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Sterapred

Generic Name: Prednisone
Class: Adrenals
ATC Class: H02AB07
VA Class: HS051
CAS Number: 53-03-2

Introduction

Synthetic glucocorticoid; minimal mineralocorticoid activity.b

Uses for Sterapred

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.c

Adrenocortical Insufficiency

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

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.a c d

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

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

Adrenogenital Syndrome

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

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.c

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

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

Hypercalcemia

Treatment of hypercalcemia associated with malignancy.a c d

Usually ameliorates hypercalcemia associated with bone involvement in multiple myeloma.c

Treatment of hypercalcemia associated with sarcoidosis.c

Treatment of hypercalcemia associated with vitamin D intoxication.c

Not effective for hypercalcemia caused by hyperparathyroidism.c

Thyroiditis

Treatment of granulomatous (subacute, nonsuppurative) thyroiditis.a c d

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

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

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

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 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.a c d e

Relieves inflammation and suppresses symptoms but not disease progression.c

Rarely indicated as maintenance therapy.c

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.a c d

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

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.c

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

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.c e 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.c

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

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

Slideshow: 12 Things You Should Know About Prednisone

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.a c d e

Usually reserved for acute exacerbations unresponsive to conservative therapy.c

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

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

Chronic skin disorders seldom an indication for systemic glucocorticoids.c

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

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

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.a c d e

Systemic therapy usually reserved for acute conditions and severe exacerbations.c

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

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.c f

Ocular Disorders

To suppress a variety of allergic and nonpyogenic ocular inflammations.c

To reduce scarring in ocular injuries.c

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 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.j

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

Oral Disorders

Has been used for oral disorders (i.e., desquamative gingivitis, recurrent aphthous stomatitis) that are unresponsive to topical therapy.e Confirm diagnosis of desquamative gingivitis via immunofluorescence biopsy assay.e

Asthma

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

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.j

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

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

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.c

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, should 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.c

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 asthmac (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).b

COPD

For severe exacerbations of 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.m

Sarcoidosis

Management of symptomatic sarcoidosis.a c d f

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

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.a

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.a d f 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.

Lipid Pneumonitis

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

Pneumocystis jiroveci (Pnemocystis carinii) Pneumonia

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

Loeffler’s Syndrome

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

Berylliosis

Symptomatic relief of acute manifestations of berylliosis.d f

Aspiration Pneumonitis

Symptomatic relief of acute manifestations of aspiration pneumonitis.d f

Anthrax

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, or hemolysis.a d e

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

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.c

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

Pericarditis

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

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, regional enteritis, or celiac disease.a c d e Low dosages of glucocorticoids, in conjunction with other supportive therapy, may occasionally be useful for patients unresponsive to usual therapy for chronic conditions.c

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

Crohn’s Disease

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

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).a c d f

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).c Acute myeloblastic leukemia, lymphosarcoma, and the blast crisis of chronic myelocytic leukemia may fail to respond or may relapse upon discontinuance of therapy.c

Treatment of breast cancere ; glucocorticoids alone not as effective as other agents (e.g., cytotoxic agents, hormones, antiestrogens) and should be reserved for unresponsive disease.c

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

Has been used in Waldenstrom's macroglobulinemia, fever associated with neoplasms, and multiple myeloma.e

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.c

Liver Disease

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

Multiple Sclerosis

Glucocorticoids are drugs of choice for the management of acute relapses of multiple sclerosis.a d 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.e

Organ Transplants

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

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

Trichinosis

Treatment of trichinosis with neurologic or myocardial involvement.a d f

Nephrotic Syndrome and Lupus Nephritis

Treatment of idiopathic nephrotic syndrome without uremia.a d f

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

Treatment of lupus nephritis.a d f

Sterapred Dosage and Administration

General

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

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.a c This regimen provides relief of symptoms while minimizing adrenal suppression, protein catabolism, and other adverse effects.a c

  • 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).c

  • 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.c

Discontinuance of Therapy

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

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

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

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

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

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

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

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

  • 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).c Administer a high dose on the first day of therapy, then withdraw therapy by tapering the dosage over several days.c (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.b May dilute oral concentrate in juice or other flavored diluent or in semisolid food (e.g., applesauce) prior to administration.b

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.b Add 100 mL of an aqueous suspension containing 3% tragacanth, 3% acacia, and 0.1% sodium benzoate and stir the mixture until homogeneous.b Dilute to 500 mL with a mixture of 67% simple syrup and 33% cherry syrup to a final concentration of 10 mg/mL.b

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

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.b f

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

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

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

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.b

Usual Dosage
Oral

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

Pneumocystis jiroveci (Pneumocystis carinii) Pneumonia
Oral

Adolescents >13 years of age with moderate to severe Pneumocystis jiroveci (formerly Pneumocystis carinii) pneumonia and acquired immunodeficiency syndrome (AIDS): 40 mg twice daily for 5 days, followed by 40 mg once daily for 5 days, and then 20 mg once daily for 11 days (or until completion of the anti-infective regimen) currently is recommended. Initiate glucocorticoid therapy within 24–72 hours of initial antipneumocystis therapy. Consult published protocols and the most current clinical guidelines.

