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prednisoLONE (Systemic)

Class: Adrenals
ATC Class: H02AB04
VA Class: HS051
CAS Number: 52438-85-4
Brands: Orapred, Pediapred, Prelone Syrup

Medically reviewed by on May 23, 2022. Written by ASHP.


Synthetic glucocorticoid; minimal mineralocorticoid activity.

Uses for prednisoLONE (Systemic)

Treatment of a wide variety of diseases and conditions, 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 prednisolone 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.


Treatment of hypercalcemia associated with malignancy.

Usually ameliorates hypercalcemia associated with bone involvement in multiple myeloma.

Treatment of hypercalcemia associated with sarcoidosis.

Treatment of hypercalcemia associated with vitamin D intoxication.

Not effective for hypercalcemia caused by hyperparathyroidism.


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 palliative 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's syndrome, rheumatic fever [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, Sjogren'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, the 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, uncontrollable eczema, cutaneous sarcoidosis, mycosis fungoides, lichen planus, severe psoriasis, 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 glucocorticoid therapy.

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 unresponsive 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 of chronic allergic conditions to disabling conditions unresponsive to more conservative therapy and when risks of long-term glucocorticoid therapy are justified.

Ocular Disorders

To suppress a variety of allergic and nonpyogenic ocular inflammations.

To reduce scarring in ocular injuries.

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.

Acute optic neuritis optimally treated with initial high-dose IV (e.g., methylprednisolone) therapy followed by chronic oral corticosteroid therapy. Aids in recovery of vision and slows progression to clinically definite multiple sclerosis. In a randomized, placebo-controlled trial, oral corticosteroid (e.g., prednisone) monotherapy did not improve the rate of vision recovery and was associated with an increased risk of new episodes of optic neuritis in either eye.

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.


Adjunctively for moderate to severe exacerbations of asthma and for maintenance in persistent asthma.

Corticosteroids used systemically (oral or IV) for treatment of moderate to severe acute exacerbations of asthma (oral prednisone usually preferred); speeds resolution of airflow obstruction and reduces rate of relapse.

Because onset of effects is delayed, do not use alone for emergency treatment.

Early systemic glucocorticoid therapy particularly important for asthma exacerbations in infants and children.

Orally as an adjunct to other therapy to speed resolution of all but the mildest exacerbations of asthma when response to a short-acting inhaled β2-agonist is not prompt or sustained after 1 hour or in those who have a history of severe exacerbations.

Oral glucocorticoids with minimal mineralocorticoid activity and relatively short half-life (e.g., prednisone, prednisolone, methylprednisolone) are preferred.

In hospital management of an acute asthma exacerbation, use systemic adjunctive glucocorticoids if response to oral inhalation therapy is not immediate, if oral corticosteroids were used as self-medication prior to hospitalization, or if the episode is severe.

For severe persistent asthma once initial control is achieved, high dosages of inhaled corticosteroids are preferable to oral glucocorticoids for maintenance because inhaled corticosteroids have fewer systemic effects.

Maintenance therapy with low doses of an orally inhaled corticosteroid is preferred treatment for adults and children with mild persistent asthma (i.e., patients with daytime symptoms of asthma more than twice weekly but less than once daily, and nocturnal symptoms of asthma more than twice per month).

Chronic Obstructive Pulmonary Disease

For severe exacerbations of chronic obstructive pulmonary disease (COPD), a short (e.g., 1–2 weeks) course of oral glucocorticoids can be added to existing therapy.

Much less dramatic effects in stable COPD than in asthma, and the role of glucocorticoids is limited to very specific indications.


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.

Advanced Pulmonary and Extrapulmonary Tuberculosis

Used systemically as adjunctive therapy with effective antimycobacterial agents (e.g., streptomycin, isoniazid) to suppress manifestations related to the host’s inflammatory response to the bacillus (Mycobacterium tuberculosis) and ameliorate complications in severe pulmonary or extrapulmonary (disseminated) tuberculosis.

In advanced pulmonary tuberculosis, adjunctive glucocorticoid therapy may enhance short-term resolution of disease manifestations (e.g., clinical and radiographic abnormalities).

In certain forms of extrapulmonary disease (e.g., meningitis, pericarditis), also may reduce mortality.

In moderate to severe tuberculous meningitis, systemic adjunctive glucocorticoids may reduce sequelae (e.g., intellectual impairment) and/or improve survival. Used concurrently with appropriate antituberculous chemotherapy in the treatment of tuberculous meningitis with subarachnoid block or impending block. Speeds resolution of abnormal CSF parameters (e.g., elevated intracranial pressure, basal exudate, CNS tuberculomas).

