Drug class: Adrenals
ATC class: H02AB07
VA class: HS051
CAS number: 53-03-2

Medically reviewed by Drugs.com on Feb 27, 2023. Written by ASHP.

Introduction

Synthetic glucocorticoid; minimal mineralocorticoid activity.

Uses for Prednisone

Treatment of a wide variety of diseases and conditions; used principally for glucocorticoid effects as an anti-inflammatory and immunosuppressant agent and for its effects on blood and lymphatic systems in the palliative treatment of various diseases.

Adrenocortical Insufficiency

Corticosteroids are administered in physiologic dosages to replace deficient endogenous hormones in patients with adrenocortical insufficiency.

Because production of both mineralocorticoids and glucocorticoids is deficient in adrenocortical insufficiency, hydrocortisone or cortisone (in conjunction with liberal salt intake) usually is the corticosteroid of choice for replacement therapy.

Usually inadequate alone for adrenocortical insufficiency because of minimal mineralocorticoid activity.

If prednisone is used for adrenocortical insufficiency, a mineralocorticoid (e.g., fludrocortisone) must also be administered, particularly in infants.

Adrenogenital Syndrome

Lifelong glucocorticoid treatment of adrenogenital syndrome (e.g., congenital adrenal hyperplasia).

In salt-losing forms, cortisone or hydrocortisone is preferred in conjunction with liberal salt intake; concomitant use of a mineralocorticoid may be necessary until the patient is at least 5–7 years of age.

For long-term therapy after early childhood, a glucocorticoid alone usually is sufficient.

In hypertensive forms, a “short-acting” glucocorticoid with minimal mineralocorticoid activity (e.g., methylprednisolone, prednisone) is preferred. Avoid long-acting glucocorticoids (e.g., dexamethasone) because of tendency toward overdosage and growth retardation.

Hypercalcemia

Treatment of hypercalcemia associated with malignancy.

Usually ameliorates hypercalcemia associated with bone involvement in multiple myeloma.

Treatment of hypercalcemia associated with sarcoidosis^{† [off-label]}.

Treatment of hypercalcemia associated with vitamin D intoxication^{† [off-label]}.

Not effective for hypercalcemia caused by hyperparathyroidism^{† [off-label]}.

Thyroiditis

Treatment of granulomatous (subacute, nonsuppurative) thyroiditis.

Anti-inflammatory actions relieves fever, acute thyroid pain, and swelling.

May reduce orbital edema in endocrine exophthalmos (thyroid ophthalmopathy).

Usually reserved for palliative therapy in severely ill patients unresponsive to salicylates and thyroid hormones.

Rheumatic Disorders and Collagen Diseases

Short-term adjunctive treatment of acute episodes or exacerbations and systemic complications of rheumatic disorders (e.g., rheumatoid arthritis, juvenile arthritis, psoriatic arthritis, acute gouty arthritis, posttraumatic osteoarthritis, synovitis of osteoarthritis, epicondylitis, acute nonspecific tenosynovitis, ankylosing spondylitis, Reiter syndrome^{† [off-label]}, rheumatic fever^{† [off-label]} [especially with carditis]) and collagen diseases (e.g., acute rheumatic carditis, systemic lupus erythematosus, systemic dermatomyositis^† [polymyositis], polyarteritis nodosa^†, vasculitis^†) refractory to more conservative measures.

Relieves inflammation and suppresses symptoms but not disease progression.

Rarely indicated as maintenance therapy.

May be used as maintenance therapy (e.g., in rheumatoid arthritis, acute gouty arthritis, systemic lupus erythematosus, acute rheumatic carditis) as part of a total treatment program in selected patients when more conservative therapies have proven ineffective.

Glucocorticoid withdrawal is extremely difficult if used for maintenance; relapse and recurrence usually occur with drug discontinuance.

Controls acute manifestations of rheumatic carditis more rapidly than salicylates and may be life-saving; cannot prevent valvular damage and no better than salicylates for long-term treatment.

Adjunctively for severe systemic complications of Wegener’s granulomatosis^†, but cytotoxic therapy is the treatment of choice.

Primary treatment to control symptoms and prevent severe, often life-threatening complications of systemic lupus erythematosus, systemic dermatomyositis (polymyositis), polyarteritis nodosa^†, relapsing polychondritis, polymyalgia rheumatica, Sjögren's syndrome, giant-cell (temporal) arteritis^†, certain cases of vasculitis, or mixed connective tissue disease syndrome^†. High dosage may be required for acute situations; after a response has been obtained, drug must often be continued for long periods at low dosage.

