Glucocorticoid-Induced Osteoporosis: Pathogenesis and Management

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.