The clinical use of glucocorticoids.
Glucocorticoids are potent anti-inflammatory agents and their administration results in a wide range of effects on inflammatory and immunologically mediated disease processes. The precise mechanisms by which glucocorticoids impair the human immune response are unknown. Intracytoplasmic glucocorticoids specific receptors are important in the specificity of glucocorticoid actions. Glucocorticoid administration results in neutrophillia, monocytopenia, lymphopenia, and eosinopenia. A principle mechanism whereby glucocorticoids limit inflammation is by limiting the access of leukocytes, particularly neutrophils, to inflammatory sites. Neutrophil function is relatively refractory while monocyte and T-cell function is more easily impaired. A variety of glucocorticoid preparations are available for use, and appreciation of their relative potency and plasma half-lives is essential for designing therapeutic regimens. High doses and frequent administration of glucocorticoids are necessary in order to induce a remission in patients with flagrantly active disease. Once a remission is induced, the glucocorticoid regimen should be adjusted to attain maximal therapeutic benefit with minimal adverse effects. Alternate day dosage regimens can often be used to maintain a remission.
D001770:Blood Bactericidal Activity; D003240:Connective Tissue Diseases / Q000188:drug therapy; D004334:Drug Administration Schedule; D005938:Glucocorticoids / Q000009:adverse effects / Q000502:physiology / Q000627:therapeutic use*; D006801:Humans; D007962:Leukocytes / Q000187:drug effects; D010587:Phagocytosis / Q000187:drug effects; D012333:RNA, Messenger / Q000096:biosynthesis; D011956:Receptors, Cell Surface / Q000378:metabolism
D005938:Glucocorticoids; D012333:RNA, Messenger; D011956:Receptors, Cell Surface