Polymyositis^† associated with malignancy and childhood dermatomyositis may not respond well.

Rarely indicated in psoriatic arthritis, diffuse scleroderma^† (progressive systemic sclerosis), or osteoarthritis; risks outweigh benefits.

Dermatologic Diseases

Treatment of pemphigus and pemphigoid^†, bullous dermatitis herpetiformis, severe erythema multiforme (Stevens-Johnson syndrome), exfoliative dermatitis, severe eczema^†, cutaneous sarcoidosis^†, mycosis fungoides, and severe seborrheic dermatitis.

Usually reserved for acute exacerbations unresponsive to conservative therapy.

Early initiation of systemic glucocorticoid therapy may be life-saving in pemphigus vulgaris and pemphigoid^†, and high or massive doses may be required.

For control of severe or incapacitating allergic conditions (e.g., contact dermatitis, atopic dermatitis) refractory to adequate trials of conventional treatment.

Chronic skin disorders seldom an indication for systemic glucocorticoids.

Used for severe psoriasis but rarely indicated systemically; if used, exacerbation may occur when the drug is withdrawn or dosage is decreased.

Rarely indicated systemically for alopecia areata^†, alopecia totalis^†, or alopecia universalis^†. May stimulate hair growth, but hair loss returns when the drug is discontinued.

Allergic Conditions

For control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment; for control of acute manifestations, including angioedema^†, serum sickness, allergic symptoms of trichinosis^†, urticarial transfusion reactions, drug hypersensitivity reactions, and severe seasonal or perennial rhinitis.

Systemic therapy usually reserved for acute conditions and severe exacerbations.

For acute conditions, usually used in high dosage and with other therapies (e.g., antihistamines, sympathomimetics).

Reserve prolonged treatment for patients with chronic, disabling allergic conditions unresponsive to more conservative therapy and for those in whom risks of long-term glucocorticoid therapy are justified.

Ocular Disorders

To suppress a variety of allergic and nonpyogenic ocular inflammations.

For the treatment of severe acute and chronic allergic and inflammatory processes involving the eye and adnexa, including allergic corneal marginal ulcers, herpes zoster ophthalmicus, anterior segment inflammation, diffuse posterior uveitis and choroiditis, sympathetic ophthalmia, allergic conjunctivitis, keratitis, chorioretinitis, optic neuritis, iritis and iridocyclitis.

Less severe allergic and inflammatory allergic conditions of the eye are treated with topical ophthalmic corticosteroids.

Systemically in stubborn cases of anterior segment eye disease and when deeper ocular structures are involved.

Asthma

Corticosteroids are used as adjunctive treatment of acute asthma exacerbations^† and for maintenance treatment of persistent asthma^†.

Systemic corticosteroids (usually prednisone, prednisolone, and dexamethasone) are used for treatment of moderate to severe acute exacerbations of asthma; speeds resolution of airflow obstruction and reduces rate of relapse.

The Global Initiative for Asthma (GINA) guidelines state that systemic corticosteroids should be used in all but the mildest exacerbations; administration within 1 hour of presentation is recommended, if possible,

Corticosteroids are used as adjunctive treatment of acute asthma exacerbations^† and for maintenance treatment of persistent asthma^†.

COPD

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) guideline states that oral glucocorticoids play a role in the acute management of COPD exacerbations, but have no role in the chronic daily treatment of COPD because of the lack of benefit and high rate of systemic complications.

Sarcoidosis

Management of symptomatic sarcoidosis.

Systemic glucocorticoids are indicated for hypercalcemia; ocular, CNS, glandular, myocardial, or severe pulmonary involvement; or severe skin lesions unresponsive to intralesional injections of glucocorticoids.

Tuberculosis

Adjunctive therapy with antimycobacterial agents (e.g., streptomycin, isoniazid)in patients with fulminating or disseminated pulmonary tuberculosis.

Lipid Pneumonitis

Promotes the breakdown or dissolution of pulmonary lesions and eliminates sputum lipids in lipid pneumonitis^†.

Pneumocystis jirovecii Pneumonia

Corticosteroids are used adjunctively in the treatment of Pneumocystis jiroveci (Pneumocystis carinii) pneumonia.

