the formulation. Rare instances of anaphylactoid reactions have occurred in patients receiving corticosteroid therapy. Although true corticosteroid hypersensitivity is rare, it is possible, though also rare, that such patients will display cross-hypersensitivity to other corticosteroids. It is advisable that patients who have a hypersensitivity reaction to any corticosteroid undergo skin testing, which, although not a conclusive predictor, may help to determine if hypersensitivity to another corticosteroid exists. Such patients should be carefully monitored during and following the administration of any corticosteroid.

Patients receiving high-dose systemic corticosteroid therapy, such as prednisone, for any period of time are at risk to develop immunosuppression; patients receiving moderate dosages of systemic corticosteroids for short periods or low doses for prolonged periods also may be at risk. When given in combination with other immunosuppressive agents, there is a risk of significant immunosuppression.

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

As glucocorticoids can produce or aggravate Cushing's syndrome, glucocorticoids should be avoided in patients with Cushing's disease unless when needed to correct hypocortisolism that may occur during use of treatments for the condition.

Pharmacological doses of systemic corticosteroids administered for prolonged periods may result in hypothalamic-pituitary-adrenal (HPA) suppression and/or manifestations of Cushing's syndrome in some patients. Acute adrenal insufficiency and even death may occur following abrupt discontinuation of systemic therapy. In addition, a withdrawal syndrome unrelated to adrenocortical insufficiency may occur following sudden discontinuation of corticosteroid therapy. These effects are thought to be due to the sudden change in glucocorticoid concentration rather than to low corticosteroid levels. Withdraw prolonged systemic corticosteroid therapy (greater than 2 weeks) gradually. HPA suppression can last for up to 12 months following cessation of systemic chronic therapy. Recovery of HPA axis function is generally prompt and complete upon discontinuation of short-term or topical corticosteroid therapy.

Like all corticosteroids, prednisone therapy may impair immune and adrenocortical function. HPA-suppressed patients may need supplemental corticosteroid treatment during periods of physiologic stress, such as surgery, acute blood loss, or infectious conditions, even after the corticosteroid has been discontinued. Patients should advise the attending physician of the corticosteroid they have received within the last 12 months, and the disease for which they were being treated. Identification cards which include the name of the patient's disease, the currently administered type and dose of corticosteroid, and the patient's physician should be carried with the patient at all times.

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

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

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

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

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

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

Use with caution in patients with glaucoma; prednisone can cause increased intraocular pressure with possible damage to the optic nerves. If steroid therapy is continued for more than 6 weeks, intraocular pressure should be monitored. Use of corticosteroids may produce posterior subcapsular cataracts and may enhance the establishment of secondary ocular infection due to bacteria, fungi or viruses. The use of oral corticosteroids is not recommended in the treatment of optic neuritis and may lead to an increase in the risk of new episodes. Corticosteroids should not be used in active ocular herpes simplex because of possible corneal perforation.

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

Corticosteroids decrease bone formation and increase bone resorption both through their effect on calcium regulation (i.e., decreasing absorption and increasing excretion) and inhibition of osteoblast function. This, together with a decrease in the protein matrix of the bone secondary to an increase in protein catabolism, and reduced sex hormone production, may lead to inhibition of bone growth in pediatric patients and the development of osteopenia or osteoporosis at any age. Growth and development of pediatric patients on prolonged corticosteroid therapy should be carefully observed. Special consideration should be given to patients at increased risk of osteoporosis (e.g., postmenopausal women) before initiating corticosteroid therapy. Consider interventions to reduce bone loss or treat glucocorticoid-induced osteoporosis in affected patients. To minimize the risk of glucocortoicoid-induced bone loss, the smallest possible effective dosage and duration should be used. Current recommendations suggest that all interventions be initiated in any patient in whom glucocorticoid therapy with at least the equivalent of 5 mg of prednisone for at least 3 months is anticipated.

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

Indicated vaccination procedures may be undertaken in patients receiving nonimmunosuppressive doses of corticosteroids as replacement therapy (e.g., for Addison's disease). Administration of live or live, attenuated vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids. Killed or inactivated vaccines may be administered. However, the response to such vaccines may be diminished and cannot be predicted. The immunosuppressive effects of steroid treatment differ, but many clinicians consider a systemic dose equivalent to either 2 mg/kg/day or 20 mg/day of prednisone as sufficiently immunosuppressive to raise concern about the safety of immunization with live-virus vaccines. In patients who have received high-dose, systemic corticosteroids for 2 weeks or longer, it is recommended to wait at least 3 months after discontinuation of therapy before administering a live-virus vaccine.

If systemic corticosteroids such as prednisone must be used during pregnancy, the potential risks should be discussed with the patient. Infants born to mothers who have received substantial doses of corticosteroids during pregnancy should be carefully observed for signs of hypoadrenalism. Based on findings from human and animal studies, corticosteroids can cause fetal harm when administered to a pregnant woman. Published epidemiological studies suggest a small but inconsistent increased risk of orofacial clefts with use of systemic corticosteroids during the first trimester. 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. Intrauterine growth restriction and decreased birth weight have also been reported with maternal use of systemic corticosteroids during pregnancy; however, the underlying maternal condition may also contribute to these risks. There are no adequate and well-controlled studies in pregnant women.

Corticosteroids distribute into breast milk, and the manufacturer states that in order to minimize infant exposure, the lowest dose should be prescribed to lactating women to achieve the desired clinical effect. Prednisone concentrations in breast milk are low, and no adverse effects have been reported in the breast-fed infant with maternal use of any corticosteroid during breast-feeding; prednisone is generally considered compatible to use during lactation. Published case reports of systemic prednisone use during pregnancy that indicate little risk to a nursing infant due to lack of reported side effects. Prednisone is converted to prednisolone in vivo, and peak concentrations in human milk appear in about 1 hour after a dose; the total daily dose reaching the infant is approximately 0.1% of the mother's total daily dose. Prednisolone and methylprednisolone have similar data available regarding systemic use during lactation. High doses of corticosteroids administered to lactating women for long periods could potentially produce problems in the breastfed infant including growth and development and interfere with endogenous corticosteroid production. At higher daily prednisone doses, avoidance of breast-feeding during times of peak milk concentrations can help limit infant exposure; however, such adjustments are rarely necessary. Consider the benefits of breast-feeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition.

Use systemic corticosteroids such as prednisone with caution in the geriatric patient; the risks and benefits of therapy should be considered for any individual patient, particularly with chronic use. According to the Beers Criteria, systemic corticosteroids are considered potentially inappropriate medications (PIMs) for use in geriatric patients with delirium or at high risk for delirium and should be avoided in these patient populations due to the possibility of new-onset delirium or exacerbation of the current condition. The Beers expert panel notes that oral and parenteral corticosteroids may be required for conditions such as exacerbation of chronic obstructive pulmonary disease (COPD) but should be prescribed in the lowest effective dose and for the shortest possible duration. The federal Omnibus Budget Reconciliation Act (OBRA) regulates medication use in residents of long-term care facilities. According to the OBRA guidelines, the need for continued use of a glucocorticoid, with the exception of topical or inhaled formulations, should be documented, along with monitoring for and management of adverse consequences. Intermediate or longer-term use may cause hyperglycemia, psychosis, edema, insomnia, hypertension, osteoporosis, mood lability, or depression.

General dosing information for systemic therapy
-Dosage requirements are variable. Individualize doses based on the condition being treated and the response of the patient.
-Gradual withdrawal of prednisolone after high-dose or prolonged therapy is recommended due to the possibility of hypothalamic-pituitary-adrenal (HPA) axis suppression. The following recommendations for withdrawal of corticosteroids based on the duration of therapy have been made: less than 2 weeks-may abruptly discontinue; 2 to 4 weeks-taper dose over 1 to 2 weeks; more than 4 weeks-taper slowly over 1 to 2 months to physiologic dose (approximately 2.5 mg/m2/day of prednisolone) and discontinue after assessment of adrenal function has demonstrated recovery.

Estimated equivalent systemic Glucocorticoid dosages. These are general approximations and may not apply to all diseases or routes of administration.
Cortisone-25 mg
Hydrocortisone-20 mg
Prednisolone-5 mg
Prednisone-5 mg
Methylprednisolone-4 mg
Triamcinolone-4 mg
Dexamethasone-0.75 mg
Betamethasone-0.75 mg


General Instructions for Delayed-release prednisone tablets (e.g., Rayos)
Dosage for Rayos is in the range of 5 mg/day to 60 mg/day PO once daily. When deciding the administration time for the delayed-release tablets, consider the pharmacokinetics and the disease or condition being treated. Prednisone is released from the tablet beginning approximately 4 hours after intake of the first dose.

General Instructions for prednisone dose packs (e.g., Sterapred Uni-Pak, Sterapred DS Uni-Pak, and generic equivalents)
NOTE: While packages are typically labeled with the following instructions, the proper dosage tapers should be determined by decreasing the initial dosage in small decrements at appropriate time intervals. Dosage adjustments may be necessary for changes in clinical status (remissions or exacerbations in the disease process), the patient's individual drug responsiveness, and patient exposure to stressful situations; in the latter situation, it may be necessary to increase dosage for a period of time. Constant monitoring is needed in regard to drug dosage.

Adult Oral dosage (Sterapred 5 mg tablets or Sterapred-DS 10 mg tablets, 21-tablet dose pack):
Day 1: 2 tablets PO before breakfast, 1 tablet PO after lunch, 1 tablet PO after supper, and 2 tablets PO at bedtime.
Day 2: 1 tablet PO before breakfast. 1 tablet PO after lunch, 1 tablet PO after supper, and 2 tablets PO at bedtime.
Day 3: 1 tablet PO before breakfast, 1 tablet PO after lunch, 1 tablet PO after supper, and 1 tablet PO at bedtime.
Day 4: 1 tablet PO before breakfast, 1 tablet PO after lunch, and 1 tablet PO at bedtime.
Day 5: 1 tablet PO before breakfast, and 1 tablet PO at bedtime.
Day 6: 1 tablet PO before breakfast.

Adult Oral dosage (Sterapred 5 mg tablets or Sterapred-DS 10 mg tablets, 48-tablet dose pack):
Day 1 through 4: 2 tablets PO before breakfast, 1 tablet PO after lunch, 1 tablet PO after supper, and 2 tablets PO at bedtime.
Day 5 through 8: 1 tablet PO before breakfast. 1 tablet PO after lunch, 1 tablet PO after supper, and 1 tablet PO at bedtime.
Day 9 through 12: 1 tablet PO before breakfast, and 1 tablet PO at bedtime.

INVESTIGATIONAL USE: For adjunctive use in the treatment of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection*, the virus that causes coronavirus disease 2019 (COVID-19)*:
Oral dosage:
Adults: 40 mg PO daily for 7 to 10 days. The World Health Organization strongly recommends the use of systemic corticosteroids in patients with severe or critical COVID-19. The National Institutes of Health (NIH) COVID-19 treatment guidelines recommend prednisone as an alternative corticosteroid for hospitalized patients who require supplemental oxygen, including those on high-flow oxygen, noninvasive ventilation, mechanical ventilation, or extracorporeal membrane oxygenation (ECMO). The NIH recommends 40 mg PO once daily (or in 2 divided doses) for up to 10 days or until hospital discharge (whichever comes first). The NIH advises clinicians to review the patient's medical history and assess the potential risks and benefits before starting prednisone.

For primary adrenocortical insufficiency (Addison's disease, congenital adrenal hyperplasia, adrenogenital syndrome) or secondary adrenocortical insufficiency:
Oral dosage:
Adults: 5 mg PO in the morning and 2.5 mg PO in the evening. The literature reports a range of 5 to 7.5 mg/day for CAH maintenance in adults, given in 1 or more divided doses. Higher doses are needed in times of physiologic stress. NOTE: Hydrocortisone and cortisone are the preferred agents.
Adolescents and Children: Maintenance dose for Addison's disease: 1.5 to 3.5 mg/m2/day; usually given in 2 divided doses. Higher doses are needed in times of physicologic stress. The maintenance dosage for pediatric patients with CAH was 3 to 6.6 mg/m2/day PO in one study that compared prednisone to hydrocortisone. The preferred glucocorticoid for CAH in infants, children, and adolescents (until final height has been reached) is hydrocortisone, which minimizes the negative effects of treatment on growth.

