sorders acquired (autoimmune) hemolytic anemia, congenital (erythroid) hypoplastic anemia (diamon-blackfan anemia), idiopathic thrombocytopenic purpura in adults, pure red cell aplasia, and selected cases of secondary thrombocytopenia. miscellaneous diagnostic testing of adrenocortical hyperfunction, trichinosis with neurologic or myocardial involvement, tuberculous meningitis with subarachnoid block or impending block when used with appropriate antituberculous chemotherapy. neoplastic diseases for palliative management of leukemias and lymphomas. nervous system acute exacerbations of multiple sclerosis, cerebral edema associated with primary or metastatic brain tumor, craniotomy, or head injury. ophthalmic diseases sympathetic ophthalmia, temporal arteritis, uveitis, and ocular inflammatory conditions unresponsive to topical corticosteroids. renal diseases to induce a diuresis or remission of proteinuria in idiopathic nephrotic syndrome or that due to lupus erythematosus. respiratory diseases berylliosis, fulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate antituberculous chemotherapy, idiopathic eosinophilic pneumonias, symptomatic sarcoidosis rheumatic disorders as adjunctive therapy for short-term administration (to tide the patient over an acute episode or exacerbation) in acute gouty arthritis, acute rheumatic carditis, ankylosing spondylitis, psoriatic arthritis, rheumatoid arthritis, including juvenile rheumatoid arthritis (selected cases may require low-dose maintenance therapy). for the treatment of dermatomyositis, polymyositis, and systemic lupus erythematosus.

s can produce reversible hypothalamic-pituitary adrenal (hpa) axis suppression with the potential for corticosteroid insufficiency after withdrawal of treatment. adrenocortical insufficiency may result from too rapid withdrawal of corticosteroids and may be minimized by gradual reduction of dosage. this type of relative insufficiency may persist for months after discontinuation of therapy; therefore, in any situation of stress occurring during that period, hormone therapy should be reinstituted. if the patient is receiving steroids already, dosage may have to be increased. metabolic clearance of corticosteroids is decreased in hypothyroid patients and increased in hyperthyroid patients. changes in thyroid status of the patient may necessitate adjustment in dosage. infections general: patients who are on corticosteroids 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 (viral, bacterial, fungal, protozoan or helminthic) in any location of the body may be associated with the use of corticosteroids alone or in combination with other immunosuppressive agents. these infections may be mild to severe. with increasing doses of corticosteroids, the rate of occurrence of infectious complications increases. corticosteroids may also mask some signs of current infection. fungal infections: corticosteroids may exacerbate systemic fungal infections and therefore should not be used in the presence of such infections unless they are needed to control life-threatening drug reactions. there have been cases reported in which concomitant use of amphotericin b and hydrocortisone was followed by cardiac enlargement and congestive heart failure (see precautions: drug interactions: amphotericin b injection and potassium-depleting agents). special pathogens: latent disease may be activated or there may be an exacerbation of intercurrent infections due to pathogens, including those caused by amoeba, candida, cryptococcus, mycobacterium, nocardia, pneumocystis, toxoplasma. it is recommended that latent amebiasis or active amebiasis be ruled out before initiating corticosteroid therapy in any patient who has spent time in the tropics or 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 corticosteroids 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. viral infections: chickenpox and measles can have a more serious or even fatal course in pediatric and adults patients on corticosteroids. in pediatric and adult patients who have not had these diseases, particular care should be taken to avoid exposure. the contribution of the underlying disease and/or prior corticosteroid treatment to the risk is also not known. if exposed to chickenpox, prophylaxis with varicella zoster immune globulin (vzig) may be indicated. if exposed to measles, prophylaxis with immune globulin (ig) may be indicated. (see the respective package inserts for vzig and ig for complete prescribing information.) if chickenpox develops, treatment with antiviral agents may 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.

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 30 mg of dexamethasone for a week followed by 4 to 12 mg every other day for one month have been shown to be effective (see precautions: neuro-psychiatric). in pediatric patients, the initial dose of dexamethasone may vary depending on the specific disease entity being treated. the range of initial doses is 0.02 to 0.3 mg/kg/day in three or four divided doses (0.6 to 9 mg/m2bsa/day). for the purpose of comparison, the following is the equivalent milligram dosage of the various corticosteroids: 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. in acute, self-limited allergic disorders or acute exacerbations of chronic allergic disorders, the following dosage schedule combining parenteral and oral therapy is suggested: dexamethasone sodium phosphate injection, 4 mg per ml: first day 1 or 2 ml, intramuscularly dexamethasone tablets, 0.75 mg: second day 4 tablets in two divided doses third day 4 tablets in two divided doses fourth day 2 tablets in two divided doses fifth day 1 tablet sixth day 1 tablet seventh day no treatment eighth day follow-up visit this schedule is designed to ensure adequate therapy during acute episodes, while minimizing the risk of overdosage in chronic cases. in cerebral edema, dexamethasone sodium phosphate injection is generally administered initially in a dosage of 10 mg intravenously followed by 4 mg every six hours intramuscularly until the symptoms of cerebral edema subside. response is usually noted within 12 to 24 hours and dosage may be reduced after two to four days and gradually discontinued over a period of five to seven days. for palliative management of patients with recurrent or inoperable brain tumors, maintenance therapy with either dexamethasone sodium phosphate injection or dexamethasone tablets in a dosage of 2 mg two or three times daily may be effective. dexamethasone suppression tests tests for cushing’s syndrome give 1.0 mg of dexamethasone orally at 11:00 p.m. blood is drawn for plasma cortisol determination at 8:00 a.m. the following morning. for greater accuracy, give 0.5 mg of dexamethasone orally every 6 hours for 48 hours. twenty-four hour urine collections are made for determination of 17-hydroxycorticosteroid excretion. test to distinguish cushing’s syndrome due to pituitary acth excess from cushing’s syndrome due to other causes. give 2.0 mg of dexamethasone orally every 6 hours for 48 hours. twenty-four hour urine collections are made for determination of 17-hydroxycorticosteroid excretion. image description

, hypertrichosis, increased requirements for insulin or oral hypoglycemic agents in diabetes, manifestations of latent diabetes mellitus, menstrual irregularities, secondary adrenocortical and pituitary unresponsiveness (particularly in times of stress, as in trauma, surgery, or illness), suppression of growth in pediatric patients. fluid and electrolyte disturbances: congestive heart failure in susceptible patients, fluid retention, hypokalemic alkalosis, potassium loss, sodium retention. gastrointestinal: abdominal distention, elevation in serum liver enzyme levels (usually reversible upon discontinuation), hepatomegaly, increased appetite, nausea, pancreatitis, peptic ulcer with possible perforation and hemorrhage, perforation of the small and large bowel (particularly in patients with inflammatory bowel disease), 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/psychiatric: convulsions, depression, emotional instability, euphoria, headache, increased intracranial pressure with papilledema (pseudotumor cerebri) usually after treatment, insomnia, mood swings, neuritis, neuropathy, paresthesia, personality changes, psychic disorders, vertigo. ophthalmic: exophthalmos, glaucoma, increased intraocular pressure, posterior subcapsular cataracts. other: abnormal fat deposits, decreased resistance to infection, hiccups, increased or decreased motility and number of spermatozoa, malaise, moon face, weight gain.