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).b

Table 1. Tapered Dosage Schedule

Day

Dosage Schedule

Day 1

Administer 10 mg twice daily (before breakfast and at bedtime) and 5 mg twice daily (after lunch and dinner).b

Day 2

Administer 5 mg 3 times daily (before breakfast, after lunch, and after dinner) and 10 mg at bedtime.b

Day 3

Administer 5 mg 4 times daily (before breakfast, after lunch, after dinner, and at bedtime).b

Day 4

Administer 5 mg 3 times daily (before breakfast, after lunch, and at bedtime).b

Day 5

Administer 5 mg twice daily (before breakfast and at bedtime).b

Day 6

Administer 5 mg before breakfast.b

Adults

Usual Dosage
Oral

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

Pneumocystis jiroveci (Pneumocystis carinii) Pneumonia
Oral

Adults with moderate to severe Pneumocystis jiroveci (formerly Pneumocystis carinii) pneumonia and acquired immunodeficiency syndrome (AIDS): 40 mg twice daily for 5 days, followed by 40 mg once daily for 5 days, and then 20 mg once daily for 11 days (or until completion of the anti-infective regimen) currently is recommended. Initiate within 24–72 hours of initial antipneumocystis therapy. Consult published protocols and the most current clinical guidelines.

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).b

Tapered Dosage Schedule

Day

Dosage Schedule

Day 1

Administer 10 mg twice daily (before breakfast and at bedtime) and 5 mg twice daily (after lunch and dinner)b

Day 2

Administer 5 mg 3 times daily (before breakfast, after lunch, and after dinner) and 10 mg at bedtimeb

Day 3

Administer 5 mg 4 times daily (before breakfast, after lunch, after dinner, and at bedtime)b

Day 4

Administer 5 mg 3 times daily (before breakfast, after lunch, and at bedtime)b

Day 5

Administer 5 mg twice daily (before breakfast and at bedtime)b

Day 6

Administer 5 mg before breakfastb

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.101 102

Tuberculous meningitis: 1 mg/kg daily for 30 days, followed by gradual tapering of the dosage over a period of weeks, has been suggested.102

Tuberculous pericarditis: 60 mg daily tapered over 6–12 weeks.

Tuberculous pleurisy: 20–40 mg daily tapered over 4–8 weeks.

Mediastinal lymphadenopathy associated with primary intrathoracic tuberculosis: 2–5 mg/kg per day (or equivalent), with dosage reduction to 1 mg/kg per day over the first week and tapered over the next 5 weeks.

Multiple Sclerosis
Oral

For acute exacerbations, the manufacturer recommends 200 mg daily for 1 week followed by 80 mg every other day for 1 month.a Alternatively, 60 mg daily tapering over 12 days following IV methylprednisolone (1 g daily for 3–5 days) has been used.

Optic Neuritis
Oral

1 mg/kg daily for 11 days following IV methylprednisolone therapy (1 g daily for 3 days).

Cautions for Sterapred

Contraindications

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

  • Systemic fungal infections.a d f

  • Concurrent administration of live or live, attenuated vaccines in patients receiving immunosuppressive doses of corticosteroids.a d f (See Specific Drugs and Laboratory Tests under Interactions.)

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).c

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.c

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.c

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

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

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.a c d f Since mineralocorticoid secretion may be impaired, sodium chloride and/or a mineralocorticoid also should be administered.c d f

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

Immunosuppression

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

Administration of live virus vaccines, including smallpox, is contraindicated in patients receiving immunosuppressive dosages of glucocorticoids.d In addition, if inactivated viral or bacterial vaccines are administered to such patients, expected serum antibody response may not be obtained.a c d 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, bursol, or intratendon administration

Increased Susceptibility to Infection

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

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.d

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.c

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

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.d

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

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.d 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.c

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

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

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.c These adverse effects may be especially serious in geriatric or debilitated patients.c A high protein diet may help to prevent adverse effects associated with protein catabolism.c

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.f

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 at least 5 mg of prednisone 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 mineral 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.c

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.c

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 for 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 prednisone than with average or large doses of cortisone or hydrocortisone.d Risk is increased with high-dose synthetic glucocorticoids for prolonged periods.c d Edema and CHF (in susceptible patients) may occur.c