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

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

For palliative management of acute lymphocytic leukemia (ALL):
Oral dosage:
Adults: 40 mg/m2 to 50 mg/m2 PO once daily indefinitely.

For the treatment of chronic lymphocytic leukemia (CLL):
-for the palliative treatment of CLL:
Oral dosage:
Adults: Multiple dosage regimens have been studied. Initial dosage may vary from 5 mg/day to 60 mg/day PO. Dosage requirements are variable though and should be individualized based on the response of the patient and tolerance to treatment. NOTE: Prednisone is approved for the palliative treatment of CLL; however, all components of combination regimens may not have been evaluated by the FDA for the treatment of CLL.
-for the first-line treatment of CLL, in combination with cladribine*:
Oral dosage:
Adults: 30 mg/m2 PO daily for 5 days in combination with cladribine 0.12 mg/kg/day IV over 2 hours for 5 days repeated every 28 days for up to 6 cycles has been studied in a randomized trial. NOTE: Prednisone is approved for the palliative treatment; however, all components of combination regimens may not have been evaluated by the FDA for the treatment of CLL.
-for the first-line treatment of CLL, in combination with chlorambucil*:
Oral dosage:
Adults: 80 mg PO once daily on Day 1, Day 2, Day 3, Day 4, and Day 5 in combination with chlorambucil 30 mg/m2 PO on Day 1 repeated every 2 weeks for up to 18 months and maximum response was evaluated in a randomized study. Alternatively, prednisone 30 mg/m2 PO daily for 7 days plus chlorambucil 12 mg/m2 PO daily for 7 days repeated every 28 days for up to 6 courses was used in another randomized study. NOTE: Prednisone is approved for the palliative treatment of CLL; however, all components of combination regimens may not have been evaluated by the FDA for the treatment of CLL.

For the short-term treatment of hypercalcemia secondary to neoplastic disease:
Oral dosage:
Adults: 50 mg/day to 100 mg/day PO for 3 to 5 days is usually effective for hypercalcemia due to hematologic cancers, lower doses may be effective for some tumors.

For the treatment of multiple myeloma*:
-for the palliative treatment of multiple myeloma in combination with melphalan*:
NOTE: Melphalan is FDA approved for the palliative treatment of multiple myeloma and has been studied in combination with prednisone.
Oral dosage:
Adults: 2 mg/kg orally daily for 4 days plus melphalan 0.25 mg/kg orally daily for 4 days repeated every 6 weeks has been studied. Treatment cycles may be repeated when the granulocyte and platelet counts returned to normal. Response may be gradual over several months.
-for newly diagnosed multiple myeloma in geriatric adults or transplant ineligible patients, in combination with melphalan and thalidomide*:
Oral dosage:
Geriatric Adults: The optimal dosage of melphalan and prednisone plus thalidomide has not been clearly established and dosages have varied in randomized controlled trials. In one study, previously untreated patients between 65 and 75 years of age received melphalan (0.25 mg/kg PO daily) for 4 days and prednisone 2 mg/kg PO once daily for 4 days, cycles were repeated every 6 weeks for 12 cycles plus thalidomide (200 mg/day PO for 2 to 4 weeks escalated up to a maximum dose of 400 mg/day PO if no severe adverse events; most patients received thalidomide 200 mg/day or less). Thalidomide was stopped after day 4 of the last cycle. In another study, patients aged 75 years and older received melphalan (0.2 mg/kg PO daily) for 4 days and prednisone 2 mg/kg PO once daily for 4 days and repeated every 6 weeks for 12 cycles plus thalidomide 100 mg/day PO at bedtime.
-for previously untreated multiple myeloma, in combination with melphalan and bortezomib*:
NOTE: Bortezomib is FDA approved in combination with melphalan and prednisone for use in previously untreated multiple myeloma.
Oral dosage:
Adults: 60 mg/m2 orally daily on days 1, 2, 3, and 4 and melphalan 9 mg/m2 orally daily on days 1, 2, 3, and 4 plus bortezomib repeated every 6 weeks for 9 cycles. In cycles 1 through 4, bortezomib 1.3 mg/m2 IV or subcutanously is given on days 1, 4, 8, and 11 followed by a 10-day rest period (days 12 through 21) and again on days 22, 25, 29, and 32 followed by a 10-day rest period (days 33 through 42); this 6-week cycle is considered one course. In cycles 5 to 9, bortezomib 1.3 mg/m2 IV or subcutanously is given on days 1, 8, 22, and 29; this 6-week cycle is considered one course.
-for the treatment of newly diagnosed multiple myeloma in patients ineligible for autologous stem-cell transplant, in combination with daratumumab, bortezomib, and melphalan*:
NOTE: Daratumumab is FDA approved in combination with bortezomib, melphalan, and prednisone for the treatment of newly diagnosed multiple myeloma in patients ineligible for autologous stem-cell transplant.
Oral dosage:
Adults: 60 mg/m2 orally daily on days 1, 2, 3, and 4; bortezomib 1.3 mg/m2 subcutaneously twice weekly on weeks 1, 2, 4, and 5 of cycle 1 followed by bortezomib 1.3 mg/m2 subcutaneously once weekly on weeks 1, 2, 4, and 5 of cycles 2 to 9; and melphalan 9 mg/m2 orally daily on days 1, 2, 3, and 4 (VMP regimen) repeated every 6 weeks for 9 cycles in combination with daratumumab was evaluated in a randomized, phase 3 trial. The manufacturer recommends the following daratumumab dosage in combination with VMP: 16 mg/kg (actual body weight) IV weekly on weeks 1 to 6, 16 mg/kg IV every 3 weeks on weeks 7 to 54, and then 16 mg/kg IV every 4 weeks starting on week 55 until disease progression. In the ALCYONE trial (median follow-up of 40.1 months), the primary endpoint of PFS time was significantly higher with daratumumab plus VMP compared VMP alone (36.4 months vs. 19.3 months; hazard ratio (HR) = 0.42; 95% CI, 0.34 to 0.51; p less than 0.0001) in adult patients (n = 706; median age, 71 years; range, 40 to 93 years) with multiple myeloma who were ineligible for high-dose chemotherapy with stem-cell transplant (SCT) due to coexisting conditions or age of 65 years or older and who had not received prior systemic therapy or SCT. At the time of this analysis, the median overall survival time was significantly improved in patients in the daratumumab plus VMP arm compared with the VMP alone arm (median time not reached in either arm; HR = 0.6; 95% CI, 0.46 to 0.8; p = 0.0003).
-for the treatment of newly diagnosed multiple myeloma in patients ineligible for autologous stem-cell transplant, in combination with daratumumab/hyaluronidase, bortezomib, and melphalan*:
NOTE: Daratumumab; hyaluronidase is FDA approved in combination with bortezomib, melphalan, and prednisone for the treatment of newly diagnosed multiple myeloma in patients ineligible for autologous stem-cell transplant.
Oral dosage:
Adults: 60 mg/m2 PO daily on days 1, 2, 3, and 4 repeated every 6 weeks on cycles 1 to 9; melphalan 9 mg/m2 PO daily on days 1, 2, 3, and 4 repeated every 6 weeks on cycles 1 to 9; bortezomib 1.3 mg/m2 subcutaneously twice weekly on weeks 1, 2, 4, and 5 for the first 6-week cycle (8 doses in cycle 1) followed by bortezomib 1.3 mg/m2 subcutaneously once weekly on weeks 1, 2, 4, and 5 for 8 more 6-week cycles (4 doses/cycle in cycles 2 to 9); and 1,800 mg daratumumab and 30,000 units hyaluronidase subcutaneously weekly on weeks 1 to 6 (6 doses), every 3 weeks on weeks 7 to 54 (16 doses), and then every 4 weeks starting on week 55 until disease progression was evaluated in a single-arm cohort (n = 67) of a multicohort, open-label trial (the PLEIADES trial). The overall response rate was 88% in patients with newly diagnosed multiple myeloma who were ineligible for transplant who received daratumumab/hyaluronidase, bortezomib, melphalan, and prednisone.
-for the treatment of newly diagnosed multiple myeloma in patients ineligible for autologous stem-cell transplant, in combination with carfilzomib and melphalan*:
Oral dosage:
Adults: Dosage not established. The progression-free survival time was not significantly improved with carfilzomib, melphalan, and prednisone compared with bortezomib, melphalan, and prednisone in a randomized, phase 3 trial (the CLARION trial); additionally, serious and fatal adverse reactions occurred more often in the carfilzomib-containing arm. There is not sufficient evidence to support the use of this drug combination for this indication.

For the treatment of inflammatory bowel disease, including Crohn's disease and ulcerative colitis:
-for the treatment of acute exacerbations of Crohn's disease:
Oral dosage:
Adults: 40 to 60 mg PO once daily for 1 to 2 weeks, initially. Taper dose by 5 mg/week until 20 mg PO once daily, and then taper dose by 2.5 to 5 mg/week; the taper should generally not exceed 3 months. Guidelines state that corticosteroids are not effective for maintenance of medically-induced remission in Crohn's disease and should not be used for long-term treatment. Corticosteroids for Crohn's disease are more effective for small-bowel involvement than for colonic involvement. Because of the potential complications of steroid use in this disease, steroids should be used selectively and in the lowest dose possible.
-for the treatment of ulcerative colitis:
Oral dosage:
Adults: 40 to 60 mg PO once daily, initially. Taper dose by 5 to 10 mg/week based on clinical symptoms, cumulative steroid exposure, and onset of action of alternate therapies; limit use to the shortest duration possible with early initiation of steroid-sparing therapy. Guidelines recommend oral corticosteroids to induce remission in persons with ulcerative colitis; however, guidelines recommend against systemic corticosteroids for the maintenance of remission.

For the treatment of serious manifestations of Behcet's syndrome*:
Oral dosage:
Adults: 1 mg/kg PO once daily is recommended.

For the treatment of juvenile rheumatoid arthritis (JRA)/juvenile idiopathic arthritis (JIA), ankylosing spondylitis, acute and subacute bursitis, acute non-specific tenosynovitis, acute gouty arthritis and gout, osteoarthritis, or epicondylitis:
Oral dosage:
Adults: Titrate to response. Usual dosage ranges from 5 to 30 mg PO once daily.
Children and Adolescents: 0.05 mg/kg/day to 2 mg/kg/day PO given in 1 to 4 divided doses.

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

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

For the treatment of selected cases of collagen disorders and mixed connective tissue disease*, such as acute rheumatic carditis, systemic dermatomyositis (polymyositis), systemic lupus erythematosus (SLE), temporal arteritis, Churg-Strauss syndrome*, polyarteritis nodosa, relapsing polychondritis, polymyalgia rheumatica, certain cases of vasculitis, or granulomatosis with polyangiitis*:
-for the treatment of unspecified collagen disorders and mixed connective tissue disease*:
Oral dosage:
Adults: 5 to 60 mg/day PO in 1 to 4 divided doses, depending upon disease being treated. Individualize dose and titrate to response. Initial doses needed may be high (60 mg/day or more). After symptoms controlled, decrease dose slowly every 5 to 7 days. Maintenance doses for chronic conditions are usually 10 to 20 mg PO once daily or 20 mg to 40 mg PO every other day.
Infants, Children, and Adolescents: 0.05 mg/kg/day to 2 mg/kg/day PO in 1 to 4 divided doses. Individualize dose and titrate to response.
-for the treatment of systemic lupus erythematosus (SLE):
Oral dosage:
Adults: Doses for the various manifestations of SLE vary widely. Initially 20 mg to 40 mg/day PO for moderate illness and 60 mg to 100 mg/day PO for severe illness; some patients may require higher doses, such as 200 to 300 mg/day PO in divided doses. After the disease is controlled, reduce the dose by 10% every 5 to 7 days; a more rapid reduction may result in relapse. Maintenance doses are usually 10 to 20 mg PO once daily or 20 to 40 mg PO every other day.
-for the treatment of dermatomyositis or polymyositis:
Oral dosage:
Adults: 0.5 to 1 mg/kg/dose (Max: 100 mg/dose) PO once daily for at least 4 weeks, then taper dose over 6 to 12 weeks to the lowest dose that sustains remission. Depending on disease severity, lower doses may be used.
Infants, Children, and Adolescents: 1 to 2 mg/kg/dose (Max: 60 mg/dose) PO once daily for at least 4 weeks, then taper dose over 12 to 24 months to the lowest dose that sustains remission.

