DailyMed Label: Cortisone Acetate

DailyMed Label: Cortisone Acetate

2006

DailyMed Prescription

Cortisone Acetate

Cortisone Acetate

Pharmacia and Upjohn Company

NDC: 0009-0015

NDC: 0009-0023

Cortisone acetate is a glucocorticoid. Glucocorticoids are adrenocortical steroids, both naturally occurring and synthetic, which are readily absorbed from the gastrointestinal tract. Cortisone acetate is a white to practically white, odorless, crystalline powder. It is insoluble in water; freely soluble in chloroform; soluble in dioxane; sparingly soluble in acetone; slightly soluble in alcohol. The chemical name for cortisone acetate is pregn-4-ene-3,11,20-trione, 21-(acetyloxy)-17-hydroxy and the molecular weight is 402.49. The structural formula is represented below: Cortisone Acetate Tablets are available in 2 strengths: 5 mg or 10 mg. Inactive ingredients: calcium stearate, corn starch, lactose, mineral oil, sorbic acid, sucrose.

Primary or secondary adrenocortical insufficiency (hydrocortisone or cortisone is the first choice; synthetic analogs may be used in conjunction with mineralocorticoids where applicable; in infancy mineralocorticoid supplementation is of particular importance) Congenital adrenal hyperplasia Hypercalcemia associated with cancer Nonsuppurative thyroiditis 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 Post-traumatic osteoarthritis Acute and subacute bursitis Synovitis of osteoarthritis Acute nonspecific tenosynovitis Epicondylitis Acute gouty arthritis During an exacerbation or as maintenance therapy in selected cases of: Systemic lupus erythematosus Acute rheumatic carditis Systemic dermatomyositis (polymyositis) Pemphigus Exfoliative dermatitis Bullous dermatitis herpetiformis Mycosis fungoides Severe erythema multiforme (Stevens-Johnson syndrome) Severe psoriasis Severe seborrheic dermatitis Control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment. Seasonal or perennial allergic rhinitis Contact dermatitis Atopic dermatitis Serum sickness Drug hypersensitivity reactions Bronchial asthma Severe acute and chronic allergic and inflammatory processes involving the eye and its adnexa such as: Allergic conjunctivitis Anterior segment inflammation Keratitis Allergic corneal marginal ulcers Diffuse posterior uveitis and choroiditis Herpes zoster ophthalmicus Iritis and iridocyclitis Optic neuritis Chorioretinitis Sympathetic ophthalmia Symptomatic sarcoidosis Loeffler's syndrome not manageable by other means Fulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate antituberculous chemotherapy Berylliosis Aspiration pneumonitis Idiopathic thrombocytopenic purpura in adults Acquired (autoimmune) hemolytic anemia Secondary thrombocytopenia in adults Erythroblastopenia (RBC anemia) Congenital (erythroid) hypoplastic anemia For palliative management of: Leukemias and lymphomas in adults Acute leukemia of childhood To induce a diuresis or remission of proteinuria in the nephrotic syndrome, without uremia, of the idiopathic type or that due to lupus erythematosus To tide the patient over a critical period of the disease in: Ulcerative colitis Regional enteritis Tuberculous meningitis with subarachnoid block or impending block when used concurrently with appropriate antituberculous chemotherapy Trichinosis with neurologic or myocardial involvement

The initial dosage of cortisone acetate may vary from 25 to 300 mg per day depending on the specific disease entity being treated. In situations of less severity, lower doses will generally suffice; while in selected patients higher initial doses may be required. The initial dosage should be maintained or adjusted until a satisfactory response is noted. If after a reasonable period of time there is a lack of satisfactory clinical response, cortisone acetate should be discontinued and the patient transferred to other appropriate therapy. IT SHOULD BE EMPHASIZED THAT DOSAGE REQUIREMENTS ARE VARIABLE AND MUST BE INDIVIDUALIZED ON THE BASIS OF THE DISEASE UNDER TREATMENT AND THE RESPONSE OF THE PATIENT . After a favorable response is noted, the proper maintenance dosage should be determined by decreasing the initial drug dosage in small decrements at appropriate time intervals until the lowest dosage which will maintain an adequate clinical response 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 cortisone acetate 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.

