cy mineralocorticoid supplementation is of particular importance); congenital adrenal hyperplasia; hypercalcemia associated with cancer; nonsuppurative thyroiditis. 5. gastrointestinal diseases to tide the patient over a critical period of the disease in: ulcerative colitis; regional enteritis. 6. hematologic disorders idiopathic thrombocytopenic purpura in adults; selected cases of secondary thrombocytopenia; acquired (autoimmune) hemolytic anemia; pure red cell aplasia; diamond-blackfan anemia. 7. neoplastic diseases for the treatment of acute leukemia and aggressive lymphomas in adults and children. 8. nervous system acute exacerbations of multiple sclerosis. 9. ophthalmic diseases uveitis and ocular inflammatory conditions unresponsive to topical corticosteroids; temporal arteritis; sympathetic ophthalmia. 10. respiratory diseases symptomatic sarcoidosis; idiopathic eosinophilic pneumonias; fulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate antituberculous chemotherapy; asthma (as distinct from allergic asthma listed above under “allergic states”), hypersensitivity pneumonitis, idiopathic pulmonary fibrosis, acute exacerbations of chronic obstructive pulmonary disease (copd), and pneumocystis carinii pneumonia (pcp) associated with hypoxemia occurring in an hiv (+) individual who is also under treatment with appropriate anti-pcp antibiotics. studies support the efficacy of systemic corticosteroids for the treatment of these conditions: allergic bronchopulmonary aspergillosis, idiopathic bronchiolitis obliterans with organizing pneumonia. 11. rheumatic disorders as adjunctive therapy for short term administration (to tide the patient over an acute episode or exacerbation) in: psoriatic arthritis; rheumatoid arthritis, including juvenile rheumatoid arthritis (selected cases may require low dose maintenance therapy); ankylosing spondylitis; acute and subacute bursitis; acute nonspecific tenosynovitis; acute gouty arthritis; epicondylitis. for the treatment of systemic lupus erythematosus, dermatomyositis (polymyositis), polymyalgia rheumatica, sjogren’s syndrome, relapsing polychondritis, and certain cases of vasculitis. 12. miscellaneous tuberculous meningitis with subarachnoid block or impending block, tuberculosis with enlarged mediastinal lymph nodes causing respiratory difficulty, and tuberculosis with pleural or pericardial effusion (appropriate antituberculous chemotherapy must be used concurrently when treating any tuberculosis complications); trichinosis with neurologic or myocardial involvement; acute or chronic solid organ rejection (with or without other agents).

