Glucocorticoids are potent anti-inflammatories, regardless of the inflammation's cause; their primary anti-inflammatory mechanism is lipocortin-1 (annexin-1) synthesis. Lipocortin-1 both suppresses phospholipase A2 , thereby blocking eicosanoid production, and inhibits various leukocyte inflammatory events ( epithelial adhesion , emigration , chemotaxis , phagocytosis , respiratory burst , etc.). In other words, glucocorticoids not only suppress immune response, but also inhibit the two main products of inflammation, prostaglandins and leukotrienes . They inhibit prostaglandin synthesis at the level of phospholipase A2 as well as at the level of cyclooxygenase /PGE isomerase (COX-1 and COX-2),  the latter effect being much like that of NSAIDs , potentiating the anti-inflammatory effect.
Dosing should be individualized based on disease and patient response:
Initial dose: 5 to 60 mg orally per day; may be give once a day or in divided doses
Maintenance dose: Adjust or maintain initial dose until a satisfactory response is obtained; then, gradually in small decrements at appropriate intervals decrease to the lowest dose that maintains an adequate clinical response
-Exogenous corticosteroids suppress adrenocorticoid activity the least when given at the time of maximal activity; consider time of maximal adrenal cortex activity (2 AM to 8 AM) when dosing.
-Alternate day therapy may be considered in patients requiring long-term treatment; it may be necessary to return to a full suppressive daily dose in the event of acute flare-ups.
Uses: As an anti-inflammatory or immunosuppressive agent when corticosteroid therapy is appropriate, such as treatment of certain allergic states; nervous system, neoplastic, or renal conditions; endocrine, rheumatologic, or hematologic disorders; collagen, dermatologic, ophthalmic, respiratory, or gastrointestinal diseases; specific infectious diseases or conditions related to organ transplantation.
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