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Glucocorticoid-Induced Osteoporosis

2001; Elsevier BV; Linguagem: Inglês

10.1016/b978-012470862-4/50045-3

Gary M. Leong, Jacqueline R. Center, N. Kathryn Henderson, John A. Eisman,

Bone health and treatments

With the widespread use of glucocorticoids for systemic diseases affecting nearly every bodily system, exogenous glucocorticoid is an important cause of osteoporosis. This chapter highlights major aspects of advances as well as current perspectives on treatment options of glucocorticoid bone disease. The adverse effect of glucocorticoid therapy on bone mineral density (BMD) is not linear with time. Bone loss and fracture risk seems to be related, at least to some extent, to the dose and duration of glucocorticoid exposure. The risk of fracture increases rapidly after the commencement of glucocorticoid therapy, but decreases again after cessation of therapy. Glucocorticoids contribute to increased fracture risk through a number of direct and indirect mechanisms that result in accelerated bone loss. The bone loss is biphasic, precipitous during the first 12 months, and more gradual but continuous in subsequent years as measured by DXA or histomorphometry. There are several issues to consider in reviewing studies on the efficacy of therapies available for glucocorticoidinduced osteoporosis. These include primary versus secondary prevention, underlying disease states, and fracture prevention. A distinction needs to be made between primary and secondary prevention trials. The former commence at or soon after glucocorticoid therapy is begun, because the greatest rate of bone loss due to glucocorticoids occurs within the first 6–12 months of use. Secondary prevention, or treatment trials are those that commence after the subject has already taken glucocorticoids for a significant period of time and in whom bone loss has already occurred. Very few prospective studies have been undertaken in children to determine the long-term effects on bone mass of chronic glucocorticoid administration. However, as the large majority of peak bone mass is acquired during the first two decades of life, glucocorticoid exposure during this critical time of bone mass accrual may impact negatively on peak bone mass.