l): persons who are on drugs which suppress the immune system are more susceptible to infections than healthy individuals. there may be decreased resistance and inability to localize infection when corticosteroids are used. infection with any pathogen including viral, bacterial, fungal, protozoan or helminthic infection, in any location of the body, may be associated with the use of corticosteroids alone or in combination with other immunosuppressive agents that affect humoral or cellular immunity, or neutrophil function. these infections may be mild to severe, and, with increasing doses of corticosteroids, the rate of occurrence of infectious complications increases. corticosteroids may also mask some signs of infection after it has already started. infections (viral): chicken pox and measles, for example, can have a more serious or even fatal course in non-immune children or adults on corticosteroids. in such children or adults who have not had these diseases, particular care should be taken to avoid exposure. how the dose, route and duration of corticosteroid administration affect the risk of developing a disseminated infection is not known. the contribution of the underlying disease and/or prior corticosteroid treatment to the risk is also not known. if exposed to chicken pox, prophylaxis with varicella zoster immune globulin (vzig) may be indicated. if exposed to measles, prophylaxis with immunoglobulin (ig) may be indicated. (see the respective package inserts for complete vzig and ig prescribing information). if chicken pox develops, treatment with antiviral agents should be considered. ophthalmic: use of corticosteroids may produce posterior subcapsular cataracts, glaucoma with possible damage to the optic nerves, and may enhance the establishment of secondary ocular infections due to bacteria, fungi or viruses. the use of oral corticosteroids is not recommended in the treatment of optic neuritis and may lead to an increase in the risk of new episodes. corticosteroids should not be used in active ocular herpes simplex. special pathogens: latent disease may be activated or there may be an exacerbation of intercurrent infections due to pathogens, including those caused by candida, mycobacterium, ameba, toxoplasma, pneumocystis, cryptococcus, nocardia, etc. corticosteroids may activate latent amebiasis. therefore, it is recommended that latent or active amebiasis be ruled out before initiating corticosteroid therapy in any patient who has spent time in the tropics or in any patient with unexplained diarrhea. similarly, corticosteroids should be used with great care in patients with known or suspected strongyloides (threadworm) infestation. in such patients, corticosteroid-induced immunosuppression may lead to strongyloides hyperinfection and dissemination with widespread larval migration, often accompanied by severe enterocolitis and potentially fatal gram negative septicemia. corticosteroids should not be used in cerebral malaria. tuberculosis: the use of prednisolone in active tuberculosis should be restricted to those cases of fulminating or disseminated tuberculosis in which the corticosteroid is used for the management of the disease in conjunction with an appropriate antituberculous regimen. if corticosteroids are indicated in patients with latent tuberculosis or tuberculin reactivity, close observation is necessary as reactivation of the disease may occur. during prolonged corticosteroid therapy, these patients should receive chemoprophylaxis. vaccination: administration of live or live, attenuated vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids. killed or inactivated vaccines may be administered, however, the response to such vaccines cannot be predicted. immunization procedures may be undertaken in patients who are receiving corticosteroids as replacement therapy, e.g., for addison’s disease.

sponse is reached. it should be kept in mind that constant monitoring is needed in regard to drug dosage. included in the situations which may make dosage adjustments necessary are changes in clinical status secondary to remissions or exacerbations in the disease process, the patient’s individual drug responsiveness, and the effect of patient exposure to stressful situations not directly related to the disease entity under treatment; in this latter situation it may be necessary to increase the dosage of pediapred ® for a period of time consistent with the patient’s condition. if after long term therapy the drug is to be stopped, it is recommended that it be withdrawn gradually rather than abruptly. in the treatment of acute exacerbations of multiple sclerosis, daily doses of 200 mg of prednisolone for a week followed by 80 mg every other day or 4 to 8 mg dexamethasone every other day for one month have been shown to be effective. in pediatric patients, the initial dose of pediapred ® may vary depending on the specific disease entity being treated. the range of initial doses is 0.14 to 2 mg/kg/day in three or four divided doses (4 to 60 mg/m 2 bsa/day). the standard regimen used to treat nephrotic syndrome in pediatric patients is 60 mg/m2/day given in three divided doses for 4 weeks, followed by 4 weeks of single dose alternate-day therapy at 40 mg/m 2 /day. the national heart, lung, and blood institute (nhlbi) recommended dosing for systemic prednisone, prednisolone or methylprednisolone in children whose asthma is uncontrolled by inhaled corticosteroids and long-acting bronchodilators is 1-2 mg/kg/day in single or divided doses. it is further recommended that short course, or “burst” therapy, be continued until a child achieves a peak expiratory flow rate of 80% of his or her personal best or symptoms resolve. this usually requires 3 to 10 days of treatment, although it can take longer. there is no evidence that tapering the dose after improvement will prevent a relapse. for the purpose of comparison, 5 ml of prednisolone sodium phosphate oral solution (33.6 mg prednisolone sodium phosphate) is equivalent to the following milligram dosage of the various glucocorticoids: cortisone, 25 triamcinolone, 4 hydrocortisone, 20 paramethasone, 2 prednisolone, 5 betamethasone, 0.75 prednisone, 5 dexamethasone, 0.75 methylprednisolone, 4 these dose relationships apply only to oral or intravenous administration of these compounds. when these substances or their derivatives are injected intramuscularly or into joint spaces, their relative properties may be greatly altered.