For the treatment of autoimmune hepatitis*:
-for the treatment of autoimmune hepatitis* as monotherapy:
Oral dosage:
Adults: 40 to 60 mg PO once daily, initially. When biochemical remission is achieved, taper dose by 2.5 to 5 mg/day every 2 to 4 weeks over 6 months to 5 to 10 mg/day or the lowest dose to maintain remission. Guidelines recommend prednisone monotherapy for persons with acute severe autoimmune hepatitis (AIH) followed by liver transplantation if no improvement within 2 weeks. Addition of azathioprine may be considered after cholestasis is resolved.
Infants, Children, Adolescents: 1 to 2 mg/kg/dose (Max: 40 to 60 mg/dose) PO once daily, initially. When biochemical remission is achieved, taper dose by 2.5 to 5 mg/day every 2 to 4 weeks over 6 months to 2.5 to 10 mg/day or the lowest dose to maintain remission. Guidelines recommend prednisone monotherapy for persons with acute severe autoimmune hepatitis (AIH) followed by liver transplantation if no improvement within 2 weeks. Addition of azathioprine may be considered after cholestasis is resolved.
-for the treatment of autoimmune hepatitis* in combination with azathioprine:
Oral dosage:
Adults: 20 to 40 mg PO once daily, initially. When biochemical remission is achieved, taper dose by 2.5 to 5 mg/day every 2 to 4 weeks over 6 months to 5 to 10 mg/day or the lowest dose to maintain remission. Guidelines recommend prednisone in combination with azathioprine as first-line therapy in adults who present with autoimmune hepatitis (AIH) who do not have cirrhosis, acute severe AIH, or acute liver failure. Add azathioprine after 2 weeks in persons with compensated cirrhosis. May attempt steroid withdrawal while continuing azathioprine.
Infants, Children, Adolescents: 1 to 2 mg/kg/dose (Max: 20 to 40 mg/dose) PO once daily, initially. When biochemical remission is achieved, taper dose by 2.5 to 5 mg/day every 2 to 4 weeks over 6 months to 2.5 to 10 mg/day or the lowest dose to maintain remission. Guidelines recommend prednisone in combination with azathioprine as first-line therapy in children who present with autoimmune hepatitis (AIH) who do not have cirrhosis, acute severe AIH, or acute liver failure. Add azathioprine after 2 weeks in persons with compensated cirrhosis. May attempt steroid withdrawal while continuing azathioprine.

For the treatment of primary amyloidosis* not associated with familial Mediterranean fever:
Oral dosage:
Adults: 0.8 mg/kg PO once daily for 7 days, in combination with melphalan; repeated every 6 weeks. The treatment combination demonstrated superior results over colchicine alone in the treatment of primary amyloidosis.

For the treatment of systemic autoimmune conditions such as acquired hemolytic anemia, congenital hypoplastic anemia, or symptomatic sarcoidosis:
Oral dosage:
Adults: Titrate to response. Usual dosage ranges from 5 mg to 30 mg PO once daily.

For asthma exacerbation:
-for inpatient management:
Oral dosage:
Adults: One recommendation is 40 to 50 mg/day or 1 mg/kg/day for 5 to 7 days; Max: 50 mg/day. Another recommendation is 40 to 80 mg/day PO given in 1 to 2 divided doses until the peak expiratory flow (PEF) reaches 70% of predicted or personal best. Total course of treatment may range from 3 to 10 days.
Children and Adolescents 12 to 17 years: One recommendation is 40 to 50 mg/day or 1 mg/kg/day for 5 to 7 days; Max: 50 mg/day. Another recommendation is 40 to 80 mg/day PO given in 1 to 2 divided doses until the peak expiratory flow (PEF) reaches 70% of predicted or personal best. Total course of treatment may range from 3 to 10 days.
Infants and Children 1 month to 11 years: 1 to 2 mg/kg/day PO in 1 to 2 divided doses for 3 to 10 days (usually 5 days). Max: 60 mg/day. A dose of 1 mg/kg/day has been shown to be just as effective as a dose of 2 mg/kg/day with fewer adverse effects, and this dose may be preferable. Continue until peak expiratory flow is 70% of predicted or personal best. Suggested age-based Max: 20 mg/day for children less than 2 years, 30 mg/day for children 3 to 5 years, and 40 mg/day for children 6 to 11 years.
-for outpatient management:
Oral dosage:
Adults: 40 to 60 mg/day PO given in 1 to 2 divided doses for 3 to 10 days or until the patient achieves peak expiratory flow (PEF) of 80% of personal best or symptoms resolve. Another recommendation is 40 to 50 mg/day usually for 5 to 7 days (or 1 mg/kg/day); Max: 50 mg/day.
Children and Adolescents 12 to 17 years: 40 to 60 mg/day PO given in 1 to 2 divided doses for 3 to 10 days or until patient achieves peak expiratory flow (PEF) of 80% of personal best or symptoms resolve. Another recommendation is 40 to 50 mg/day usually for 5 to 7 days (or 1 mg/kg/day); Max: 50 mg/day.
Infants and Children less than 12 years: 1 to 2 mg/kg/day PO in 1 or 2 divided doses for 3 to 10 days (usually 5 days) or until the patient achieves peak expiratory flow (PEF) of 80% of personal best or symptoms resolve. Max: 60 mg/day. A dose of 1 mg/kg/day is as effective as a dose of 2 mg/kg/day with fewer adverse effects, and this dose may be preferable. Suggested age-based Max: 20 mg/day for children less than 2 years, 30 mg/day for children 3 to 5 years, and 40 mg/day for children 6 to 11 years.

For asthma maintenance treatment in patients with severe, persistent asthma:
Oral dosage:
Adults: 7.5 to 60 mg/day PO administered once daily in the morning or every other day as needed for symptom control; use lowest effective dose; alternate day therapy may produce less adrenal suppression. Dosing in the afternoon at 3:00 PM may be helpful for patients prone to nocturnal symptoms, with no increase in adrenal suppression. Consider add-on low dose oral corticosteroids (CS) (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 CS only after exclusion of other contributory factors and consideration of other add-on treatments.
Children and Adolescents 12 to 17 years: 7.5 to 60 mg/day PO given once daily in the morning or every other day as needed for symptom control; use lowest effective dose; alternate day therapy may produce less adrenal suppression. In pediatric patients, the use of oral corticosteroids is usually limited to a few weeks until asthma control is improved and the patient can be stabilized on other, preferred treatments.
Infants and Children less than 12 years: 0.25 to 2 mg/kg/day PO administered once daily in the morning or every other day as needed for symptom control; use lowest effective dose; alternate day therapy may produce less adrenal suppression. Max: 60 mg/day. Usual age-based Max: 20 mg/day for children less than 2 years of age; 30 mg/day for children 3 to 5 years; 40 mg/day for children 6 to 11 years. In pediatric patients, the use of oral corticosteroids is usually limited to a few weeks until asthma control is improved and the patient can be stabilized on other, preferred treatments.

For the treatment of thrombocytopenia or immune thrombocytopenic purpura (ITP):
-in patients with chronic immune thrombocytopenic purpura (ITP):
Oral dosage:
Adults: Initially, 1 mg/kg PO once daily; however, lower doses of 5 mg/day to 10 mg/day PO are preferable for long-term treatment.
-for autoimmune thrombocytopenia associated with SLE:
Oral dosage:
Adults, Adolescents, and Children: 0.25 mg/kg/day PO was as effective as higher doses of 1 mg/kg/day.

For the treatment of exacerbations of chronic obstructive pulmonary disease (COPD):
Oral dosage:
Adults: 40 mg PO once daily for 5 days is the most commonly recommended regimen. A multicenter, randomized, controlled trial confirmed that this shorter duration of low dose prednisone is equivalent to using 40 mg of prednisone for a longer duration (i.e., 14 days). The use of systemic steroids for no more than 5 to 7 days is recommended by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines. Data from studies indicate that systemic glucocorticoids shorten recovery time; improve lung function (FEV-1), improve oxygenation, and reduce the risk of early relapse, treatment failure, and the length of hospitalization.

For the treatment of myasthenia gravis in patients who are poorly controlled with cholinesterase inhibitor therapy:
Oral dosage:
Adults: Initially, 15 mg/day to 20 mg/day PO. Increase by 5 mg every 2 to 3 days as needed. Maximum: 60 mg/day PO. For chronic use, may change to every other day therapy.

For the treatment of acute or recurrent pericarditis*:
-for the treatment of acute pericarditis:
Oral dosage:
Adults: 0.2 to 0.5 mg/kg/dose PO once daily for 2 to 4 weeks in combination with colchicine in cases of contraindication or incomplete response to aspirin/NSAID, and when an infectious cause has been excluded, or when there is a specific indication such as autoimmune disease. Taper dose over at least 6 weeks.
-for the treatment of recurrent pericarditis*:
Oral dosage:
Adults: 0.2 to 0.5 mg/kg/dose PO once daily for 2 to 4 weeks in combination with aspirin/NSAID and colchicine in cases of incomplete response to aspirin/NSAID, and when an infectious cause has been excluded; limit to patients with specific indications, such as systemic inflammatory diseases, post-pericardiotomy syndromes, or pregnancy, or NSAID contraindications. Taper dose over at least 6 weeks.

For the treatment of psoriatic arthritis or severe plaque psoriasis:
Oral dosage:
Adults: Titrate to response. Usual dosage ranges from 5 to 30 mg PO once daily. Use the lowest effective dose (usually less than 7.5 mg/day, per guidelines). Usual Max: 60 mg/day PO. Guidelines for psoriasis/psoriatic arthritis recommend short-term use (avoid long-term use) of systemic corticosteroids for acute relief of symptoms/flares with caution; local corticosteroid injections are often preferable for oligoarthritis, dactylitis or in enthesitis.

For the treatment of proteinuria in nephrotic syndrome, without uremia, of the idiopathic type or due to lupus nephritis:
Oral dosage:
Adults: 40 mg/day to 80 mg/day PO until urine is protein-free; slowly taper as indicated. Some patients may require long-term therapy.
Children and Adolescents: 2 mg/kg/day or 60 mg/m2/day (Maximum: 80 mg) PO once daily until urine is protein-free for 3 consecutive days. Then 1 mg/kg to 1.5 mg/kg or 40 mg/m2 PO every other day for 4 weeks. If needed, the long-term maintenance dose is 0.5 to 1 mg/kg PO every other day for 3 to 6 months.
-for the treatment of lupus nephritis:
Oral dosage:
Adults: American College of Rheumatology guidelines recommend 0.5 to 1 mg/kg/day PO (the higher dose is recommended if crescents seen) after induction therapy with methylprednisolone (500 to 1,000 mg/day IV for 3 doses) and other induction drugs. Taper the dose after a few weeks to the lowest effective dose that maintains control. Insufficient data exist to recommend a specific steroid taper because nephritis and extrarenal manifestations vary from patient to patient. Prednisone up to 10 mg/day has been used long term for maintenance, along with other medications.

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

For the treatment of severe erythema multiforme or Stevens-Johnson syndrome:
Oral dosage:
Adults: In patients with severe skin reactions, higher initial doses (e.g., 60 mg/day PO) are usually required. Adjust until a satisfactory response is noted; taper as clinically indicated. High-dose corticosteroids are controversial; administration has been associated with decreased survival. Prednisone doses of 60 mg/day to 250 mg/day PO are equivalent to the recommended hydrocortisone doses of 240 mg/day to 1,000 mg/day.

For the treatment of corticosteroid-responsive dermatoses and dermatologic disorders such as atopic dermatitis or eczema, bullous dermatitis herpetiformis, contact dermatitis, exfoliative dermatitis, mycosis fungoides, pemphigus, or severe seborrheic dermatitis:
Oral dosage:
Adults: 5 to 60 mg PO once daily, initially. Adjust dose to achieve a satisfactory response, and then reduce dose by small increments to lowest dose that will maintain an adequate response. Taper long-term therapy gradually when discontinuing.
Infants, Children, and Adolescents: 0.14 to 2 mg/kg/dose PO once daily, initially. Adjust dose to achieve a satisfactory response, and then reduce dose by small increments to lowest dose that will maintain an adequate response. Taper long-term therapy gradually when discontinuing.