Coronavirus Disease 2019 (COVID-19)

Adjunctive therapy in the treatment of serious complications from COVID-19^†.

Loeffler’s Syndrome

Symptomatic relief of acute manifestations of symptomatic Loeffler’s syndrome not manageable by other means.

Berylliosis

Symptomatic relief of acute manifestations of berylliosis.

Aspiration Pneumonitis

Symptomatic relief of acute manifestations of aspiration pneumonitis.

Anthrax

Has been used as an adjunct to anti-infective therapy in the treatment of anthrax^†; evidence of effect based on small observational studies. Some clinicians recommend that adjunctive corticosteroids be considered in patients with extensive edema especially of the head or neck, suspected bacterial meningitis, or vasopressor-resistant shock.

Hematologic Disorders

Management of acquired (autoimmune) hemolytic anemia, idiopathic thrombocytopenic purpura (ITP), secondary thrombocytopenia, erythroblastopenia, congenital (erythroid) hypoplastic anemia, or hemolysis^†.

High or even massive dosages decrease bleeding tendencies and normalize blood counts; does not affect the course or duration of hematologic disorders.

Glucocorticoids, immune globulin IV (IGIV), or splenectomy are first-line therapies for moderate to severe ITP, depending on the extent of bleeding involved.

May not affect or prevent renal complications in Henoch-Schoenlein purpura.

Insufficient evidence of effectiveness in aplastic anemia in children, but widely used.

Pericarditis

Has been used in the treatment of pericarditis^†, but generally considered second- or third-line treatment.

GI Diseases

Short-term therapy for acute exacerbations and systemic complications of ulcerative colitis, regional enteritis, or celiac disease^†. Low dosages of glucocorticoids, in conjunction with other supportive therapy, may occasionally be useful for patients unresponsive to usual therapy for chronic conditions.

Steroids should be used with caution in patients with active or latent peptic ulcers, diverticulitis, fresh intestinal anastomoses, and nonspecific ulcerative colitis; may increase risk of perforation.

Crohn’s Disease

Oral corticosteroids may be used for short-term treatment of moderate to severely active Crohn’s disease^†.

Neoplastic Diseases

Alone or as a component of various chemotherapeutic regimens in the palliative treatment of neoplastic diseases of the lymphatic system (e.g., leukemias and lymphomas in adults and acute leukemias in children).

In adults, acute lymphocytic (lymphoblastic) leukemia, chronic lymphocytic leukemia, and Hodgkin’s disease respond well to combination regimens that include a glucocorticoid (usually prednisone or prednisolone). Acute myeloblastic leukemia, lymphosarcoma, and the blast crisis of chronic myelocytic leukemia may fail to respond or may relapse upon discontinuance of therapy.

Myasthenia Gravis

Has been used in the management of myasthenia gravis^†, usually when there is an inadequate response to anticholinesterase therapy.

Some experts state that corticosteroids should be used as the initial immunosuppressive agent in ocular myasthenia gravis; however, may cause transient worsening within the first 2 weeks. Monitor patients carefully.

Organ Transplants

Used in massive dosages with or without other immunosuppressive drugs to prevent rejection of transplanted organs^†.

Incidence of secondary infections is high with immunosuppressive drugs; limit to clinicians experienced in their use.

Trichinosis

Treatment of trichinosis with neurologic or myocardial involvement.

Nephrotic Syndrome and Lupus Nephritis

Treatment of idiopathic nephrotic syndrome without uremia.

Can induce diuresis and remission of proteinuria in nephrotic syndrome secondary to primary renal disease, especially when there is minimal renal histologic change.

Treatment of lupus nephritis.

Bacterial Meningitis

Has been used in the treatment of bacterial meningitis^†.

In a Cochrane review, corticosteroids were found to reduce hearing loss and neurological sequelae, but did not improve overall mortality. The benefits were limited to high-income countries; there was no beneficial effect of corticosteroid therapy in low-income countries.

Related/similar drugs

Rinvoq, Benlysta, Cimzia, Nplate, Otezla, Saphnelo, Vumerity

Prednisone Dosage and Administration

General

• Dosage depends on the condition being treated and the patient response.

Alternate-day Therapy

• Alternate-day therapy, in which a single dose (twice the usual daily dosage) is administered every other morning, is the dosage regimen of choice for long-term oral glucocorticoid treatment of most conditions. This regimen provides relief of symptoms while minimizing adrenal suppression, protein catabolism, and other adverse effects.

