Table of contents

  • Brand Names
  • Chemistry
  • Pharmacologic Category
  • Mechanism of Action
  • Therapeutic Use
  • Pregnancy and Lactation Implications
  • Contraindications
  • Warnings and Precautions
  • Adverse Reactions
  • Genes that may be involved
  • Substrate of
  • Drug Interactions
  • Nutrition/Nutraceutical Interactions
  • Dosage
  • Pharmacokinetics and Pharmacodynamics
  • Special Considerations

Brand Names


Germany: Cortison; Italy: Cortis, Cortone; Netherlands: Cortisonacetaat; Slovakia: Cortison; UK: Cortisone.


Japan: Cortone.

Drug combinations


Cortisone Acetate: C~23~H~30~O~6~. Mw: 402.48. (1) Pregn-4-ene-3,11,20-trione, 21-(acetyloxy)-17-hydroxy-; (2) 17,21-Dihydroxypregn-4-ene-3,11,20-trione 21-acetate. CAS-50-04-4; CAS-53-06-5 (cortisone).

Pharmacologic Category

Hormones and Synthetic Substitutes; Adrenals. Systemic Corticosteroid. (ATC-Code: H02AB10; S01BA03).

Mechanism of action

Principally an anti-inflammatory or immunosuppressant agent. Has potent anti-inflammatory activity and some mineralocorticoid properties. In physiologic doses, replaces deficient endogenous hormones. In pharmacologic doses, decreases inflammation and suppresses the immune response. Stabilizes leukocyte lysosomal membranes, preventing release of destructive acid hydrolases from leukocytes, reduces leukocyte adhesion to capillary endothelium, inhibits macrophage accumulation in inflamed areas, and 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, resulting in negative nitrogen balance. Reduces intestinal absorption and increases renal excretion of calcium. Suppresses release of corticotropin from the pituitary, resulting in cessation of endogenous corticosteroid secretion (secondary adrenocortical insufficiency). Suppresses the immune response by reducing activity and volume of the lymphatic system, producing lymphocytopenia. Promotes sodium reabsorption, and potassium and hydrogen excretion, along with subsequent water retention through a mineralocorticoid action on the part of the renal distal tubule that facilitates sodium transport.

Therapeutic use

Adrenocortical insufficiency.

Pregnancy and lactiation implications

Adverse events observed in animals. Cortisone is found in cord blood; endogenous maternal cortisol (active) is metabolized by placental enzymes to cortisone (inactive), regulating the amount of maternal glucocorticoids reaching the fetus. An association between first trimester systemic corticosteroid use and oral clefts reported. Excretion in breast milk unknown (use caution).

Unlabeled use


Hypersensitivity to cortisone or any component of the formulation. Serious infections, except septic shock or tuberculous meningitis. Administration of live virus vaccines.

Warnings and precautions

May cause hypercorticism or suppression of hypothalamic-pituitary-adrenal axis, particularly in younger children or in patients receiving high doses for prolonged periods (may lead to adrenal crisis). Withdrawal and discontinuation of a corticosteroid should be done slowly and carefully. Prolonged use may also increase the incidence of secondary infection, mask acute infection (including fungal infections), prolong or exacerbate viral infections, or limit response to vaccines (exposure to chickenpox should be avoided; corticosteroids should not be used to treat ocular herpes simplex, cerebral malaria or viral hepatitis). Use in active tuberculosis should be restricted. Prolonged treatment with corticosteroids has been associated with the development of Kaposi’s sarcoma. Acute myopathy reported with high-dose corticosteroids, usually in neuromuscular transmission disorders (may involve ocular and/or respiratory muscles). Corticosteroid use may cause psychiatric disturbances (depression, euphoria, insomnia, mood swings, personality changes). Pre-existing psychiatric conditions may be exacerbated by corticosteroid use. Use with caution in the following cases: heart failure (long-term use associated with fluid retention and hypertension), diabetes mellitus (may alter glucose production/regulation leading to hyperglycemia), GI disease (diverticulitis, peptic ulcer, ulcerative colitis; risk of perforation), hepatic impairment (long-term use associated with fluid retention), myasthenia gravis (exacerbation of symptoms), following acute MI (risk of myocardial rupture), cataracts and/or glaucoma (risk of increased intraocular pressure, open-angle glaucoma, and cataracts), osteoporosis (increased bone loss and osteoporotic fractures), renal impairment (risk of fluid retention), and history of seizure disorder (seizures reported with adrenal crisis). Metabolic clearance of corticosteroids increases in hyperthyroidism and decreases in hypothyroidism. Because of the risk of adverse effects, systemic corticosteroids should be used cautiously in the elderly. May affect growth velocity in children.



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