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Ann Intern Med. 1990 Mar 1;112(5):352-64.

Glucocorticoid-induced osteoporosis: pathogenesis and management.

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  • 1University of Kansas Medical Center, Kansas City.

Abstract

PURPOSE:

To review the clinical picture, pathogenesis, and management of glucocorticoid-induced osteoporosis.

DATA IDENTIFICATION:

Studies published since 1970 were identified from a MEDLINE search, articles accumulated by the authors, and through bibliographies of identified articles.

STUDY SELECTION:

Information for review was taken from 160 of the more than 200 articles examined.

DATA EXTRACTION:

Pertinent studies were selected; the relative strengths and weaknesses of these studies are discussed.

RESULTS OF DATA SYNTHESIS:

Studies in tissue and organ cultures suggest that glucocorticoids have a direct effect on bone, causing inhibition of bone formation and enhancing bone resorption. Glucocorticoids decrease calcium absorption from the intestine and increase renal excretion. Osteoporosis occurs in at least 50% of persons who require long-term glucocorticoid therapy. Long-term trials of therapy for the prevention of glucocorticoid-induced osteoporosis have not been done, but reasonable recommendations include the use of a glucocorticoid with a short half-life in the lowest dose possible, maintenance of physical activity, adequate calcium and vitamin D intake, sodium restriction and use of thiazide diuretics, and gonadal hormone replacement. In refractory cases, the use of calcitonin, bisphosphonates, sodium fluoride, or anabolic steroids should be considered.

CONCLUSIONS:

Osteoporosis is common in patients requiring long-term treatment with glucocorticoids. Careful attention to preventive management may minimize the severity of this serious complication.

Comment in

  • Corticosteroids and bone mass. [Ann Intern Med. 1990]
PMID:
2407167
[PubMed - indexed for MEDLINE]
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