Glucocorticoid-induced osteoporosis: pathogenesis and management.

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.