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

Increased calcium excretion and possible hypocalcemia.c d

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.d

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

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

Endocrine and Metabolic Effects

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

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

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

Exaggerated response to glucocorticoids in hypothyroidism.c d

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.c

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

Should be used with caution in patients with hypertension or CHF.a c d

Sensitivity Reactions

Urticaria and other allergic, anaphylactic, or hypersensitivity reactions reported.a d f

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.c

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

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.c

Nervous System Effects

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

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.d

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

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

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.d

Specific Populations

Pregnancy

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

Lactation

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

Pediatric Use

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

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

With long-term use, may delay growth and maturation in children and adolescents.c d Monitor carefully the growth and development of pediatric patients receiving prolonged corticosteroid therapy.a c d Titrate dosage to the lowest effective level.c 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.c

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, 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.c May be especially serious in geriatric or debilitated patients.c

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

Use with caution in patients with osteoporosis.d

Hepatic Impairment

Patients with cirrhosis show an exaggerated response to glucocorticoids.c d

Renal Impairment

Use with caution.d

Common Adverse Effects

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

Interactions for Sterapred

Metabolized by CYP3A4.c

Drugs Affecting Hepatic Microsomal Enzymes

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

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

Specific Drugs and Laboratory Tests

Drug or Test

Interaction

Comments

Amphotericin B

May enhance the potassium-wasting effect of glucocorticoidsc

During concomitant use, observe closelyc

Anticoagulants, oral

Conflicting reports of diminished as well as enhanced response to anticoagulantsd

Monitor coagulation indices to maintain desired anticoagulant effectd

Anticholinesterase agents

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

If possible, withdraw anticholinesterase therapy ≥24 hours before initiating corticosteroid therapyc

Antidiabetic therapy

Glucocorticoids may increase blood glucose concentration

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

Barbiturates

Increased clearance of prednisonea d

May need to increase dosage of prednisonea d

Cyclosporine

Concomitant administration of prednisone and cyclosporine may result in inhibition of metabolism of either agent.i Seizures reportedly have occurred in adult and pediatric patients receiving high-dose glucocorticoid therapy concurrently with cyclosporinec

Consider possibility of exacerbated toxicity (convulsions), as well as need for dosage adjustment with concomitant usec d

Diuretics, potassium-depleting

Enhance the potassium-wasting effects of glucocorticoidsc

Monitor for development of hypokalemiac

Ephedrine

Increased metabolism of corticosteroidsc

May need to increase dosage of the corticosteroidc

Estrogens

May potentiate effects of certain corticosteroidsc

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

Ketoconazole

Decreased metabolism of corticosteroidsa c d

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

NSAIAs

Increases the risk of GI adverse effects (ulceration)c

Increased clearance of salicylates;a d when corticosteroids are discontinued, serum salicylate concentration may increase, possibly resulting in salicylate intoxicationa c

Use concurrently with cautionc

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

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

Use aspirin and corticosteroids with caution in hypoprothrombinemiaa d

Phenytoin

Increased clearance of prednisonea c d

May require increases in the dosage of prednisonec d

Rifampin

Increased clearance of prednisonea c d

May require increases in the dosage of prednisonea c d

Tests for nitroblue tetrazolium

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

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 thyroiditisc

Tests involving skin antigens

Depresses skin reactivity to antigen-antibody interactionsc

Vaccines and toxoids

May cause a diminished response to toxoids and live or inactivated vaccinesa c d

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

Can aggravate neurologic reactions to some vaccines (supraphysiologic dosages) c

(See Immunosuppression under Cautions)

Sterapred Pharmacokinetics

Distribution

Extent

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

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

Special Populations

In patients with hypothyroidism, metabolic clearance of corticosteroids decreased.c

In patients with hyperthyroidism, metabolic clearance of corticosteroids increased.c

Changes in thyroid status may necessitate adjustment of glucocorticoid dosage.c

Stability

Storage

Oral

Tablets

15–30°C.d f Protect Sterapred from light and moisture.f

Solution

15–30°C.d

Extemporaneous Suspension

Stable at 2–8°C for 2 months.b (See Oral Administration under Dosage and Administration.)

