Glucocorticoids suppress inflammation in addition to humoral and cell-mediated immune responses.
Corticosteroids are well absorbed from the gastrointestinal tract. Prednisone is metabolized in the liver to prednisolone, the active compound. Further hepatic metabolism results in the inactivation of steroids. They are 90% protein-bound.
Cutaneous side effects include acne, hirsutism, striae, purpura, and impaired wound healing. Osteoporosis, myopathy, and aseptic necrosis of bone may occur. Gastrointestinal side effects include peptic ulceration with bleeding or perforation and pancreatitis. Hypertension and edema secondary to fluid retention occur. Steroid psychosis and benign intracranial hypertension are the central nervous system adverse reactions. Ocular effects include cataracts and glaucoma. Patients may suffer growth arrest, secondary amenorrhea, impotence, and suppression of the hypothalamic-pituitary-adrenal axis. Glucose intolerance, hyperosmolar nonketotic coma, and centripetal obesity occur. The risk for infection is increased. Intraarticular corticosteroids may cause a crystal-induced transient synovitis. Immobilization and ice compress will facilitate resolution; persistence of the synovitis beyond 24 hours raises the possibility of an arthrocentesis-related infectious arthritis. Topical steroids, especially the more potent fluorinated compounds, may cause cutaneous telangiectasia, striae, epidermal and dermal atrophy, rosacea-like facial eruption, and senile-type purpura. When used with occlusive dressings, infection, folliculitis, and decreased heat exchange may occur.
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