In acute tuberculous pericarditis, systemic adjunctive glucocorticoid therapy rapidly reduces the size of pericardial effusions and the need for drainage procedures and decreases mortality (probably through control of hemodynamically threatening effusion).

In tuberculous pleurisy, hastens the resolution of pain, dyspnea, and fever.

Used adjunctively with antimycobacterial agents for the treatment of tuberculosis with enlarged mediastinal lymph nodes causing respiratory difficulty. The safety and efficacy of adjunctive glucocorticoid therapy in patients with tuberculous lymphadenitis, miliary or laryngeal tuberculosis, or HIV-associated tuberculosis has not been fully elucidated.

Eosinophilic Pneumonias

Used in the management of idiopathic eosinophilic pneumonias.

Hypersensitivity Pneumonitis

Used in the management of hypersensitivity pneumonitis.

Pulmonary Fibrosis

Used in the management of idiopathic pulmonary fibrosis.

Lipid Pneumonitis†

Promotes the breakdown or dissolution of pulmonary lesions and eliminates sputum lipids.

>Pneumocystis carinii Pneumonia

Used adjunctively with appropriate anti-infective therapy in the management of moderate to severe Pneumocystis carinii pneumonia in patients with acquired immunodeficiency syndrome (AIDS) to decrease the likelihood of deterioration of oxygenation, respiratory failure, and/or death.

Allergic Bronchopulmonary Aspergillosis

Used in the management of allergic bronchopulmonary aspergillosis.

Bronchiolitis Obliterans

Used in the management of idiopathic bronchiolitis obliterans with organizing pneumonia.

Loeffler’s Syndrome

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


Symptomatic relief of acute manifestations of berylliosis.

Aspiration Pneumonitis

Symptomatic relief of acute manifestations of aspiration pneumonitis.


Adjunct to anti-infective therapy in the treatment of anthrax in an attempt to ameliorate toxin-mediated effects associated with Bacillus anthracis infections.

Used for cutaneous anthrax if there are signs of systemic involvement or extensive edema involving the neck and thoracic region. Has been used for anthrax meningitis, and inhalational anthrax that occurs as the result of exposure to anthrax spores in the context of biologic warfare or bioterrorism if extensive edema, respiratory compromise, or meningitis is present.

Hematologic Disorders

Management of acquired (autoimmune) hemolytic anemia, idiopathic thrombocytopenic purpura (ITP), secondary thrombocytopenia, erythroblastopenia, congenital (erythroid) hypoplastic anemia (Diamond-Blackfan 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.


To reduce the pain, fever, and inflammation of pericarditis, including that associated with MI.

Glucocorticoids can provide effective symptomatic relief, but aspirin considered the treatment of choice for postmyocardial infarction pericarditis because of greater evidence establishing benefit.

Important to distinguish between pain caused by pericarditis and that caused by ischemia since management will differ.

Consider possibility that cardiac rupture may account for recurrent pain since use of glucocorticoids may be a risk factor in its development.

Glucocorticoids may cause thinning of developing scar and myocardial rupture.

Management of tuberculous pericarditis. (See Advanced Pulmonary and Extrapulmonary Tuberculosis under Uses.)

GI Diseases

Short-term palliative therapy for acute exacerbations and systemic complications of ulcerative colitis or 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.

Do not use if a probability of impending perforation, abscess, or other pyogenic infection.

Crohn’s Disease

Management of mildly to moderately active and moderately to severely active Crohn’s disease.

Some experts state that conventional glucocorticoids should not be used for the management of mildly to moderately active disease because of their high incidence of adverse effects, and their use should be reserved for patients with moderately to severely active disease.

Parenteral glucocorticoids recommended for patients with severe fulminant Crohn’s disease. Once patients respond to parenteral therapy, they should gradually be switched to an equivalent regimen of an oral glucocorticoid.

Glucocorticoids should not be used for maintenance therapy of Crohn’s disease because they usually do not prevent relapses and the drugs may produce severe adverse reactions with long-term administration.

Glucocorticoids have been used in the management of moderately to severely active Crohn’s disease and in mild esophageal or gastroduodenal Crohn’s disease in pediatric patients.

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.

Treatment of breast cancer: Glucocorticoids alone not as effective as other agents (e.g., cytotoxic agents, hormones, antiestrogens) and should be reserved for unresponsive disease.

Glucocorticoids alone or as a component of various combination chemotherapeutic regimens for palliative treatment of advanced, symptomatic (i.e., painful) hormone-refractory prostate cancer.

