Management of glucocorticoid-induced osteoporosis: prevalence, and emerging treatment options

Abstract

An excess amount of glucocorticoids represents the primary and most frequent etiological factor influencing secondary osteoporosis. Patients receiving glucocorticoids, but also those with the endogenous form of hypercorticism, are at high risk for the loss of bone density, with the subsequent occurrence of pathological fractures. In this review, we summarize the currently available methods of prevention and the treatment of glucocorticoid-induced osteoporosis. We also include a proposal for both a prophylactic and therapeutic approach that takes into account the risk factors typical for long-term users of glucocorticoids.

Keywords: bisphosphonates; bone mineral density; calcium and vitamin D; glucocorticoid-induced osteoporosis; osteoporotic fractures; teriparatide.

Figure 1

Effects of glucocorticoids on bone. Derived from., Abbreviations: TST, testosterone; LH, luteinizing hormone; FSH, follicle-stimulating hormone; GI, gastrointestinal; Ca, calcium.

Figure 2

Diagnostic and therapeutic steps in making decisions for the prevention of glucocorticoid-induced osteoporosis. Reproduced from Geusens PP, de Nijs RNJ, Lems WF, et al. Prevention of glucocorticoid osteoporosis: a consensus document of the Dutch Society for Rheumatology. Ann Rheum Dis. 2004;63:324–325. Copyright © 2004, with permission from BMJ Publishing Group Ltd.