• If alternate-day therapy is preferred, only use a “short-acting” glucocorticoid that suppresses the HPA axis <1.5 days after a single oral dose (e.g., prednisone, prednisolone, methylprednisolone).

• Some conditions (e.g., rheumatoid arthritis, ulcerative colitis) require daily glucocorticoid therapy because symptoms of the underlying disease cannot be controlled by alternate-day therapy.

Discontinuance of Therapy

• A steroid withdrawal syndrome consisting of lethargy, fever, myalgia can develop following abrupt discontinuance. Symptoms often occur without evidence of adrenal insufficiency (while plasma glucocorticoid concentrations were still high but were falling rapidly).

• If used for only brief periods (a few days) in emergency situations, may reduce and discontinue dosage quite rapidly.

• Very gradually withdraw systemic glucocorticoids until recovery of HPA-axis function occurs following long-term therapy with pharmacologic dosages. (See Adrenocortical Insufficiency under Cautions.)

• Exercise caution when transferring from systemic glucocorticoid to oral or nasal inhalation corticosteroid therapy.

• Many methods of slow withdrawal or “tapering” have been described.

• In one suggested regimen, decrease by 2.5–5 mg every 3–7 days until the physiologic dose (5 mg) is reached.

• Other recommendations state that decrements usually should not exceed 2.5 mg every 1–2 weeks.

• When physiologic dosage is reached, single 20-mg oral morning doses of hydrocortisone can be substituted for whatever glucocorticoid the patient was receiving. After 2–4 weeks, may decrease hydrocortisone dosage by 2.5 mg every week until a single morning dosage of 10 mg daily reached.

• For certain acute allergic conditions (e.g., contact dermatitis such as poison ivy) or acute exacerbations of chronic allergic conditions, glucocorticoids may be administered short term (e.g., for 6 days). Administer a high dose on the first day of therapy, then withdraw therapy by tapering the dosage over several days. (See Allergic Conditions under Dosage and Administration.)

Administration

Oral Administration

Administered orally as tablets, solution, or solution concentrate; also has been administered as an extemporaneously prepared suspension. May dilute oral concentrate in juice or other flavored diluent or in semisolid food (e.g., applesauce) prior to administration.

To prepare an extemporaneous suspension containing prednisone 10 mg/mL, mix 5 g of prednisone as tablets with 200 mL of 0.1% sodium benzoate solution. Add 100 mL of an aqueous suspension containing 3% tragacanth, 3% acacia, and 0.1% sodium benzoate and stir the mixture until homogeneous. Dilute to 500 mL with a mixture of 67% simple syrup and 33% cherry syrup to a final concentration of 10 mg/mL.

May prepare 4 L of the tragacanth-acacia suspension in a container that can be closed for vigorous agitation. Initially, dissolve 4 g of sodium benzoate in 2 L of purified water. Add 120 g of powdered tragacanth and 120 g of acacia in that order and shake the container vigorously. Add additional water gradually over 24–48 hours with agitation at regular intervals until a volume of 4 L and a smooth suspension results. To mask the odor, may add 1 mL of anise oil.

Dosage

After a satisfactory response is obtained, decrease dosage in small decrements to the lowest level that maintains an adequate clinical response, and discontinue the drug as soon as possible.

Monitor patients continually for signs that indicate dosage adjustment is necessary, such as remissions or exacerbations of the disease and stress (surgery, infection, trauma).

High dosages may be required for acute situations of certain rheumatic disorders and collagen diseases. After a response has been obtained, drug often must be continued for long periods at low dosage.

High or massive dosages may be required in the treatment of pemphigus, exfoliative dermatitis, bullous dermatitis herpetiformis, severe erythema multiforme, or mycosis fungoides. Early initiation of systemic glucocorticoid therapy may be life-saving in pemphigus vulgaris. Reduce dosage gradually to the lowest effective level, but discontinuance may not be possible.

Pediatric Patients

Base pediatric dosage on severity of the disease and patient response rather than on strict adherence to dosage indicated by age, body weight, or body surface area.

Usual Dosage

Oral

0.14–2 mg/kg daily or 4–60 mg/m² daily in 4 divided doses.