Systemic fungal infections and known hypersensitivity to components.

Drug-induced secondary adrenocortical insufficiency 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. Since mineralocorticoid secretion may be impaired, salt and/or a mineralocorticoid should be administered concurrently. There is an enhanced effect of corticosteroids on patients with hypothyroidism and in those with cirrhosis. Corticosteroids should be used cautiously in patients with ocular herpes simplex because of possible corneal perforation. The lowest possible dose of corticosteroid should be used to control the condition under treatment, and when reduction in dosage is possible, the reduction should be gradual. Psychic derangements may appear when corticosteroids are used, ranging from euphoria, insomnia, mood swings, personality changes, and severe depression, to frank psychotic manifestations. Also, existing emotional instability or psychotic tendencies may be aggravated by corticosteroids. Steroids should be used with caution in nonspecific ulcerative colitis, if there is a probability of impending perforation, abscess or other pyogenic infection; diverticulitis; fresh intestinal anastomoses, active or latent peptic ulcer; renal insufficiency; hypertension; osteoporosis; and myasthenia gravis. Growth and development of infants and children on prolonged corticosteroid therapy should be carefully observed. Kaposi's sarcoma has been reported to occur in patients receiving corticosteroid therapy. Discontinuation of corticosteroids may result in clinical remission. The pharmacokinetic interactions listed below are potentially clinically important. Drugs that induce hepatic enzymes such as phenobarbital, phenytoin and rifampin may increase the clearance of corticosteroids and may require increases in corticosteroid dose to achieve the desired response. Drugs such as troleandomycin and ketoconazole may inhibit the metabolism of corticosteroids and thus decrease their clearance. Therefore, the dose of corticosteroid should be titrated to avoid steroid toxicity. Corticosteroids may increase the clearance of chronic high dose aspirin. This could lead to decreased salicylate serum levels or increase the risk of salicylate toxicity when corticosteroid is withdrawn. Aspirin should be used cautiously in conjunction with corticosteroids in patients suffering from hypoprothrombinemia. The effect of corticosteroids on oral anticoagulants is variable. There are reports of enhanced as well as diminished effects of anticoagulants when given concurrently with corticosteroids. Therefore, coagulation indices should be monitored to maintain the desired anticoagulant effect. Persons who are on immunosuppressant doses of corticosteroids should be warned to avoid exposure to chicken pox or measles. Patients should also be advised that if they are exposed, medical advice should be sought without delay.

The pharmacokinetic interactions listed below are potentially clinically important. Drugs that induce hepatic enzymes such as phenobarbital, phenytoin and rifampin may increase the clearance of corticosteroids and may require increases in corticosteroid dose to achieve the desired response. Drugs such as troleandomycin and ketoconazole may inhibit the metabolism of corticosteroids and thus decrease their clearance. Therefore, the dose of corticosteroid should be titrated to avoid steroid toxicity. Corticosteroids may increase the clearance of chronic high dose aspirin. This could lead to decreased salicylate serum levels or increase the risk of salicylate toxicity when corticosteroid is withdrawn. Aspirin should be used cautiously in conjunction with corticosteroids in patients suffering from hypoprothrombinemia. The effect of corticosteroids on oral anticoagulants is variable. There are reports of enhanced as well as diminished effects of anticoagulants when given concurrently with corticosteroids. Therefore, coagulation indices should be monitored to maintain the desired anticoagulant effect.

Cortisone Acetate Tablets, USP are available in the following strengths and package sizes: 5 mg (white, round, scored, imprinted UPJOHN 15)         Bottles of 50                NDC 0009-0015-01 10 mg (white, round, scored, imprinted UPJOHN 23)         Bottles of 100              NDC 0009-0023-01 Store at controlled room temperature 20° to 25°C (68° to 77°F) [see USP].