Cerebral Malaria

Glucocorticoids are not effective and can have detrimental effects in the management of cerebral malaria caused by Plasmodium falciparum; no longer recommended for this condition.

Liver Disease

In patients with subacute hepatic necrosis and chronic active hepatitis, high-dose glucocorticoids can decrease serum bilirubin, ascites, and mortality rate. In nonalcoholic cirrhosis in women, the drugs increase survival rate in the absence of ascites, but not when ascites is present. May decrease mortality rate in patients with alcoholic cirrhosis with hepatic encephalopathy, but should not be used in less seriously ill patients.

Multiple Sclerosis

Glucocorticoids are drugs of choice for the management of acute relapses of multiple sclerosis. Have replaced corticotropin as the therapy of choice because of a more rapid onset of action, more consistent effects, and fewer adverse effects.

Anti-inflammatory and immunomodulating effects accelerate neurologic recovery by restoring the blood-brain barrier, reducing edema, and possibly improving axonal conduction.

Shortens the duration of relapse and accelerates recovery; remains to be established whether the overall degree of recovery improves or the long-term course is altered.

Myasthenia Gravis

Management of myasthenia gravis, usually when there is an inadequate response to anticholinesterase therapy.

Organ Transplants

Used in massive dosage 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.


Treatment of trichinosis with neurologic or myocardial involvement.

Nephrotic Syndrome and Lupus Nephritis

Treatment of idiopathic nephrotic syndrome without uremia.

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

Treatment of lupus nephritis.

prednisoLONE (Systemic) Dosage and Administration


  • Route of administration and dosage depend 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 Warnings.)

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


Oral Administration

Administer orally as tablets, syrup, or oral solution.


Dosage of prednisolone sodium phosphate is expressed in terms of prednisolone.

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

Syrup or tablets: Initially, 0.14–2 mg/kg daily or 4–60 mg/m2 daily in 4 divided doses.

Oral solution: Initially, 0.14–2 mg/kg daily or 4–60 mg/m2 daily in 3 or 4 divided doses.


For the treatment of refractory bronchial asthma and related bronchospasm (severe persistent asthma) not controlled with high maintenance dosages of an inhaled corticosteroid and a long-acting bronchodilator, add an oral corticosteroid (e.g., prednisone, prednisolone, methylprednisolone) at a dosage of 1–2 mg/kg daily in single or divided doses. Continue a short course of oral corticosteroid therapy (usually 3–10 days) until a peak expiratory flow rate of 80% of personal best is achieved or until symptoms resolve. May need a longer duration of treatment in some children. No evidence that tapering the dosage after improvement will prevent relapse.

Nephrotic Syndrome

Usual dosage: 60 mg/m2 given in 3 divided doses for 4 weeks, followed by 4 weeks of alternate-day therapy at single doses of 40 mg/m2.


Usual Dosage

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

Acute Exacerbations of Multiple Sclerosis

Usual dosage: 200 mg daily for 1 week, followed by 80 mg every other day for a month.

Cautions for prednisoLONE (Systemic)


  • Known hypersensitivity to prednisolone, 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. (See Specific Drugs under Interactions.)



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 prednisolone very gradually following long-term therapy with pharmacologic dosages. (See Discontinuance of Therapy under Dosage and Administration: Dosage.)

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

Until recovery occurs, signs and symptoms of adrenal insufficiency may develop if subjected to stress (e.g., infection, surgery, trauma, illness) and replacement therapy may be required. 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 temporarily and then withdraw drug more gradually.


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 Warnings.)

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 long-acting preparations

  • maintenance physiologic dosages (replacement therapy)

  • if it is administered topically, ophthalmically, intra-articularly, bursally, or into a tendon

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.

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 adults 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., VZIG, IG, acyclovir).

Fatal outcome (e.g., in those developing hemorrhagic varicella) may not always be avoided even if appropriate therapy is initiated aggressively.

Immunosuppression may result in activation of latent infection or exacerbation of intercurrent infections (e.g., those caused by Candida, Mycobacterium, Toxoplasma, Strongyloides, Pneumocystis, Cryptococcus, Nocardia, Ameba).

Use with great care in patients with known or suspected Strongyloides (threadworm) infection. Immunosuppression may lead to Strongyloides hyperinfection and dissemination with widespread larval migration, often accompanied by severe enterocolitis and potentially fatal gram-negative septicemia.

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).

Tendon rupture, particularly of the Achilles tendon.

Osteoporosis and related fractures are one of the most serious adverse effects of long-term glucocorticoid therapy. The American College of Rheumatology (ACR) currently considers patients receiving or planning to receive the equivalent of at least 5 mg of prednisone (i.e., 5 mg of prednisolone) daily for 3 months or longer to be at risk for bone loss.