Coronavirus Disease 2019 (COVID-19)†

Oral

When a corticosteroid is used, NIH COVID-19 Treatment Guidelines Panel recommends dexamethasone (0.15 mg/kg [maximum 6 mg] given IV or orally once daily for up to 10 days). If dexamethasone not available, may consider equivalent dosages of an alternative corticosteroid (e.g., prednisone). Consult most recent NIH treatment guidelines for additional information on use of corticosteroids in pediatric patients with COVID-19.

Allergic Conditions

Oral

For certain conditions (e.g., contact dermatitis, including poison ivy), 30 mg (6 tablets) for the first day, which is then tapered by 5 mg daily until 21 tablets have been administered (see Table 1).

Adults

Usual Dosage

Oral

Initially, 5–60 mg daily, depending on the disease being treated, usually in 2–4 divided doses.

Coronavirus Disease 2019 (COVID-19)†

Oral

NIH COVID-19 Treatment Guidelines Panel recommends prednisone 40 mg given once daily or in 2 divided doses. Consult most recent NIH treatment guidelines for additional information on use of corticosteroids in patients with COVID-19.

Allergic Conditions

Oral

For certain conditions (e.g., contact dermatitis, including poison ivy), 30 mg (6 tablets) for the first day, which is then tapered by 5 mg daily until 21 tablets have been administered (see Table 2).

Advanced Pulmonary or Extrapulmonary Tuberculosis

Oral

For severe systemic and respiratory complications of advanced pulmonary tuberculosis: 40–60 mg daily, tapered over 4–8 weeks.

Tuberculous meningitis: 1 mg/kg daily for 30 days, followed by gradual tapering of the dosage over a period of weeks, has been suggested.

Cautions for Prednisone

Contraindications

• Known hypersensitivity to prednisone, any ingredient in the respective formulation, or any other corticosteroid.

• Systemic fungal infections.

• Concurrent administration of live or live, attenuated vaccines in patients receiving immunosuppressive doses of corticosteroids.

Warnings/Precautions

Warnings

Adrenocortical Insufficiency

When given in supraphysiologic doses for prolonged periods, glucocorticoids may cause decreased secretion of endogenous corticosteroids by suppressing pituitary release of corticotropin (secondary adrenocortical insufficiency).

The degree and duration of adrenocortical insufficiency is highly variable among patients and depends on the dose, frequency and time of administration, and duration of glucocorticoid therapy.

Acute adrenal insufficiency (even death) may occur if the drugs are withdrawn abruptly or if patients are transferred from systemic glucocorticoid therapy to local (e.g., inhalation) therapy.

Withdraw prednisone very gradually following long-term therapy with pharmacologic dosages.

Adrenal suppression may persist up to 12 months in patients who receive large dosages for prolonged periods.

Until recovery occurs, may develop signs and symptoms of adrenal insufficiency if subjected to stress (e.g., infection, surgery, trauma, illness) and may require replacement therapy. Since mineralocorticoid secretion may be impaired, sodium chloride and/or a mineralocorticoid also should be administered.

If the disease flares up during withdrawal, may need to increase dosage and follow with a more gradual withdrawal.

Immunosuppression

Increased susceptibility to infections secondary to glucocorticoid-induced immunosuppression. Certain infections (e.g., varicella [chickenpox], measles) can have a more serious or even fatal outcome in such patients. (See Increased Susceptibility to Infection under Cautions.)

Administration of live virus vaccines, including smallpox, is contraindicated in patients receiving immunosuppressive dosages of glucocorticoids. In addition, if inactivated viral or bacterial vaccines are administered to such patients, expected serum antibody response may not be obtained. The USPHS Advisory Committee on Immunization Practices (ACIP) and American Academy of Family Physicians (AAFP) state that administration of live virus vaccines usually is not contraindicated in patients receiving corticosteroid therapy under the following circumstances:

• short-term (<2 weeks) therapy

• low to moderate dosage

• long-term alternate-day treatment with short-acting preparations

• maintenance physiologic dosages (replacement therapy)

• topical, ophthalmic, intra-articular, bursal, or intratendon administration

Increased Susceptibility to Infection

Glucocorticoids, especially in large doses, increase susceptibility to and mask symptoms of infection.

Infections with any pathogen, including viral, bacterial, fungal, protozoan, or helminthic infections in any organ system, may be associated with glucocorticoids alone or in combination with other immunosuppressive agents; reactivation of latent infections may occur.

Infections may be mild, but they can be severe or fatal, and localized infections may disseminate.