For the treatment of ACE-inhibitor induced angioedema once acute symptoms are controlled:
Oral dosage:
Adults: Short courses of 30 to 50 mg/day PO can be given during the late phase of an acute reaction, once oral therapy is appropriate. FDA-approved dosage: 5 to 60 mg/day PO, depending on disease severity for angioedema; taper as clinically indicated.

For the treatment of allergic disorders including anaphylaxis or anaphylactoid reactions, angioedema, acute noninfectious laryngeal edema, hypersensitivity reactions (e.g., drug or food allergy), serum sickness, urticaria, or severe perennial allergies or seasonal allergies, including allergic rhinitis:
Oral dosage:
Adults: 5 to 60 mg/day PO day initially, depending on the specific disease entity and the severity of the condition being treated. Use lowest effective dose. Corticosteroids are not indicated as initial treatment for anaphylaxis, but can be given as adjunctive therapy after the administration of epinephrine.
Infants, Children, and Adolescents: 1 to 2 mg/kg/day PO (Max: 60 mg/day) in 1 to 4 divided doses for acute control. Treatment duration dependent on specific allergic/hypersensitivity condition, but is usually 2 to 3 weeks. May follow with subsequent treatment with 1 to 2 mg/kg/day (Max: 60 mg/day) PO in 1 to 4 divided doses for 1 to 2 weeks until symptomatic control, then conversion to alternate-day treatment of 1 to 2 mg/kg/day, with tapering by no more than 5 to 10 mg per month. Corticosteroids are not indicated as initial treatment for anaphylaxis, but can be given as adjunctive therapy after the administration of epinephrine.

For the treatment of the acute respiratory distress syndrome (ARDS):
Oral dosage:
Adults: Corticosteroid use in ARDS is controversial. If there are no signs of improvement 7 to 14 days after ARDS onset, 2 mg/kg/day to 4 mg/kg/day PO for 7 to 14 days has been recommended.

For the treatment of idiopathic pulmonary fibrosis:
Oral dosage:
Adults: The initial dosage may vary from 5 to 60 mg PO per day. Guidelines use a dose of 0.5 mg/kg/day PO for 4 weeks, then 0.25 mg/kg/day PO for 8 weeks. Taper to 0.125 mg/kg/day or 0.25 mg/kg/day PO on alternate days. Guidelines suggest use of prednisone with cyclophosphamide or azathioprine, and a minimum of 6 months duration. Objective responses may not be noted until at least 3 months of therapy. Exact duration of treatment and need for long-term maintenance should be individualized to clinical response and tolerance of therapy. Chronic doses of prednisone (15 mg to 20 mg PO once daily) may be adequate as maintenance therapy.

For treatment of idiopathic eosinophilic pneumonia or aspiration or hypersensitivity pneumonitis:
Oral dosage:
Adults: The initial dosage may vary from 5 to 60 mg PO per day. Gradually taper after 1 to 2 weeks and discontinue by 4 to 6 weeks, guided by symptoms.
Children and Adolescents: The initial dosage may vary from 5 to 60 mg PO per day. Weight-based dosing: 0.14 mg/kg to 2 mg/kg (4 to 60 mg/m2) PO daily, given in 1 to 4 divided doses. Gradually taper after 1 to 2 weeks and discontinue by 4 to 6 weeks, as guided by symptoms.

For use as an adjunct in the management of extradural malignant spinal cord compression* (MSCC*) associated with metastatic disease:
Oral dosage:
Adults: A range of 40 mg/day to 80 mg/day PO is suggested. Higher quality data are needed to establish the benefits vs. risks and optimal dose and duration of therapy. Experts generally agree that patients who have neurologic deficits should receive a corticosteroid; many patients with MSCC require corticosteroids to help preserve neurologic function, such as ambulation.

For the treatment of Hodgkin lymphoma in combination with antineoplastic agents:
-in combination with mechlorethamine, vincristine, vinblastine, and procarbazine (MVVPP regimen):
Oral dosage:
Adults: 40 mg/m2/day PO on Day 1 through Day 22, then taper. Chemotherapy cycle is repeated every 57 days.
-in combination with mechlorethamine, vincristine, procarbazine, doxorubicin, bleomycin, and vinblastine (MOPP/APB regimen):
Oral dosage:
Adults: 40 mg/m2/day PO on Day 1 through Day 14; cycle is repeated every 28 days.
-for the treatment of previously untreated, high-risk classical Hodgkin lymphoma, in combination with brentuximab vedotin, doxorubicin, vincristine, etoposide, and cyclophosphamide:
NOTE: Brentuximab vedotin is FDA approved for this indication.
Oral dosage:
Children 2 years and older and Adolescents: 20 mg/m2 orally twice daily on days 1 to 7 in combination with brentuximab vedotin 1.8 mg/kg (not to exceed 180 mg/dose) IV on day 1; doxorubicin 25 mg/m2 IV on days 1 and 2; vincristine 1.4 mg/m2 IV on day 8; etoposide 125 mg/m2 IV on days 1, 2, and 3; and cyclophosphamide 600 mg/m2 IV on days 1 and 2 repeated every 3 weeks for up to 5 cycles. Administer primary prophylaxis with a granulocyte colony-stimulating factor starting in cycle 1 due to the high incidence of febrile neutropenia. At a median follow-up time of 42.1 (range, 0.1 to 80.9) months, the 3-year event-free survival rate was significantly improved in patients (median age, 15.6 years; range, 3.4 to 21.99 years) with newly diagnosed, stage IIB with bulk tumor or stage IIIB, IVA, or IVB classic Hodgkin lymphoma who received brentuximab vedotin plus AVEPC compared with doxorubicin, bleomycin, vincristine, etoposide, prednisone, and cyclophosphamide (ABVE-PC) (92.1% vs. 82.5%; hazard ratio = 0.41; 95% CI, 0.25 to 0.67) in a multicenter, randomized, phase 3 trial (n = 587). The 3-year overall survival rates were 99.3% and 98.5% in the brentuximab vedotin plus AVEPC and ABVE-PC arms, respectively.

For the systemic treatment of ophthalmic inflammatory conditions such as endophthalmitis*, optic neuritis, allergic conjunctivitis, keratitis, allergic corneal ulcer, iritis, chorioretinitis, anterior segment inflammation, uveitis, choroiditis, or sympathetic ophthalmia:
Oral dosage:
Adults: 5 to 60 mg/day PO administered in 1 to 4 divided doses, depending upon disease being treated. Topically applied corticosteroids are as effective as systemic corticosteroids for anterior ocular inflammation.
Infants, Children, and Adolescents: 0.14 to 2 mg/kg/day PO in 1 to 4 divided doses is the general initial dose range for prednisone (dose equivalent to prednisolone). Topically applied corticosteroids are as effective as systemic corticosteroids for anterior ocular inflammation.

For the treatment of Loeffler's syndrome, berylliosis, erythroblastopenia, or trichinosis:
Oral dosage:
Adults: 5 mg to 60 mg PO per day, administered in 1 to 4 divided doses, depending upon disease being treated. Depending on the indication, the initial dose may be gradually tapered after 1 to 2 weeks and discontinued by 4 to 6 weeks, as guided by symptoms.
Adolescents and Children: 0.14 to 2 mg/kg/day PO or 4 to 60 mg/m2/day PO, given in 4 divided doses. Depending on indication, gradually taper the initial dose after 1 to 2 weeks and discontinue by 4 to 6 weeks, guided by symptoms.

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

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

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

For the treatment of heart transplant rejection*:
Oral dosage:
Adults: Guidelines recommend 1 mg/kg/day to 3 mg/kg/day PO for 3 to 5 days for asymptomatic mild or moderate acute cellular rejection (ISHLT 1R or 2R). A corticosteroid taper may be considered. Not first-line for symptomatic rejection (ISHLT 1R, 2R, or 3R) or for asymptomatic severe rejection (ISHLT 3R).

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

For adjunct therapy in patients with chorioretinitis associated with congenital toxoplasmosis*:
Oral dosage:
Infants and Children: 0.5 mg/kg/dose PO twice daily (Max: 20 mg/dose) with rapid taper in combination with pyrimethamine, sulfadiazine, and leucovorin is recommended for patients with severe chorioretinitis by the American Academy of Pediatrics (AAP) guidelines.
Neonates: 0.5 mg/kg/dose PO twice daily in combination with pyrimethamine, sulfadiazine, and leucovorin is recommended for patients with CSF protein 1 g/dL or more or severe chorioretinitis in vision-threatening macular area. Initiate prednisone after 72 hours of anti-Toxoplasma therapy and continue until CSF protein is less than 1 g/dL or resolution of severe chorioretinitis.

For adjunct therapy in patients with Mycobacterium avium complex infection* (MAC) experiencing moderate to severe immune reconstitution inflammatory syndrome (IRIS):
Oral dosage:
Adults: 20 to 40 mg PO once daily for 4 to 8 weeks can be considered for patients with moderate to severe immune reconstitution inflammatory syndrome (IRIS).

For the treatment of peripheral T-cell lymphoma (PTCL)*:
-for the first-line treatment of PTCL in combination with gemcitabine, cisplatin, and thalidomide*:
Oral dosage:
Adults and Adolescents 14 years and older: 60 mg/m2 orally on days 1, 2, 3, 4, and 5 in combination with gemcitabine (800 mg/m2 IV over 30 minutes on days 1 and 8), cisplatin (25 mg/m2 IV on days 1, 2, and 3), and thalidomide (200 mg orally daily) repeated every 21 days until disease progression or for up to 6 cycles was evaluated in patients with previously untreated PTCL in a randomized trial. Patients received aspirin 100 mg orally daily during thalidomide therapy. The use of granulocyte colony-stimulation factor was permitted as indicated.
-for the treatment of previously untreated CD30-expressing PTCL, in combination with brentuximab vedotin, cyclophosphamide, and doxorubicin*:
NOTE: Brentuximab vedotin is FDA approved in combination with cyclophosphamide, doxorubicin, and prednisone for this indication.
Oral dosage:
Adults: 100 mg orally daily on days 1, 2, 3, 4, and 5 in combination with brentuximab vedotin 1.8 mg/kg (not to exceed 180 mg/dose) IV on day 1, cyclophosphamide 750 mg/m2 IV on day 1, and doxorubicin 50 mg/m2 IV on day 1 given every 21 days for 6 to 8 cycles of therapy. The progression-free survival time (evaluated via an independent review facility) was significantly improved in patients with CD30-expressing systemic anaplastic large-cell lymphoma (sALCL) or PTCL who received brentuximab vedotin plus cyclophosphamide, doxorubicin, and prednisone (CHP) compared with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) (48.2 months vs. 20.8 months; hazard ratio (HR) = 0.71; 95% CI, 0.54 to 0.93) in a multicenter, randomized, double-blind, phase 3 trial (the ECHELON-2 trial; n = 452). Overall survival was also significantly improved in the brentuximab vedotin-containing arm (HR = 0.66; 95% CI, 0.46 to 0.95). In this trial, 70% of patients had sALCL and 30% of patients had PTCL (e.g., including PTCL not otherwise specified (16%), angioimmunoblastic T-cell lymphoma (12%), adult T-cell leukemia/lymphoma (2%), and enteropathy-associated T-cell lymphoma (less than 1%)).

For the treatment of Kawasaki disease*:
Oral dosage:
Infants, Children, and Adolescents: 2 mg/kg/day PO in 3 divided doses until CRP is normalized, then taper over 2 to 3 weeks. This regimen, administered after an initial course of IV steroids that is continued until the patient is afebrile and concurrently with IVIG (2 grams/kg IV once) and aspirin, may be considered for primary treatment of high-risk patients with acute disease or in the retreatment of patients who have recurrent or recrudescent fever after initial IVIG treatment.