To minimize the risk of glucocorticoid-induced bone loss, should use the smallest possible effective dosage and duration and use topical and inhaled preparations whenever possible. Obtain baseline measurement of bone mass density (BMD) at the lumbar spine and/or hip when initiating long-term (e.g., exceeding 6 months) glucocorticoid therapy and initiate appropriate preventive therapy. May repeat longitudinal measurements as often as every 6 months to detect possible bone loss. Less frequent (e.g., annually) follow-up probably is sufficient in patients who are receiving therapy to prevent bone loss.

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

Skeletal wasting is most rapid during the initial 6 months of therapy, and trabecular bone is affected to a greater degree than is cortical bone.

Withdraw glucocorticoids if osteoporosis develops, unless their use is life-saving.

Calcium and vitamin D supplementation, bisphosphonate (e.g., alendronate, risedronate), and a weight-bearing exercise program that maintains muscle mass are suitable first-line therapies aimed at reducing the risk of adverse bone effects.

Calcitonin may be considered as second-line therapy for patients who refuse or do not tolerate bisphosphonate therapy or in whom the drugs are contraindicated.

Fluid and Electrolyte Disturbances

Sodium retention with resultant edema, potassium loss, and elevation of blood pressure may occur but is less common with prednisolone 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 IOP which may result in glaucoma or may occasionally damage the optic nerve. If corticosteroid therapy is continued for >6 weeks, monitor IOP.

May enhance the establishment of secondary fungal, bacterial, and 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. Congestive heart failure may occur in susceptible patients.

Should be used with caution in patients with hypertension or congestive heart failure.

Sensitivity Reactions

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

General Precautions


Prior to initiation of long-term glucocorticoid therapy, perform baseline ECGs, BPs, 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 and weight determinations, chest and spinal radiographs, and hematopoietic, electrolyte, glucose tolerance, ocular pressure, and BP evaluations.

Genitourinary 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.

Use with caution in patients with myasthenia gravis.

GI Effects

Use with caution in patients with diverticulitis, nonspecific ulcerative colitis (if there is a probability of impending perforation, abscess, or other 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


Category C. If substantial dosage is received during pregnancy, carefully observe infant for signs of hypoadrenalism.


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. Evidence of safety and efficacy for prednisolone in pediatric patients based on treatment of nephrotic syndrome (in patients older than 2 years of age) and aggressive leukemias and lymphomas (in patients older than 1 month of age). Evidence of safety and efficacy for other pediatric indications (e.g., severe asthma and wheezing) are based on controlled trials in adults.

The 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.

Glucocorticoid-induced osteoporosis and associated fractures are common in children and adolescents receiving long-term systemic therapy. In addition, may prevent achievement of peak bone mass during adolescence by inhibiting bone formation. Methods for monitoring bone mineralization (e.g., dual-energy x-ray absorptiometry [DEXA]) in children and adolescents are similar to those in adults.

Ensure children and adolescents consistently ingest adequate calcium and vitamin D, either through diet or supplementation.

Geriatric Use

With prolonged therapy, 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 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.

Interactions for prednisoLONE (Systemic)

Metabolized by CYP3A4.

Drugs Affecting Hepatic Microsomal Enzymes

Inhibitors of CYP3A4: Potential pharmacokinetic interaction (decreased prednisolone metabolism).

Inducers of CYP3A4: Potential pharmacokinetic interaction (enhanced metabolism of prednisolone).

Specific Drugs and Laboratory Tests

Drug or Test



Amphotericin B

May enhance the potassium-wasting effect of glucocorticoids

During concomitant use, observe closely

Anticoagulants, oral

Conflicting reports of diminished as well as enhanced response to anticoagulants

Monitor coagulation indices to maintain desired anticoagulant effect

Anticholinesterase agents

Severe weakness with concomitant use of anticholinesterase agents and corticosteroids in patients with myasthenia gravis

If possible, withdraw antichlolinesterase therapy ≥24 hours before initiating corticosteroid therapy

Antidiabetic therapy

Glucocorticoids may increase blood glucose concentration

May require dosage adjustment of concurrent insulin and/or oral hypoglycemic agents


Increased metabolism of prednisolone

May need to increase dosage of prednisolone

Cardiac glycosides

With concurrent use, increased risk for arrhythmias as a result of potential hypokalemia.