Actions

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

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

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

  • Inhibits macrophage accumulation in inflamed areas.c

  • Reduces capillary wall permeability and edema formation.c

  • Antagonizes histamine activity and release of kinin from substrates.c

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

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

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

  • Reduces intestinal absorption and increases renal excretion of calcium.c e

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

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

  • Depresses reactivity of tissue to antigen-antibody interactions.c

Advice to Patients

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

  • 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.c

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

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

  • 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.a c

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

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

Preparations

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

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

Prednisone

Routes

Dosage Forms

Strengths

Brand Names

Manufacturer

Bulk

Powder

Oral

Solution

5 mg/5 mL

Prednisone Oral Solution (with alcohol 5%)

Roxane

Solution, concentrate

5 mg/mL

Prednisone Intensol (with alcohol 30%)

Roxane

Tablets

1 mg*

Prednisone Tablets

Roxane

2.5 mg*

Prednisone Tablets

Roxane

5 mg*

Sterapred 5 mg Unipak

Merz

Sterapred 5 mg 12 Day Unipak

Merz

Prednisone Tablets

Mutual, Roxane, Trigen, Watson

10 mg*

Sterapred DS Unipak

Merz

Sterapred DS 12 Day Unipak

Merz

Prednisone Tablets

Mutual, Roxane, Trigen, Watson

20 mg*

Prednisone Tablets

Mutual, Roxane, Trigen, Watson

50 mg*

Prednisone Tablets

Roxane, Watson

Comparative Pricing

This pricing information is subject to change at the sole discretion of DS Pharmacy. This pricing information was updated 02/2014. Actual costs to patients will vary depending on the use of specific retail or mail-order locations and health insurance copays.

PredniSONE 1MG Tablets (ROXANE): 90/$23.99 or 180/$33.97

PredniSONE 10MG Tablets (WEST-WARD): 30/$11.99 or 60/$13.98

PredniSONE 2.5MG Tablets (ROXANE): 30/$12.99 or 60/$16.98

PredniSONE 20MG Tablets (QUALITEST): 30/$11.99 or 60/$15.89

PredniSONE 5MG/5ML Solution (ROXANE): 30/$14.99 or 60/$20.98

PredniSONE 5MG Tablets (WEST-WARD): 100/$12.99 or 200/$14.98

PredniSONE 50MG Tablets (ROXANE): 30/$17.99 or 60/$25.98

AHFS DI Essentials. © Copyright, 2004-2014, Selected Revisions July 1, 2006. American Society of Health-System Pharmacists, Inc., 7272 Wisconsin Avenue, Bethesda, Maryland 20814.

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

References

101. Dooley DP, Carpenter JL, Rademacher S. Adjunctive corticosteriod therapy fortuberculosis: a critical reappraisal of the literature. Clin Infect Dis. 1997; 25:872-87. [IDIS 395793] [PubMed 9356803]

102. Alzeer AH, FitzGerald JM. Corticosteroids and tuberculosis: risks and use as adjunct therapy Tuber Lung Dis. 1993; 74:6-11.

a. Pharmacia & Upjohn. Deltasone (prednisone) tablets prescribing information. Kalamazoo, MI; 2002 Apr.

b. AHFS drug information 2004. McEvoy GK, ed. Prednisone. Bethesda, MD: American Society of Health-System Pharmacists; 2004:2916-7.

c. AHFS drug information 2004. McEvoy GK, ed. Corticosteroids general statement. Bethesda, MD: American Society of Health-System Pharmacists; 2004:2886-98.

d. Roxane Laboratories. Prednisone tablets, oral solution, prednisone Intensol concentrated solution prescribing information. Columbus, OH; 2002 Feb.

e. USP DI: drug information for the health care provider. 24th ed. Greenwood Village, CO: Thomson Micromedex; 2004;1:940-6

f. Merz Pharmaceuticals. Sterapred Uni-pak (prednisone tablets) prescribing information. Greensboro, NC; 2003 Nov.

g. Bello CE, Garrett SD. Therapeutic issues in oral glucocorticoid use. Lippincotts Prim Care Pract. 1999; 3:333-41. [PubMed 10711134]

h. Walsh LJ, Wong CA, Oborne J et al. Adverse effects of oral corticosteroids in relation to dose in patients with lung disease. Thorax. 2001; 56:279-84. [PubMed 11254818]

i. Baciewicz AM, Baciewicz FA. Cyclosporine pharmacokinetic drug interactions. Am J Surg. 1989; 157:264-71. [PubMed 2644865]

j. Behrman RE, Kliegman RM, Jenson HB, eds. Nelson textbook of pediatrics. 17th ed. Philadelphia: Saunders; 2004:1407-8.

k. Centers for Disease Control and Prevention. General recommendations on immunization: recommendations of the Advisory Committee on Immunization Practices and the American Academy of Family Physicians. MMWR. 2002; 51(RR-2):1-44

l. Celltech Americas. Prednisolone sodium phosphate oral solution prescribing information. Rochester, NY; 2001 Dec.

m. National Heart, Lung, and Blood Institute/World Health Organization. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. Bethesda, MD: National Heart, Lung, and Blood Institute, Global Initiative for Chronic Obstructive Lung Disease, World Health Organization; 2004. Available at . Accessed Sep. 2, 2004.

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