For the treatment of systemic anaplastic large-cell lymphoma (sALCL)*:
-for the treatment of previously untreated sALCL, in combination with brentuximab vedotin, cyclophosphamide, and doxorubicin*:
NOTE: Brentuximab vedotin is FDA approved in combination with cyclophosphamide, doxorubicin, and prednisone for this indication.
Oral dosage:
Adults: 100 mg orally daily on days 1, 2, 3, 4, and 5 in combination with brentuximab vedotin 1.8 mg/kg (not to exceed 180 mg/dose) IV on day 1, cyclophosphamide 750 mg/m2 IV on day 1, and doxorubicin 50 mg/m2 IV on day 1 given every 21 days for 6 to 8 cycles of therapy. The progression-free survival (PFS) time (evaluated via an independent review facility) was significantly improved in patients with CD30-expressing sALCL or peripheral T-cell lymphoma who received brentuximab vedotin plus cyclophosphamide, doxorubicin, and prednisone (CHP) compared with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) (48.2 months vs. 20.8 months; hazard ratio (HR) = 0.71; 95% CI, 0.54 to 0.93) in a multicenter, randomized, double-blind, phase 3 trial (the ECHELON-2 trial; n = 452). Overall survival was also significantly improved in the brentuximab vedotin-containing arm (HR = 0.66; 95% CI, 0.46 to 0.95). In patients with sALCL (n = 314; anaplastic lymphoma kinase (ALK)-negative sALCL, 48%; ALK-positive sALCL, 22%), the PFS times were 55.7 months and 54.2 months in patients who received brentuximab vedotin plus CHP and CHOP, respectively (HR = 0.59; 95% CI, 0.42 to 0.84).

For the treatment of Pneumocystis pneumonia (PCP)*:
Oral dosage:
Adults: 40 to 60 mg PO 2 to 3 times daily; taper dose after 5 to 7 days over 1 to 2 weeks. A suggested taper is 40 mg PO twice daily on days 1 to 5; then 40 mg PO once daily on days 6 to 10; then 20 mg PO once daily on days 11 to 21. Start therapy as early as possible and within 72 hours after starting specific PCP therapy. Recommended for patients with moderate to severe infection, defined by a PaO2 less than 70 mmHg at room air or an alveolar-arterial DO2 gradient of 35 mmHg or more. The benefits of starting corticosteroids after 72 hours are unclear.
Adolescents: 40 to 60 mg PO 2 to 3 times daily; taper dose after 5 to 7 days over 1 to 2 weeks. A suggested taper is 40 mg PO twice daily on days 1 to 5; then 40 mg PO once daily on days 6 to 10; then 20 mg PO once daily on days 11 to 21. Start therapy as early as possible and within 72 hours after starting specific PCP therapy. Recommended for patients with moderate to severe infection, defined by a PaO2 less than 70 mmHg at room air or an alveolar-arterial DO2 gradient of 35 mmHg or more. The benefits of starting corticosteroids after 72 hours are unclear.
Infants and Children: 1 mg/kg/dose PO twice daily on days 1 to 5; then 0.5 to 1 mg/kg/dose PO twice daily on days 6 to 10; then 0.5 mg/kg/dose PO once daily on days 11 to 21. Start therapy as early as possible and within 72 hours after starting specific PCP therapy. Recommended for patients with moderate to severe infection, defined by a PaO2 less than 70 mmHg at room air or an alveolar-arterial DO2 gradient more than 35 mmHg.

For the treatment of drug-susceptible tuberculosis infection or drug-resistant tuberculosis infection as adjunctive therapy in combination with antituberculous therapy:
Oral dosage:
Adults: 2.67 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.
Infants, Children, and Adolescents: 2 to 4 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.

For the treatment of aggressive lymphomas, including aggressive non-Hodgkin's lymphoma (NHL):
-for the treatment of previously untreated diffuse large B-cell lymphoma (not otherwise specified) or high-grade B-cell lymphoma in patients who have an International Prognostic Index score of 2 or greater, in combination with polatuzumab vedotin, rituximab, cyclophosphamide, and doxorubicin*:
NOTE: Polatuzumab vedotin is FDA approved in combination with rituximab, cyclophosphamide, doxorubicin, and prednisone for this indication.
Oral dosage:
Adults: 100 mg orally daily on days 1, 2, 3, 4, and 5 in combination with polatuzumab vedotin 1.8 mg/kg IV, rituximab 375 mg/m2 IV, cyclophosphamide 750 mg/m2 IV, and doxorubicin 50 mg/m2 IV on day 1 repeated every 21 days for 6 cycles has been evaluated in a randomized, double-blind, placebo-controlled, phase 3 trial (n = 879; the POLARIX trial). Rituximab 375 mg/m2 IV was continued for 2 additional cycles of therapy (cycles 7 and 8).

For the treatment of pharyngitis*:
Oral dosage:
Adults: 60 mg PO once daily for 1 to 2 days.
Children and Adolescents 5 to 17 years: 2 mg/kg/dose (Max: 60 mg/dose) PO once daily for 1 to 2 days.

For the treatment of cellulitis* in nondiabetic persons:
Oral dosage:
Adults: 40 mg PO once daily for 7 days.

For the treatment of e-cigarette or vaping product use-associated lung injury*:
Oral dosage:
Adults: 40 to 60 mg PO once daily, initially, followed by a taper such as 20 mg PO once daily for 1 week, then 10 mg PO once daily for 1 week; base length of steroid taper on patient's clinical course of recovery and close follow-up.
Adolescents: 40 to 60 mg PO once daily, initially, followed by a taper such as 20 mg PO once daily for 1 week, then 10 mg PO once daily for 1 week; base length of steroid taper on patient's clinical course of recovery and close follow-up.

For the treatment of encephalitis*:
-for the treatment of viral encephalitis* as adjunctive therapy:
Oral dosage:
Adults: 1 mg/kg/dose (Max: 60 to 80 mg/dose) PO once daily for 3 to 5 days.
Infants, Children, and Adolescents: 1 mg/kg/dose (Max: 60 to 80 mg/dose) PO once daily for 3 to 5 days.
-for the treatment of immune-mediated encephalitis* as step-down therapy:
Oral dosage:
Adults: 0.5 to 2 mg/kg/dose (Max: 60 mg/dose) PO once daily, followed by an extended taper over up to 12 months.
Infants, Children, and Adolescents: 0.5 to 2 mg/kg/dose (Max: 60 mg/dose) PO once daily, followed by an extended taper over up to 12 months.

For the treatment of thyroiditis:
-for the treatment of subacute thyroiditis:
Oral dosage:
Adults: 40 mg PO once daily for 1 to 2 weeks, followed by a gradual taper over 2 to 4 weeks or more depending on clinical response. The FDA-approved dosage is 5 to 60 mg/day.
-for the treatment of amiodarone-induced thyroiditis:
Oral dosage:
Adults: 40 mg PO once daily for 2 to 4 weeks, followed by a gradual taper over 2 to 3 months depending on clinical response. The FDA-approved dosage is 5 to 60 mg/day.

For the treatment of rheumatoid arthritis:
Oral dosage:
Adults: 5 to 10 mg PO once daily, initially. Taper dose to the lowest effective dose. Doses more than 10 mg/day are rarely indicated.

For the treatment of complex regional pain syndrome*:
Oral dosage:
Adults: 10 mg PO 3 times daily for up to 12 weeks, followed by a taper.

For the treatment of complications associated with infectious mononucleosis* secondary to Epstein-Barr virus infection*:
Oral dosage:
Adults: 60 to 80 mg/day PO administered in two divided doses and tapered over 1 to 2 weeks has been used to treat complications including airway obstruction due to tonsillar enlargement; autoimmune hemolytic anemia, severe thrombocytopenia, and aplastic anemia; CNS involvement; myocarditis; and pericarditis.

For the treatment of alcohol-associated hepatitis*:
Oral dosage:
Adults: 40 mg PO once daily in persons with severe alcohol-associated hepatitis (Maddrey discriminant function [MDF] of 32 or more; model for end-stage liver disease [MELD] score more than 20) to improve 28-day mortality.

Maximum Dosage Limits:
Corticosteroid dosage must be individualized and is highly variable depending on the nature and severity of the disease, and on patient response. There is no absolute maximum dosage.

Patients with Hepatic Impairment Dosing
Prednisone is a prodrug and bioactivation to prednisolone occurs in the liver, but even in severe hepatic disease this bioactivation appears to be nearly complete. No specific dosage adjustment appears to be necessary in patients with hepatic disease. The use of prednisolone instead of prednisone has been preferred historically for patients with severe hepatic impairment, but most pharmacokinetic data suggest there is no basis for this preference. Doses are equivalent (i.e., 1 mg prednisone is equivalent to 1 mg of prednisolone).

Patients with Renal Impairment Dosing
Specific guidelines for dosage adjustments in renal impairment are not available; it appears that no dosage adjustments are needed.

*non-FDA-approved indication

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; Dextromethorphan; Guaifenesin; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.

Acetaminophen; Dextromethorphan; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.

Acetaminophen; Guaifenesin; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.

Acetazolamide: (Moderate) Corticosteroids may increase the risk of hypokalemia if used concurrently with acetazolamide. Hypokalemia may be especially severe with prolonged use of corticotropin, ACTH. Monitor serum potassium levels to determine the need for potassium supplementation and/or alteration in drug therapy.

Acetohexamide: (Moderate) Monitor blood glucose during concomitant corticosteroid and sulfonylurea use; a sulfonylurea dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells.

Adagrasib: (Moderate) Monitor for corticosteroid-related adverse events if prednisone is used with adagrasib. Concurrent use may increase the exposure of prednisone. Prednisone is a CYP3A substrate and adagrasib is a strong CYP3A inhibitor. Other strong CYP3A inhibitors have been reported to decrease the metabolism of certain corticosteroids by up to 60%.

Albiglutide: (Moderate) Monitor blood glucose during concomitant corticosteroid and incretin mimetic use; an incretin mimetic dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells.

Aldesleukin, IL-2: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.

Alemtuzumab: (Moderate) Concomitant use of alemtuzumab with immunosuppressant doses of corticosteroids may increase the risk of immunosuppression. Monitor patients carefully for signs and symptoms of infection.

Aliskiren; Hydrochlorothiazide, HCTZ: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.

Alogliptin; Metformin: (Moderate) Monitor blood glucose during concomitant corticosteroid and metformin use; a metformin dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells.

Alpha-glucosidase Inhibitors: (Moderate) Monitor patients receiving antidiabetic agents closely for worsening glycemic control when corticosteroids are instituted and for signs of hypoglycemia when corticosteroids are discontinued. Systemic and inhaled corticosteroids are known to increase blood glucose and worsen glycemic control in patients taking antidiabetic agents. The main risk factors for impaired glucose tolerance due to corticosteroids are the dose of steroid and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells.

Altretamine: (Minor) Concurrent use of altretamine with other agents which cause bone marrow or immune suppression such as corticosteroids may result in additive effects.

Ambenonium Chloride: (Moderate) Concomitant use of anticholinesterase agents, such as ambenonium chloride, and corticosteroids may produce severe weakness in patients with myasthenia gravis. If possible, anticholinesterase agents used to treat myasthenia should be withdrawn at least 24 hours before initiating corticosteroid therapy.

Amifampridine: (Moderate) Carefully consider the need for concomitant treatment with systemic corticosteroids and amifampridine, as coadministration may increase the risk of seizures. If coadministration occurs, closely monitor patients for seizure activity. Seizures have been observed in patients without a history of seizures taking amifampridine at recommended doses. Systemic corticosteroids may increase the risk of seizures in some patients.

Amiloride; Hydrochlorothiazide, HCTZ: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.

Aminolevulinic Acid: (Minor) Corticosteroids administered prior to or concomitantly with photosensitizing agents used in photodynamic therapy may decrease the efficacy of the treatment.

Aminosalicylate sodium, Aminosalicylic acid: (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.

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.

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.