Do not use, except in life-threatening situations, in patients with viral infections or bacterial infections not controlled by anti-infectives.

Some infections (e.g., varicella [chickenpox], measles) can have a more serious or even fatal outcome, particularly in children.

Children and any adult who are not likely to have been exposed to varicella or measles should avoid exposure to these infections while receiving glucocorticoids.

If exposure to varicella or measles occurs in susceptible patients, treat appropriately (e.g., varicella zoster immune globulin [VZIG], immune globulin [IG]).

Prolonged use of systemic corticosteroids in patients with COVID-19^† may increase risk of reactivation of latent infections (e.g., HBV, herpesvirus, strongyloidiasis, tuberculosis). Risk of reactivation of latent infections following a 10-day course of dexamethasone (6 mg once daily) or equivalent corticosteroid therapy (e.g., prednisone) not well established. When initiating prednisone in patients with COVID-19, consider appropriate screening and treatment to reduce the risk of Strongyloides hyperinfection in those at high risk (e.g., patients from tropical, subtropical, or warm, temperate regions or those engaged in agricultural activities) and reduce the risk of fulminant reactivation of HBV.

Not effective and can have detrimental effects in the management of cerebral malaria.

Can reactivate tuberculosis. Include chemoprophylaxis in patients with a history of active tuberculosis undergoing prolonged glucocorticoid therapy. Observe closely for evidence of reactivation. Restrict use in active tuberculosis to those with fulminating or disseminated tuberculosis in which glucocorticoids are used in conjunction with appropriate antimycobacterial chemotherapy.

Can reactivate latent amebiasis. Exclude possible amebiasis in any patient who has been in the tropics or who has unexplained diarrhea prior to initiating therapy.

Musculoskeletal Effects

Muscle wasting, muscle pain or weakness, delayed wound healing, and atrophy of the protein matrix of the bone resulting in osteoporosis, vertebral compression fractures, aseptic necrosis of femoral or humeral heads, or pathologic fractures of long bones are manifestations of protein catabolism that may occur during prolonged therapy with glucocorticoids. These adverse effects may be especially serious in geriatric or debilitated patients. A high protein diet may help to prevent adverse effects associated with protein catabolism.

An acute, generalized myopathy can occur with the use of high doses of glucocorticoids, particularly in patients with disorders of neuromuscular transmission (e.g., myasthenia gravis) or in patients receiving concomitant therapy with neuromuscular blocking agents (e.g., pancuronium). Use with caution in patients with myasthenia gravis.

Osteoporosis and related fractures are one of the most serious adverse effects of long-term glucocorticoid therapy. The American College of Rheumatology (ACR) has published guidelines on prevention and treatment of glucocorticoid-induced osteoporosis. Recommendations are made according to a patient's risk of fracture.

Fluid and Electrolyte Disturbances

Sodium retention with resultant edema, potassium loss, and elevation of blood pressure may occur, but is less common with prednisone than with average or large doses of cortisone or hydrocortisone. Risk is increased with high-dose synthetic glucocorticoids for prolonged periods. Edema and CHF (in susceptible patients) may occur.

Dietary salt restriction is advisable and potassium supplementation may be necessary.

Increased calcium excretion and possible hypocalcemia.

Ocular Effects

Prolonged use may result in posterior subcapsular and nuclear cataracts (particularly in children), exophthalmos, and/or increased intraocular pressure (IOP) which may result in glaucoma or may occasionally damage the optic nerve.

May enhance the establishment of secondary fungal or viral infections of the eye.

Do not use in patients with active ocular herpes simplex infections for fear of corneal perforation.

Endocrine and Metabolic Effects

With prolonged therapy, may produce various endocrine disorders including hypercorticism (cushingoid state) and amenorrhea or other menstrual difficulties.

Increased or decreased motility and number of sperm in some men.

May decrease glucose tolerance, produce hyperglycemia, and aggravate or precipitate diabetes mellitus, especially in patients predisposed to diabetes mellitus. If glucocorticoid therapy is required in patients with diabetes mellitus, may be necessary to change insulin or oral antidiabetic agent dosage or diet.

Exaggerated response to glucocorticoids in hypothyroidism.

Cardiovascular Effects

Use with extreme caution in recent MI since an association between use of glucocorticoids and left ventricular free-wall rupture has been suggested.

Sodium retention with resultant edema, potassium loss, hypokalemic alkalosis, and hypertension may occur in patients receiving glucocorticoids. CHF may occur in susceptible patients.

