Barbara P. Lukert, MD; Lawrence G. Raisz, MD
Lukert BP, Raisz LG. Glucocorticoid-Induced Osteoporosis: Pathogenesis and Management. Ann Intern Med. 1990;112:352-364. doi: 10.7326/0003-4819-112-5-352
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Published: Ann Intern Med. 1990;112(5):352-364.
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.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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