Aprepitant, Fosaprepitant: (Moderate) Use caution if prednisone and aprepitant, fosaprepitant are used concurrently and monitor for an increase in prednisone-related adverse effects for several days after administration of a multi-day aprepitant regimen. The active metabolite of prednisone, prednisolone, is a CYP3A4 substrate. Aprepitant, when administered as a 3-day oral regimen (125 mg/80 mg/80 mg), is a moderate CYP3A4 inhibitor and inducer and may increase plasma concentrations of prednisone. For example, a 5-day oral aprepitant regimen increased the AUC of another CYP3A4 substrate, midazolam (single dose), by 2.3-fold on day 1 and by 3.3-fold on day 5. After a 3-day oral aprepitant regimen, the AUC of midazolam (given on days 1, 4, 8, and 15) increased by 25% on day 4, and then decreased by 19% and 4% on days 8 and 15, respectively. As a single 125 mg or 40 mg oral dose, the inhibitory effect of aprepitant on CYP3A4 is weak, with the AUC of midazolam increased by 1.5-fold and 1.2-fold, respectively. After administration, fosaprepitant is rapidly converted to aprepitant and shares many of the same drug interactions. However, as a single 150 mg intravenous dose, fosaprepitant only weakly inhibits CYP3A4 for a duration of 2 days; there is no evidence of CYP3A4 induction. Fosaprepitant 150 mg IV as a single dose increased the AUC of midazolam (given on days 1 and 4) by approximately 1.8-fold on day 1; there was no effect on day 4. Less than a 2-fold increase in the midazolam AUC is not considered clinically important.

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) Coadministration may result in decreased exposure to prednisone. Butalbital is a CYP3A4 inducer; prednisone is a CYP3A4 substrate. Monitor for decreased response to prednisone during concurrent use. (Moderate) 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; Codeine: (Moderate) Coadministration may result in decreased exposure to prednisone. Butalbital is a CYP3A4 inducer; prednisone is a CYP3A4 substrate. Monitor for decreased response to prednisone during concurrent use. (Moderate) 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.

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.

Aspirin, ASA; Pravastatin: (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.

Atazanavir: (Moderate) Coadministration of prednisone with atazanavir may cause elevated prednisone serum concentrations, potentially resulting in Cushing's syndrome and adrenal suppression. Prednisone is a CYP3A4 substrate; atazanavir is a strong inhibitor of CYP3A4. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use.

Atazanavir; Cobicistat: (Moderate) Coadministration of prednisone with atazanavir may cause elevated prednisone serum concentrations, potentially resulting in Cushing's syndrome and adrenal suppression. Prednisone is a CYP3A4 substrate; atazanavir is a strong inhibitor of CYP3A4. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. (Moderate) Coadministration of prednisone with cobicistat may cause elevated prednisone serum concentrations, potentially resulting in Cushing's syndrome and adrenal suppression. Cobicistat is a CYP3A4 and P-glycoprotein (P-gp) inhibitor, while prednisone is a CYP3A4 and P-gp substrate. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use.

Atenolol; Chlorthalidone: (Moderate) 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.

Atracurium: (Moderate) Limit the period of use of neuromuscular blockers and corticosteroids and only use when the specific advantages of the drugs outweigh the risks for acute myopathy. An acute myopathy has been observed with the use of high doses of corticosteroids in patients receiving concomitant long-term therapy with neuromuscular blockers. Clinical improvement or recovery after stopping therapy may require weeks to years.

Atropine; Benzoic Acid; Hyoscyamine; Methenamine; Methylene Blue; Phenyl Salicylate: (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.

Azathioprine: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.

Azilsartan; Chlorthalidone: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.

Basiliximab: (Minor) Because systemically administered corticosteroids have immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives.

Benazepril; Hydrochlorothiazide, HCTZ: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.

Bendroflumethiazide; Nadolol: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.

Benzoic Acid; Hyoscyamine; Methenamine; Methylene Blue; Phenyl Salicylate: (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.

Bexarotene: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents, such as bexarotene.

Bismuth Subsalicylate: (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.

Bismuth Subsalicylate; Metronidazole; Tetracycline: (Moderate) Monitor for gastrointestinal toxicity during concurrent corticosteroid and salicylate use. Concomitant use increases the risk of GI bleeding. In patients receiving concomitant corticosteroids and chronic use of salicylates, withdrawal of corticosteroids may result in salicylism because corticosteroids enhance renal clearance of salicylates and their withdrawal is followed by return to normal rates of renal clearance.

Bisoprolol; Hydrochlorothiazide, HCTZ: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.

Bortezomib: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.

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.

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.

Butabarbital: (Moderate) Coadministration may result in decreased exposure to prednisone. Butabarbital is a CYP3A4 inducer; prednisone is a CYP3A4 substrate. Monitor for decreased response to prednisone during concurrent use.

Butalbital; Acetaminophen: (Moderate) Coadministration may result in decreased exposure to prednisone. Butalbital is a CYP3A4 inducer; prednisone is a CYP3A4 substrate. Monitor for decreased response to prednisone during concurrent use.

Butalbital; Acetaminophen; Caffeine: (Moderate) Coadministration may result in decreased exposure to prednisone. Butalbital is a CYP3A4 inducer; prednisone is a CYP3A4 substrate. Monitor for decreased response to prednisone during concurrent use.

Butalbital; Acetaminophen; Caffeine; Codeine: (Moderate) Coadministration may result in decreased exposure to prednisone. Butalbital is a CYP3A4 inducer; prednisone is a CYP3A4 substrate. Monitor for decreased response to prednisone during concurrent use.

Cabozantinib: (Minor) Monitor for an increase in prednisone-related adverse reactions if coadministration with cabozantinib is necessary; a dose adjustment of prednisone may be necessary. Prednisone is a P-glycoprotein (P-gp) substrate. Cabozantinib is a P-gp inhibitor and has the potential to increase plasma concentrations of P-gp substrates; however, the clinical relevance of this finding is unknown.

Caffeine; Sodium Benzoate: (Moderate) Corticosteroids may cause protein breakdown, which could lead to elevated blood ammonia concentrations, especially in patients with an impaired ability to form urea. Corticosteroids should be used with caution in patients receiving treatment for hyperammonemia.

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) Hepatic microsomal enzyme inducers, including carbamazepine, can increase the metabolism of prednisone. Dosage adjustments may be necessary, and closer monitoring of clinical and/or adverse effects is warranted when carbamazepine is used with prednisone.

Carbinoxamine; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.

Carmustine, BCNU: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.

Carvedilol: (Minor) Increased concentrations of prednisone may occur if it is coadministered with carvedilol; exercise caution. Carvedilol is a P-glycoprotein (P-gp) inhibitor and prednisone is a P-gp substrate.

Ceritinib: (Minor) Monitor for steroid-related adverse reactions if coadministration of ceritinib with prednisone is necessary, due to increased prednisone exposure. Ceritinib is a strong CYP3A4 inhibitor and prednisolone, the active metabolite of prednisone, is a CYP3A4 substrate. Another strong CYP3A4 inhibitor has been reported to decrease the metabolism of certain corticosteroids by up to 60%, leading to increased risk of corticosteroid side effects; however, plasma concentrations of prednisolone are less affected by strong CYP3A4 inhibitors, especially for long-term use.

Certolizumab pegol: (Moderate) The safety and efficacy of certolizumab in patients with immunosuppression have not been evaluated. Patients receiving immunosuppressives along with certolizumab may be at a greater risk of developing an infection. Many of the serious infections occurred in patients on immunosuppressive therapy who received certolizumab.

Chlorambucil: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.

Chlorothiazide: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.

Chlorpheniramine; 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; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.

Chlorpropamide: (Moderate) Monitor blood glucose during concomitant corticosteroid and sulfonylurea use; a sulfonylurea dose adjustment may be necessary. Corticosteroids may increase blood glucose concentrations. Risk factors for impaired glucose tolerance due to corticosteroids include the corticosteroid dose and duration of treatment. Corticosteroids stimulate hepatic glucose production and inhibit peripheral glucose uptake into muscle and fatty tissues, producing insulin resistance. Decreased insulin production may occur in the pancreas due to a direct effect on pancreatic beta cells.

Chlorthalidone: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.

Chlorthalidone; Clonidine: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.

Cholestyramine: (Moderate) Cholestyramine may increase the clearance of corticosteroids, such as prednisone.

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.

Clofarabine: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.

Cobicistat: (Moderate) Coadministration of prednisone with cobicistat may cause elevated prednisone serum concentrations, potentially resulting in Cushing's syndrome and adrenal suppression. Cobicistat is a CYP3A4 and P-glycoprotein (P-gp) inhibitor, while prednisone is a CYP3A4 and P-gp substrate. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use.

Codeine; Phenylephrine; Promethazine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.

Daclatasvir: (Moderate) Systemic exposure of prednisone, a P-glycoprotein (P-gp) substrate, may be increased when administered concurrently with daclatasvir, a P-gp inhibitor. Taking these drugs together could increase or prolong the therapeutic effects of prednisone; monitor patients for potential adverse effects.

Dapagliflozin: (Moderate) 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) Coadministration of prednisone with darunavir may cause elevated prednisone serum concentrations, potentially resulting in Cushing's syndrome and adrenal suppression. Prednisone is a CYP3A4 substrate; darunavir is a strong inhibitor of CYP3A4. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use.

Darunavir; Cobicistat: (Moderate) Coadministration of prednisone with cobicistat may cause elevated prednisone serum concentrations, potentially resulting in Cushing's syndrome and adrenal suppression. Cobicistat is a CYP3A4 and P-glycoprotein (P-gp) inhibitor, while prednisone is a CYP3A4 and P-gp substrate. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. (Moderate) Coadministration of prednisone with darunavir may cause elevated prednisone serum concentrations, potentially resulting in Cushing's syndrome and adrenal suppression. Prednisone is a CYP3A4 substrate; darunavir is a strong inhibitor of CYP3A4. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use.

Darunavir; Cobicistat; Emtricitabine; Tenofovir alafenamide: (Moderate) Coadministration of prednisone with cobicistat may cause elevated prednisone serum concentrations, potentially resulting in Cushing's syndrome and adrenal suppression. Cobicistat is a CYP3A4 and P-glycoprotein (P-gp) inhibitor, while prednisone is a CYP3A4 and P-gp substrate. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use. (Moderate) Coadministration of prednisone with darunavir may cause elevated prednisone serum concentrations, potentially resulting in Cushing's syndrome and adrenal suppression. Prednisone is a CYP3A4 substrate; darunavir is a strong inhibitor of CYP3A4. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use.

Dasabuvir; Ombitasvir; Paritaprevir; Ritonavir: (Moderate) Coadministration of prednisone with ritonavir (a strong CYP3A4 inhibitor) may cause prednisone serum concentrations to increase, potentially resulting in Cushing's syndrome and adrenal suppression. Consider use of an alternative corticosteroid whose concentrations are less affected by strong CYP3A4 inhibitors, such as beclomethasone and prednisolone, especially during long-term treatment.

Deferasirox: (Moderate) Because gastric ulceration and GI bleeding have been reported in patients taking deferasirox, use caution when coadministering with other drugs known to increase the risk of peptic ulcers or gastric hemorrhage including corticosteroids.

Denileukin Diftitox: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.

Denosumab: (Moderate) The safety and efficacy of denosumab use in patients with immunosuppression have not been evaluated. Patients receiving immunosuppressives along with denosumab may be at a greater risk of developing an infection.

Desmopressin: (Major) Desmopressin 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.

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.

Doxacurium: (Moderate) Limit the period of use of neuromuscular blockers and corticosteroids and only use when the specific advantages of the drugs outweigh the risks for acute myopathy. An acute myopathy has been observed with the use of high doses of corticosteroids in patients receiving concomitant long-term therapy with neuromuscular blockers. Clinical improvement or recovery after stopping therapy may require weeks to years.

Dronedarone: (Moderate) Dronedarone is metabolized by and is an inhibitor of CYP3A; dronedarone also inhibits P-gp. Prednisone is a substrate for CYP3A4 and P-gp. The concomitant administration of dronedarone with CYP3A4 and P-gp substrates may result in increased exposure of the substrate and should, therefore, be undertaken with caution.

Droperidol: (Moderate) Caution is advised when using droperidol in combination with corticosteroids which may lead to electrolyte abnormalities, especially hypokalemia or hypomagnesemia, as such abnormalities may increase the risk for QT prolongation or cardiac arrhythmias.

Dulaglutide: (Moderate) 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.