Should be used with caution in patients with hypertension or CHF.

Sensitivity Reactions

Urticaria and other allergic, anaphylactic, or hypersensitivity reactions reported.

General Precautions

Monitoring

Prior to initiation of long-term glucocorticoid therapy, perform baseline ECGs, blood pressures, chest and spinal radiographs, glucose tolerance tests, and evaluations of HPA-axis function in all patients.

Perform upper GI radiographs in patients predisposed to GI disorders, including those with known or suspected peptic ulcer disease.

During long-term therapy, perform periodic height, weight, chest and spinal radiographs, hematopoietic, electrolyte, glucose tolerance, and ocular and BP evaluations.

GU Effects

Increased or decreased motility and number of sperm in some men.

Nervous System Effects

May precipitate mental disturbances ranging from euphoria, insomnia, mood swings, depression, and personality changes to frank psychoses. Use may aggravate emotional instability or psychotic tendencies.

GI Effects

Use with caution in patients with diverticulitis, nonspecific ulcerative colitis (if there is a probability of impending perforation, abscess, or pyogenic infection), or those with recent intestinal anastomoses.

Signs of peritoneal irritation following GI perforation may be absent in patients receiving corticosteroids.

Use with caution in patients with active or latent peptic ulcer. Suggest concurrent administration of antacids between meals to prevent peptic ulcer formation in patients receiving high dosages of corticosteroids.

Dermatologic Effects

Kaposi’s sarcoma has been reported to occur in patients receiving glucocorticoid therapy; discontinuance of such therapy may result in remission of the disease.

Specific Populations

Pregnancy

Corticosteroids have been shown to be teratogenic in many species when administered in clinical doses. No adequate and well-controlled studies in pregnant women. Use during pregnancy only potential benefit justifies potential risk to fetus.

Lactation

Glucocorticoids are distributed into milk and could suppress growth, interfere with endogenous glucocorticoid production, or cause other adverse effects in nursing infants. Use with caution.

Pediatric Use

The effects of glucocorticoids on the pathophysiology and course of diseases are considered to be similar in adults and children.

Adverse effects in pediatric patients are similar to those in adults. As in adults, perform periodic evaluations of height, weight, ocular pressure, and BP. Children, like adults, also should undergo clinical evaluation for the presence of infection, psychosocial disturbances, thromboembolism, peptic ulcers, cataracts, and osteoporosis.

With long-term use, may delay growth and maturation in children and adolescents. Monitor carefully the growth and development of pediatric patients receiving prolonged corticosteroid therapy. Titrate dosage to the lowest effective level. Alternate-day therapy with glucocorticoids that cause shorter HPA-axis suppression than does dexamethasone (e.g., prednisone, prednisolone, methylprednisolone) may minimize growth suppression and should be instituted if growth suppression occurs.

Safety and efficacy of dexamethasone and other corticosteroids (e.g., prednisone) for COVID-19^† treatment not fully evaluated in pediatric patients. Use caution when extrapolating recommendations for adults with COVID-19 to pediatric patients <18 years of age. The NIH COVID-19 Treatment Guidelines Panel recommends use of dexamethasone (see Pediatric Patients under Dosage, in Dosage and Administration) for hospitalized pediatric patients with COVID-19 who are receiving high-flow oxygen, noninvasive ventilation, invasive mechanical ventilation, or extracorporeal membrane oxygenation (ECMO); dexamethasone not routinely recommended for pediatric patients who require only low levels of oxygen support (i.e., nasal cannula only). If dexamethasone not available, the NIH panel states that alternative corticosteroids (e.g., prednisone) at equivalent dosages may be considered. Use of corticosteroids for treatment of severe COVID-19 in pediatric patients who are profoundly immunocompromised not evaluated to date and may be harmful; therefore, the NIH panel states consider such use only on a case-by-case basis. IV corticosteroids have been used as first-line therapy in pediatric patients with multisystem inflammatory syndrome in children (MIS-C); however, the NIH panel recommends consultation with a multidisciplinary team when considering and managing immunomodulating therapy for children with this condition. Optimal choice and combination of immunomodulating therapies for children with MIS-C not definitely established. Consult the most recent NIH COVID-19 treatment guidelines for additional information on use of corticosteroids in pediatric patients with COVID-19.

