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Glucocorticosteroid Therapy: Mechanisms of Action and Clinical Considerations

ANTHONY S. FAUCI, M.D.; DAVID C. DALE, M.D.; and JAMES E. BALOW, M.D.
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▸Requests for reprints should be addressed to Anthony S. Fauci, M.D., National Institute of Allergy and Infectious Diseases, Bldg. 10, Room 11B-09, National Institutes of Health, Bethesda, MD 20014.


Bethesda, Maryland


Ann Intern Med. 1976;84(3):304-315. doi:10.7326/0003-4819-84-3-304
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The administration of glucocorticosteroids results in a wide range of effects on inflammatory and immunologically mediated disease processes. Glucocorticosteroids cause neutrophilic leukocytosis together with eosinopenia, monocytopenia, and lymphocytopenia. A principal mechanism whereby corticosteroids suppress inflammation is their impeding the access of neutrophils and monocytes to an inflammatory site. Granulocyte function is relatively refractory, whereas monocyte-macrophage function seems to be particularly sensitive to corticosteroids. Corticosteroid administration causes a transient lymphocytopenia of all detectable lymphocyte subpopulations, particularly the recirculating thymus-derived lymphocyte. The mechanism of this lymphocytopenia is probably a redistribution of circulating cells to other body compartments. There is considerable disagreement about the direct effects of corticosteroid administration on human lymphocyte function. The corticosteroid regimen should be adjusted to attain maximal therapeutic benefit with minimal adverse side effects. Often, alternate-day dosage regimens effectively maintain disease remission with minimization or lack of Cushingoid and infectious complications.

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