Elvitegravir; Cobicistat; Emtricitabine; Tenofovir Alafenamide: (Moderate) Coadministration of prednisone with cobicistat may cause elevated prednisone serum concentrations, potentially resulting in Cushing's syndrome and adrenal suppression. Cobicistat is a CYP3A4 and P-glycoprotein (P-gp) inhibitor, while prednisone is a CYP3A4 and P-gp substrate. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use.

Elvitegravir; Cobicistat; Emtricitabine; Tenofovir Disoproxil Fumarate: (Moderate) Coadministration of prednisone with cobicistat may cause elevated prednisone serum concentrations, potentially resulting in Cushing's syndrome and adrenal suppression. Cobicistat is a CYP3A4 and P-glycoprotein (P-gp) inhibitor, while prednisone is a CYP3A4 and P-gp substrate. Corticosteroids, such as beclomethasone and prednisolone, whose concentrations are less affected by strong CYP3A4 inhibitors, should be considered, especially for long-term use.

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.

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 corticosteroid efficacy if prednisone is used with enzalutamide; a dosage increase may be necessary. Concurrent use may decrease the exposure of prednisone. Prednisone is a CYP3A4 substrate and enzalutamide is a strong CYP3A4 inducer.

Ephedrine: (Moderate) Ephedrine may enhance the metabolic clearance of corticosteroids. Decreased blood concentrations and lessened physiologic activity may necessitate an increase in corticosteroid dosage.

Ephedrine; Guaifenesin: (Moderate) Ephedrine may enhance the metabolic clearance of corticosteroids. Decreased blood concentrations and lessened physiologic activity may necessitate an increase in corticosteroid dosage.

Epinephrine: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and epinephrine use due to risk for additive hypokalemia; potassium supplementation may be necessary. Corticosteroids may potentiate the hypokalemic effects of epinephrine.

Eprosartan; Hydrochlorothiazide, HCTZ: (Moderate) Monitor potassium concentrations during concomitant corticosteroid and thiazide diuretic use due to risk for additive hypokalemia; potassium supplementation may be necessary. Both corticosteroids and thiazide diuretics cause increased renal potassium loss.

Erlotinib: (Moderate) Monitor for symptoms of gastrointestinal (GI) perforation (e.g., severe abdominal pain, fever, nausea, and vomiting) if coadministration of erlotinib with prednisone is necessary. Permanently discontinue erlotinib in patients who develop GI perforation. The pooled incidence of GI perforation clinical trials of erlotinib ranged from 0.1% to 0.4%, including fatal cases; patients receiving concomitant prednisone 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.

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) Etravirine is a CYP3A4 inducer/substrate and a P-glycoprotein (PGP) inhibitor and prednisone is a CYP3A4 and PGP substrate. Caution is warranted if these drugs are coadministered.

Exenatide: (Moderate) 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.

Fluoxymesterone: (Moderate) Coadministration of corticosteroids and fluoxymesterone may increase the risk of edema, especially in patients with underlying cardiac or hepatic disease. Corticosteroids with greater mineralocorticoid activity, such as fludrocortisone, may be more likely to cause edema. Administer these drugs in combination with caution.

Fosamprenavir: (Moderate) Concomitant use of prednisone and fosamprenavir may result in altered prednisone plasma concentrations. Prednisone is a substrate of the hepatic isoenzyme CYP3A4 and drug transporter P-glycoprotein (P-gp). Amprenavir, the active metabolite of fosamprenavir, is an inducer of P-gp and a potent inhibitor and moderate inducer of CYP3A4.

Fosinopril; Hydrochlorothiazide, HCTZ: (Moderate) 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.

Fosphenytoin: (Moderate) Monitor for decreased corticosteroid efficacy if prednisone is used with fosphenytoin; a dosage increase may be necessary. Concurrent use may decrease the exposure of prednisone. Prednisone is a CYP3A substrate and fosphenytoin is a strong CYP3A inducer.

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.

Glecaprevir; Pibrentasvir: (Moderate) Caution is advised with the coadministration of glecaprevir and prednisone as coadministration may increase serum concentrations of prednisone and increase the risk of adverse effects. Prednisone is a substrate of P-glycoprotein (P-gp); glecaprevir is a P-gp inhibitor. (Moderate) Caution is advised with the coadministration of pibrentasvir and prednisone as coadministration may increase serum concentrations of prednisone and increase the risk of adverse effects. Prednisone is a substrate of P-glycoprotein (P-gp); pibrentasvir is a P-gp inhibitor.

Glimepiride: (Moderate) 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.

Glimepiride; Rosiglitazone: (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.

Golimumab: (Moderate) The safety and efficacy of golimumab in patients with immunosuppression have not been evaluated. Patients receiving immunosuppressives along with golimumab may be at a greater risk of developing an infection.

Guaifenesin; Phenylephrine: (Moderate) The therapeutic effect of phenylephrine may be increased in patient receiving corticosteroids, such as hydrocortisone. Monitor patients for increased pressor effect if these agents are administered concomitantly.

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.

Hydralazine; 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: (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.

Hydroxyurea: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.

Hyoscyamine; Methenamine; Methylene Blue; Phenyl Salicylate; Sodium Biphosphate: (Moderate) 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.

Idelalisib: (Major) Avoid concomitant use of idelalisib, a strong CYP3A inhibitor, with prednisone, a CYP3A substrate, as prednisone toxicities may be significantly increased. The AUC of a sensitive CYP3A substrate was increased 5.4-fold when coadministered with idelalisib. In addition, because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents. While therapy is designed to take advantage of this effect, patients may be predisposed to over-immunosuppression resulting in an increased risk for the development of severe infections. If coadministration is necessary, close clinical monitoring is advised and therapy should be accompanied by appropriate antimicrobial therapies as indicated.

Imatinib: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.

Incretin Mimetics: (Moderate) 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.

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.

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.

Isavuconazonium: (Moderate) Concomitant use of isavuconazonium with prednisone may result in increased serum concentrations of prednisone. Prednisolone, the active metabolite of prednisone, is a substrate of the hepatic isoenzyme CYP3A4; additionally prednisone is a substrate of the drug transporter P-glycoprotein (P-gp). Isavuconazole, the active moiety of isavuconazonium, is an inhibitor of CYP3A4 and P-gp. Caution and close monitoring for adverse effects, such as corticosteroid-related side effects, are advised if these drugs are used together.

Isoniazid, INH; Pyrazinamide, PZA; Rifampin: (Moderate) Monitor for decreased corticosteroid efficacy if prednisone is used with rifampin; a dosage increase may be necessary. Concurrent use may decrease the exposure of prednisone. Prednisone is a CYP3A4 substrate and rifampin is a strong CYP3A4 inducer.

Isoniazid, INH; Rifampin: (Moderate) Monitor for decreased corticosteroid efficacy if prednisone is used with rifampin; a dosage increase may be necessary. Concurrent use may decrease the exposure of prednisone. Prednisone 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.

Itraconazole: (Moderate) Prednisone is metabolized by the liver to the active metabolite prednisolone. Itraconazole is a potent inhibitor of CYP3A4, and prednisolone is a CYP3A4 substrate. Monitor patients for corticosteroid-related side effects if both prednisone and itraconazole are taken.

Ketoconazole: (Moderate) Monitor for corticosteroid-related adverse events if prednisone is used with ketoconazole. Concurrent use may increase the exposure of prednisone. Prednisone is a CYP3A4 substrate and ketoconazole is a strong CYP3A4 inhibitor. Ketoconazole has been reported to decrease the metabolism of certain corticosteroids by up to 60%. In a study, ketoconazole inhibited 6 beta-hydroxylase and increased the exposure of biologically active unbound prednisolone after oral prednisone administration.

L-Asparaginase Escherichia coli: (Moderate) Concomitant use of L-asparaginase with corticosteroids can result in additive hyperglycemia. L-Asparaginase transiently inhibits insulin production contributing to hyperglycemia seen during concurrent corticosteroid therapy. Insulin therapy may be required in some cases. Administration of L-asparaginase after rather than before corticosteroids reportedly has produced fewer hypersensitivity reactions.

Ledipasvir; Sofosbuvir: (Moderate) Caution and close monitoring of prednisone-associated adverse reactions is advised with concomitant administration of ledipasvir. Prednisone is a substrate of the drug transporter P-glycoprotein (P-gp); ledipasvir is a P-gp inhibitor. Taking these drugs together may increase prednisone plasma concentrations.

Letermovir: (Moderate) A clinically relevant increase in the plasma concentration of prednisolone (the active metabolite of prednisone) may occur if given with letermovir. In patients who are also receiving treatment with cyclosporine, the magnitude of this interaction may be amplified. Prednisolone is a CYP3A4 substrate. Letermovir is a moderate CYP3A4 inhibitor; however, when given with cyclosporine, the combined effect on CYP3A4 substrates may be similar to a strong CYP3A4 inhibitor. Concurrent administration with a strong CYP3A4 inhibitor decreased the metabolism of certain corticosteroids by up to 60%, leading to increased risk of corticosteroid side effects.

Levoketoconazole: (Moderate) Monitor for corticosteroid-related adverse events if prednisone is used with ketoconazole. Concurrent use may increase the exposure of prednisone. Prednisone is a CYP3A4 substrate and ketoconazole is a strong CYP3A4 inhibitor. Ketoconazole has been reported to decrease the metabolism of certain corticosteroids by up to 60%. In a study, ketoconazole inhibited 6 beta-hydroxylase and increased the exposure of biologically active unbound prednisolone after oral prednisone administration.

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 corticosteroid-related adverse events if prednisone is used with lonafarnib. Concurrent use may increase the exposure of prednisone. Prednisone is a CYP3A4 substrate and lonafarnib is a strong CYP3A4 inhibitor. Other strong CYP3A4 inhibitors have been reported to decrease the metabolism of certain corticosteroids by up to 60%.

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) Coadministration of prednisone with ritonavir (a strong CYP3A4 inhibitor) may cause prednisone serum concentrations to increase, potentially resulting in Cushing's syndrome and adrenal suppression. Consider use of an alternative corticosteroid whose concentrations are less affected by strong CYP3A4 inhibitors, such as beclomethasone and prednisolone, especially during long-term treatment.

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) Lumacaftor; ivacaftor may reduce the efficacy of prednisone and prednisolone by decreasing systemic exposure of the corticosteroid. If used together, a higher systemic corticosteroid dose may be required to obtain the desired therapeutic effect. Prednisolone, the active metabolite of prednisone, is a CYP3A4 substrate, and lumacaftor is a strong CYP3A inducer.

Lumacaftor; Ivacaftor: (Moderate) Lumacaftor; ivacaftor may reduce the efficacy of prednisone and prednisolone by decreasing systemic exposure of the corticosteroid. If used together, a higher systemic corticosteroid dose may be required to obtain the desired therapeutic effect. Prednisolone, the active metabolite of prednisone, is a CYP3A4 substrate, and lumacaftor is a strong CYP3A inducer.

Lumateperone: (Minor) The manufacturer of lumateperone recommends that concurrent use of prednisone be avoided and lists prednisone as a CYP3A4 inducer. Lumateperone is a CYP3A4 substrate. However, prednisone is not an established CYP3A4 inducer, and the potential outcome of using this combination is unknown. Be alert for a potential reduction in lumateperone efficacy.

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 rinfabate: (Moderate) Additional monitoring may be required when coadministering systemic or inhaled corticosteroids and mecasermin, recombinant, rh-IGF-1. In animal studies, corticosteroids impair the growth-stimulating effects of growth hormone (GH) through interference with the physiological stimulation of epiphyseal chondrocyte proliferation exerted by GH and IGF-1. Dexamethasone administration on long bone tissue in vitro resulted in a decrease of local synthesis of IGF-1. Similar counteractive effects are expected in humans. If systemic or inhaled glucocorticoid therapy is required, the steroid dose should be carefully adjusted and growth rate monitored.

Mecasermin, Recombinant, rh-IGF-1: (Moderate) Additional monitoring may be required when coadministering systemic or inhaled corticosteroids and mecasermin, recombinant, rh-IGF-1. In animal studies, corticosteroids impair the growth-stimulating effects of growth hormone (GH) through interference with the physiological stimulation of epiphyseal chondrocyte proliferation exerted by GH and IGF-1. Dexamethasone administration on long bone tissue in vitro resulted in a decrease of local synthesis of IGF-1. Similar counteractive effects are expected in humans. If systemic or inhaled glucocorticoid therapy is required, the steroid dose should be carefully adjusted and growth rate monitored.