Decreased plasma clearance of prednisolone; increased activity of both cyclosporine and corticosteroid

Consider possibility of exacerbated toxicity (seizures), as well as need for dosage adjustment with concomitant use

Diuretics, potassium-depleting

Enhance the potassium-wasting effects of glucocorticoids

Monitor for development of hypokalemia


Increased metabolism of corticosteroids

Increase dosage of prednisolone


May potentiate effects of certain corticosteroids

Dosage adjustment of corticosteroids may be required if estrogens are added to or withdrawn from a stable dosage regimen


Decreased metabolism of prednisolone

May need to decrease dosage of concomitant glucocorticoids to avoid potential adverse effects


Increases the risk of adverse GI effects (ulceration)

Increased clearance of salicylates. When corticosteroids are discontinued, serum salicylate concentration may increase, possibly resulting in salicylate intoxication

With indomethacin and prednisolone administration, plasma concentrations of free prednisolone were increased; total plasma prednisolone concentrations were unchanged. Indomethacin may have a steroid-sparing effect

Use concurrently with caution

Observe patients receiving both drugs closely for adverse effects of either salicylates or corticosteroid

May be necessary to increase salicylate dosage when corticosteroids are administered concurrently or decrease salicylate dosage when corticosteroids are discontinued

Use aspirin and corticosteroids with caution in hypoprothrombinemia


Increased metabolism of prednisolone

May need to increase dosage of prednisolone


Increased metabolism of prednisolone

May need to increase dosage of prednisolone

Tests for nitroblue tetrazolium

May produce false-negative results in the nitroblue tetrazolium test for systemic bacterial infection

Tests for thyroid function

May decrease iodine 131 uptake and protein-bound iodine concentrations, making it difficult to monitor the therapeutic response of patients receiving the drugs for thyroiditis

Tests involving skin antigens

Depresses skin reactivity to antigen-antibody interactions


Decreased clearance of corticosteroids

May need to decrease dosage of concomitant corticosteroids to avoid potential adverse effects

Vaccines and toxoids

May cause a diminished response to toxoids and live or inactivated vaccines

May potentiate replication of some organisms contained in live, attenuated vaccines

Can aggravate neurologic reactions to some vaccines (supraphysiologic dosages)

(See Immunosuppression under Cautions)

prednisoLONE (Systemic) Pharmacokinetics



Following oral administration in patients with asthma, effects may not be evident for several hours.


The duration of anti-inflammatory activity of prednisolone approximately equals the duration of HPA-axis suppression, about 1.25–1.5 days for a single 50-mg oral dose.



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

Plasma Protein Binding

Has a high affinity for transcortin and competes with cortisol for binding to this binding protein. Because only unbound drug is pharmacologically active, patients with low serum albumin concentrations may be more susceptible to glucocorticoid effects.



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.







Tight containers at 4–25°; may be refrigerated.


20–25°C; do not refrigerate.


  • Principally an anti-inflammatory or immunosuppressant agent.

  • 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 increase 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.

Advice to Patients

  • 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.

  • Advise patients receiving orally inhaled glucocorticoid therapy who are currently being withdrawn or who have been withdrawn from systemic therapy to immediately resume full therapeutic dosages of systemic glucocorticoids and to contact their clinician for further instructions during stressful periods (e.g., severe infection, severe asthmatic attack).

  • 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 to breast-feed.

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


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



Dosage Forms


Brand Names






5 mg/5 mL*

prednisoLONE Syrup

Ethex, Hi-Tech, Morton Grove, Paddock, Pharmaceutical Associates, WE Pharmaceuticals

15 mg/5 mL*

prednisoLONE Syrup

Alpharma, Ethex, Hi-Tech, Morton Grove, Paddock, Pharmaceutical Associates, WE Pharmaceuticals

Prednisolone Oral Solution (with alcohol 5% and propylene glycol)


Prelone Syrup (with alcohol 5% and propylene glycol)



5 mg*

prednisoLONE Tablets


prednisoLONE Sodium Phosphate


Dosage Forms


Brand Names




5 mg (of prednisolone) per 5 mL

Pediapred (with methylparaben)


prednisoLONE Sodium Phosphate Oral Solution

Ethex, Hi-Tech, Morton Grove, Paddock, Pharmaceutical Associates, WE Pharmaceuticals

15 mg (of prednisolone) per 5 mL

Orapred (with alcohol 2% and povidone)


prednisoLONE Sodium Phosphate Oral Solution

Ethex, Morton Grove, Pharmaceutical Associates, WE Pharmaceuticals

AHFS DI Essentials™. © Copyright 2022, Selected Revisions June 1, 2006. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.

† Use is not currently included in the labeling approved by the US Food and Drug Administration.

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