Geriatric Use

With prolonged therapy, muscle wasting, muscle pain or weakness, delayed wound healing, atrophy of the protein matrix of the bone resulting in osteoporosis, vertebral compression fractures, aseptic necrosis of femoral or humeral heads, or pathologic fractures of long bones may occur. May be especially serious in geriatric or debilitated patients.

Before initiating glucocorticoid therapy in postmenopausal women, consider that such women are especially prone to osteoporosis.

Use with caution in patients with osteoporosis.

Hepatic Impairment

Patients with cirrhosis show an exaggerated response to glucocorticoids.

Renal Impairment

Use with caution.

Common Adverse Effects

Associated with long-term therapy: Bone loss, cataracts, indigestion, muscle weakness, back pain, bruising, oral candidiasis.

Drug Interactions

Metabolized by CYP3A4.

Drugs Affecting Hepatic Microsomal Enzymes

Inhibitors of CYP3A4: Potential pharmacokinetic interaction (decreased prednisone clearance).

Inducers of CYP3A4: Potential pharmacokinetic interaction (increased clearance of prednisone).

Specific Drugs and Laboratory Tests

Prednisone Pharmacokinetics

Distribution

Extent

Most corticosteroids are rapidly removed from blood and distributed to muscles, liver, skin, intestines, and kidneys. Distributed into breast milk and cross placenta.

Corticosteroids metabolized in most tissues, but primarily in liver, to inactive compounds.

Special Populations

In patients with hypothyroidism, metabolic clearance of corticosteroids decreased.

In patients with hyperthyroidism, metabolic clearance of corticosteroids increased.

Changes in thyroid status may necessitate adjustment of glucocorticoid dosage.

Stability

Storage

Oral

Tablets

205–25°C.

Solution

15–30°C.

Extemporaneous Suspension

Stable at 2–8°C for 2 months.

Actions

• Principally an anti-inflammatory or immunosuppressant agent. Exhibits anti-inflammatory activity and minimal mineralocorticoid properties.

• Has approximately half the mineralocorticoid activity of hydrocortisone and cortisone.

• Decreases inflammation by stabilizing leukocyte lysosomal membranes, preventing release of destructive acid hydrolases from leukocytes, or reducing leukocyte adhesion to capillary endothelium.

• Inhibits macrophage accumulation in inflamed areas.

• Reduces capillary wall permeability and edema formation.

• Antagonizes histamine activity and release of kinin from substrates.

• Reduces fibroblast proliferation, collagen deposition, and subsequent scar tissue formation.

• Stimulates erythroid cells of bone marrow, prolongs survival time of erythrocytes and platelets, and produces neutrophilia and eosinopenia.

• Promotes gluconeogenesis, redistribution of fat from peripheral to central areas of the body, and protein catabolism, which results in negative nitrogen balance.

• Reduces intestinal absorption and increases renal excretion of calcium.

• Suppresses the immune response by reducing activity and volume of the lymphatic system, producing lymphocytopenia.

• Decreases immunoglobulin and complement concentrations and passage of immune complexes through basement membranes.

• Depresses reactivity of tissue to antigen-antibody interactions.

• In patients receiving long-term therapy, importance of not discontinuing the drug abruptly.

• Importance of notifying a clinician of any infections, signs of infections (e.g., fever, sore throat, pain during urination, muscle aches), or injuries that develop during therapy or within 12 months after therapy is discontinued.

• Importance of carrying identification cards listing the diseases being treated, the glucocorticoid regimen, and the name and telephone number of the clinician.

• When surgery is required, importance of informing the attending physician, dentist, or anesthesiologist of recent (within 12 months) glucocorticoid therapy.

• In immunosuppressed patients, importance of avoiding exposure to certain infections (e.g., chickenpox, measles) and of the importance of obtaining medical advice if such exposure occurs.

• Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs, as well as any concomitant illnesses.

• Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.

• Importance of informing patients of other important precautionary information. (See Cautions.)

Additional Information

The American Society of Health-System Pharmacists, Inc. represents that the information provided in the accompanying monograph was formulated with a reasonable standard of care, and in conformity with professional standards in the field. Readers are advised that decisions regarding use of drugs are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and that the information contained in the monograph is provided for informational purposes only. The manufacturer’s labeling should be consulted for more detailed information. The American Society of Health-System Pharmacists, Inc. does not endorse or recommend the use of any drug. The information contained in the monograph is not a substitute for medical care.

Preparations

Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.

* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name

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