Meglitinides: (Moderate) 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: (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. 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; 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.

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.

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.

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) Use caution if mitotane and prednisone are used concomitantly, and monitor for decreased efficacy of prednisone and a possible change in dosage requirements. Mitotane is a strong CYP3A4 inducer and prednisone is a CYP3A4 substrate; coadministration may result in decreased plasma concentrations of prednisone.

Mitoxantrone: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.

Mivacurium: (Moderate) 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.

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.

Nelarabine: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.

Neostigmine: (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.

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: (Major) The use of prednisone to prevent nevirapine-associated rash is not recommended. In a clinical trial, concomitant use of prednisone was associated with an increase in incidence and severity of rash during the first 6 weeks of nevirapine therapy.

Nirmatrelvir; Ritonavir: (Moderate) Coadministration of prednisone with ritonavir (a strong CYP3A4 inhibitor) may cause prednisone serum concentrations to increase, potentially resulting in Cushing's syndrome and adrenal suppression. Consider use of an alternative corticosteroid whose concentrations are less affected by strong CYP3A4 inhibitors, such as beclomethasone and prednisolone, especially during long-term treatment.

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.

Ombitasvir; Paritaprevir; Ritonavir: (Moderate) Coadministration of prednisone with ritonavir (a strong CYP3A4 inhibitor) may cause prednisone serum concentrations to increase, potentially resulting in Cushing's syndrome and adrenal suppression. Consider use of an alternative corticosteroid whose concentrations are less affected by strong CYP3A4 inhibitors, such as beclomethasone and prednisolone, especially during long-term treatment.

Oritavancin: (Moderate) Prednisolone is metabolized by CYP3A4; oritavancin is a weak CYP3A4 inducer. Plasma concentrations and efficacy of prednisolone may be reduced if these drugs are administered concurrently.

Oxymetholone: (Moderate) Concomitant use of oxymetholone with corticosteroids or corticotropin, ACTH may cause increased edema. Manage edema with diuretic and/or digitalis therapy.

Ozanimod: (Moderate) Concomitant use of ozanimod with prednisone may increase the risk of immunosuppression. Monitor patients carefully for signs and symptoms of infection. In clinical studies for ulcerative colitis, the use of systemic corticosteroids did not appear to influence safety or efficacy of ozanimod.

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.

Pazopanib: (Moderate) Pazopanib is a weak inhibitor of CYP3A4. Coadministration of pazopanib and prednisone, a CYP3A4 substrate, may cause an increase in systemic concentrations of prednisone. Use caution when administering these drugs concomitantly. In addition, concomitant administration may predispose the patient to over-immunosuppression resulting in an increased risk for the development of severe infections.

Pegaspargase: (Moderate) Monitor for an increase in glucocorticoid-related adverse reactions such as hyperglycemia and osteonecrosis during concomitant use of pegaspargase and glucocorticoids.

Peginterferon Alfa-2a: (Moderate) Additive myelosuppressive effects may be seen when alpha interferons are given concurrently with other myelosuppressive agents, such as antineoplastic agents or immunosuppressives.

Penicillamine: (Major) Agents such as immunosuppressives have adverse reactions similar to those of penicillamine. Concomitant use of penicillamine with these agents is contraindicated because of the increased risk of developing severe hematologic and renal toxicity.

Phenobarbital: (Moderate) Coadministration may result in decreased exposure to prednisone. Phenobarbital is a CYP3A4 inducer; prednisone is a CYP3A4 substrate. Monitor for decreased response to prednisone during concurrent use.

Phenobarbital; Hyoscyamine; Atropine; Scopolamine: (Moderate) Coadministration may result in decreased exposure to prednisone. Phenobarbital is a CYP3A4 inducer; prednisone is a CYP3A4 substrate. Monitor for decreased response to prednisone during concurrent use.

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.

Phenytoin: (Moderate) Monitor for decreased corticosteroid efficacy if prednisone is used with phenytoin; a dosage increase may be necessary. Concurrent use may decrease the exposure of prednisone. Prednisone is a CYP3A substrate and phenytoin is a strong CYP3A inducer.

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) Posaconazole and prednisone should be coadministered with caution due to an increased potential for adverse events. Posaconazole is a potent inhibitor of CYP3A4, an isoenzyme partially responsible for the metabolism of prednisone. Further, both prednisone and posaconazole are substrates of the drug efflux protein, P-glycoprotein, which when administered together may increase the absorption or decrease the clearance of the other drug. This complex interaction may cause alterations in the plasma concentrations of both posaconazole and prednisone, ultimately resulting in an increased risk of adverse events.

Potassium Phosphate; Sodium Phosphate: (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia.

Potassium-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.

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 prednisone. Primidone is a CYP3A4 inducer; prednisone is a CYP3A4 substrate. Monitor for decreased response to prednisone 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.

Propylthiouracil, PTU: (Moderate) The metabolism of corticosteroids is increased in hyperthyroidism and decreased in hypothyroidism. Dosage adjustments may be necessary when initiating, changing or discontinuing thyroid hormones or antithyroid agents.

Purine analogs: (Minor) Concurrent use of purine analogs with other agents which cause bone marrow or immune suppression such as other antineoplastic agents or immunosuppressives may result in additive effects.

Pyridostigmine: (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.

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.

Rifampin: (Moderate) Monitor for decreased corticosteroid efficacy if prednisone is used with rifampin; a dosage increase may be necessary. Concurrent use may decrease the exposure of prednisone. Prednisone is a CYP3A4 substrate and rifampin is a strong CYP3A4 inducer.

Rifapentine: (Moderate) Monitor for decreased corticosteroid efficacy if prednisone is used with rifapentine; a dosage increase may be necessary. Concurrent use may decrease the exposure of prednisone. Prednisone 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.

Ritonavir: (Moderate) Coadministration of prednisone with ritonavir (a strong CYP3A4 inhibitor) may cause prednisone serum concentrations to increase, potentially resulting in Cushing's syndrome and adrenal suppression. Consider use of an alternative corticosteroid whose concentrations are less affected by strong CYP3A4 inhibitors, such as beclomethasone and prednisolone, especially during long-term treatment.

Rituximab: (Moderate) Rituximab and corticosteroids are commonly used together; however, monitor the patient for immunosuppression and signs and symptoms of infection during combined chronic therapy.

Rituximab; Hyaluronidase: (Moderate) Rituximab and corticosteroids are commonly used together; however, monitor the patient for immunosuppression and signs and symptoms of infection during combined chronic therapy.

Rocuronium: (Moderate) 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: (Major) Saquinavir may inhibit CYP3A4 metabolism of prednisone, resulting in increased plasma prednisone concentrations and reduced serum cortisol concentrations. There have been reports of clinically significant drug interactions in patients receiving ritonavir with other corticosteroids, resulting in systemic corticosteroid effects including Cushing syndrome and adrenal suppression. Similar results are expected with saquinavir. Consider using an alternative treatment to prednisone, such as a corticosteroid not metabolized by CYP3A4 (i.e., beclomethasone or prednisolone). If corticosteroid therapy is to be discontinued, consider tapering the dose over a period of time to decrease the potential for withdrawal.

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.

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.

Simeprevir: (Minor) Simeprevir, a P-glycoprotein (P-gp) inhibitor and a mild intestinal CYP3A4 inhibitor, may increase the side effects of prednisone, which is a P-gp and CYP3A4 substrate. Monitor patients for adverse effects of prednisone, such as enhanced adrenal suppression.

Siponimod: (Moderate) Monitor patients carefully for signs and symptoms of infection during coadministration of siponimod and prednisone. 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.

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 Iodide: (Moderate) Corticosteroids, such as prednisone, are known to decrease the uptake of iodide into thyroid tissue. In order to increase thyroid uptake and optimize exposure of thyroid tissue to the radionucleotide sodium iodide I-131, consider withholding prednisone prior to treatment with sodium iodide I-131.

Sodium Phenylbutyrate: (Moderate) The concurrent use of corticosteroids with sodium phenylbutyrate may increase plasma ammonia levels (hyperammonemia) by causing the breakdown of body protein. Patients with urea cycle disorders being treated with sodium phenylbutyrate usually should not receive regular treatment with corticosteroids.

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; Voxilaprevir: (Moderate) Plasma concentrations of prednisone, a P-glycoprotein (P-gp) substrate, may be increased when administered concurrently with voxilaprevir, a P-gp inhibitor. Monitor patients for increased side effects if these drugs are administered concurrently.

Somatropin, rh-GH: (Moderate) Corticosteroids can retard bone growth and therefore, can inhibit the growth-promoting effects of somatropin. If corticosteroid therapy is required, the corticosteroid dose should be carefully adjusted.

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.

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.

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; 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.

Tesamorelin: (Moderate) Use caution when coadministering tesamorelin with prednisone as their concurrent use may decrease the effectiveness of the steroids. Tesamorelin stimulates the production of growth hormone, which is known to inhibit the enzyme 11-beta-hydroxysteroid dehydrogenase type 1 (11-beta-HSD-1); cortisone and prednisone require the 11-beta-HSD-1 enzyme for conversion to their active metabolites. Patients with hypoadrenalism receiving treatment with cortisone or prednisone may required increased maintenance or stress doses after initiation of tesamorelin.

Testosterone: (Moderate) Monitor for fluid retention during concurrent corticosteroid and testosterone use. Concurrent use may result in increased fluid retention.

Theophylline, Aminophylline: (Minor) Serum theophylline concentrations have been reported to be lower during concomitant administration of prednisone, but the actual magnitude of the interaction was slight.

Thiazide diuretics: (Moderate) 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.

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.

Tositumomab: (Minor) Because systemically administered corticosteroids exhibit immunosuppressive effects when given in high doses and/or for extended periods, additive effects may be seen with other immunosuppressives or antineoplastic agents.

Trandolapril; Verapamil: (Minor) The absorption of verapamil can also be reduced by the cyclophosphamide, vincristine, procarbazine, prednisone (COPP) chemotherapeutic drug regimen.

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 prednisone with tucatinib is necessary, due to increased prednisone exposure; Cushings syndrome and adrenal suppression could potentially occur with long-term use. Prednisolone, the active metabolite of prednisone, is a CYP3A4 substrate; tucatinib is a strong CYP3A4 inhibitor. 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.

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: (Minor) Concomitant use of vemurafenib and prednisone may result in altered concentrations of prednisone or its active metabolite, prednisolone. Vemurafenib is an inhibitor of P-glycoprotein (PGP) and an inducer of CYP3A4. Prednisone is a substrate of PGP and its active metabolite, prednisolone, is a CYP3A4 substrate. Use caution and monitor patients for toxicity and efficacy.

Verapamil: (Minor) The absorption of verapamil can also be reduced by the cyclophosphamide, vincristine, procarbazine, prednisone (COPP) chemotherapeutic drug regimen.

Vigabatrin: (Major) Vigabatrin should not be used with corticosteroids, which are associated with serious ophthalmic effects (e.g., retinopathy or glaucoma) unless the benefit of treatment clearly outweighs the risks.

Vincristine Liposomal: (Moderate) Use sodium phosphate cautiously with corticosteroids, especially mineralocorticoids or corticotropin, ACTH, as concurrent use can cause hypernatremia.

Voriconazole: (Moderate) Monitor for potential adrenal dysfunction with concomitant use of voriconazole and prednisone. 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 prednisone 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.

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.

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

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

Affected cytochrome P450 isoenzymes and drug transporters: P-gp, CYP3A4
In vitro, prednisone was identified as a substrate of p-glycoprotein (P-gp). Prednisone is metabolized by the liver to the active metabolite prednisolone via the 11b-hydroxydehydrogenase enzyme, which is not part of the CYP system, but prednisolone is metabolized by the CYP3A4-mediated 6b-hydroxylase enzyme to inactive compounds.


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


-Special Populations
Hepatic Impairment
There is an enhanced effect of corticosteroids in patients with cirrhosis.

Renal Impairment
This drug is known to be substantially excreted by the kidney, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function.