ion); pancreatitis; peptic ulcer with possible perforation and hemorrhage; ulcerative esophagitis. metabolic: negative nitrogen balance due to protein catabolism. musculoskeletal: aseptic necrosis of femoral and humeral heads; loss of muscle mass; muscle weakness; osteoporosis; pathologic fracture of long bones; steroid myopathy; tendon rupture; vertebral compression fractures. neurological: convulsions; headache; increased intracranial pressure with papilledema (pseudotumor cerebri) usually following discontinuation of treatment; psychic disorders; vertigo. ophthalmic: exophthalmos; glaucoma; increased intraocular pressure; posterior subcapsular cataracts. other: increased appetite; malaise; nausea; weight gain. to report suspected adverse reactions, contact royal pharmaceuticals at 1-800-510-3401 or fda at 1-800-fda-1088 or www.fda.gov/medwatch.

d clinical evaluation for the presence of infection, psychosocial disturbances, thromboembolism, peptic ulcers, cataracts, and osteoporosis. children who are treated with corticosteroids by any route, including systemically administered corticosteroids, may experience a decrease in their growth velocity. this negative impact of corticosteroids on growth has been observed at low systemic doses and in the absence of laboratory evidence of hpa axis suppression (i.e., cosyntropin stimulation and basal cortisol plasma levels). growth velocity may therefore be a more sensitive indicator of systemic corticosteroid exposure in children than some commonly used tests of hpa axis function. the linear growth of children treated with corticosteroids by any route should be monitored, and the potential growth effects of prolonged treatment should be weighed against clinical benefits obtained and the availability of other treatment alternatives. in order to minimize the potential growth effects of corticosteroids, children should be titrated to the lowest effective dose.

sis and storage; increased glomerular filtration rate and resulting increase in urinary excretion of urate (creatinine excretion remains unchanged); and increased calcium excretion. depressed production of eosinophils and lymphocytes occurs, but erythropoiesis and production of polymorphonuclear leukocytes are stimulated. inflammatory processes (edema, fibrin deposition, capillary dilatation, migration of leukocytes and phagocytosis) and the later stages of wound healing (capillary proliferation, deposition of collagen, cicatrization) are inhibited. prednisolone can stimulate secretion of various components of gastric juice. suppression of the production of corticotropin may lead to suppression of endogenous corticosteroids. prednisolone has slight mineralocorticoid activity, whereby entry of sodium into cells and loss of intracellular potassium is stimulated. this is particularly evident in the kidney, where rapid ion exchange leads to sodium retention and hypertension. prednisolone is rapidly and well absorbed from the gastrointestinal tract following oral administration. pediapred ® oral solution produces a 14% higher peak plasma level of prednisolone which occurs 20% faster than that seen with tablets. prednisolone is 70-90% protein bound in the plasma and it is eliminated from the plasma with a half-life of 2 to 4 hours. it is metabolized mainly in the liver and excreted in the urine as sulfate and glucuronide conjugates. the systemic availability, metabolism and elimination of prednisolone after administration of single weight-based doses (0.8 mg/kg) of intravenous (iv) prednisolone and oral prednisone were reported in a small study of 19 young (23 to 34 years) and 12 elderly (65 to 89 years) subjects. results showed that the systemic availability of total and unbound prednisolone, as well as interconversion between prednisolone and prednisone were independent of age. the mean unbound fraction of prednisolone was higher, and the steady-state volume of distribution (vss) of unbound prednisolone was reduced in elderly patients. plasma prednisolone concentrations were higher in elderly subjects, and the higher aucs of total and unbound prednisolone were most likely reflective of an impaired metabolic clearance, evidenced by reduced fractional urinary clearance of 6β-hydroxyprednisolone. despite these findings of higher total and unbound prednisolone concentrations, elderly subjects had higher aucs of cortisol, suggesting that the elderly population is less sensitive to suppression of endogenous cortisol or their capacity for hepatic inactivation of cortisol is diminished.