Journal of Steroid Biochemistry & Molecular Biology 88 (2004) 337–349 Review The treatment of glucocorticoid-induced osteoporosis Dana Cohen, Jonathan D. Adachi ∗ 501-25 Charlton Ave E, Hamilton, Ont., Canada L8N 1Y2 Received 22 August 2003; accepted 12 January 2004 Abstract Glucocorticoid use results in an increase risk for fractures. Over the past 10 years, we have a greater understanding of the epidemiology, pathophysiology, prevention and treatment of glucocorticoid induced osteoporosis. This article reviews these recent findings and selective practice guidelines. © 2004 Elsevier Ltd. All rights reserved. Keywords: Glucocorticoids; Osteoporosis; Treatment 1. Introduction The use of glucocorticoids in the treatment of disease is ubiquitous in medicine today. In the fields of rheuma- tology, respirology, neurology, hematology, dermatology, gastroenterology and transplant medicine, glucocorticoids have vastly improved the treatment of numerous diseases that were once associated with significant morbidity and mortality. Often these drugs are prescribed on a long-term basis at supraphysiologic doses, and are associated with a number of side effects. The most common and serious of which, however, is bone loss leading to osteoporosis [1]. Glucocorticoid-induced osteoporosis (GIOP) is a widely recognized complication of these drugs, associated with increased risk of fractures to patients. It is estimated that between 30 and 50% of patients on long-term glucocor- ticoids will experience fractures [2], and that this risk to patients increases rapidly from the onset of therapy [3,4]. Today, loss of bone density and fractures due to GIOP may be prevented through the use of bone sparing agents. Due to the prevalence of glucocorticoid usage and the high costs incurred both personally and to society fol- lowing a fracture, it is imperative that there be a greater awareness of the issues surrounding GIOP and of therapies that may be offered to patients both for prevention and treatment. ∗ Corresponding author. Tel.: +1-905-529-1317; fax: +1-905-521-1297. E-mail address: jd.adachi@sympatico.ca (J.D. Adachi). 2. Epidemiology In a large, retrospective cohort study evaluating the rela- tionship between oral glucocorticoid use and fracture risk in the UK, it was estimated that approximately 0.9% of the total adult population was using oral glucocorticoids at any one time [5]. On extrapolation of this percentage to the UK population as a whole it was suggested that around 409,000 people were using glucocorticoids, and while the majority were taking doses of 2.5–7.5 mg of prednisolone daily, an estimated 93,000 people were taking doses greater than 7.5 mg, and had done so for greater than 6 months [5]. A significant dose response was observed for vertebral and hip fractures, such that fracture risk in glucocorticoid users was determined to be about 20% for daily doses of 5 mg or lower of prednisolone, however, rose to an approximate 60% increased risk compared to control group for those on a daily dose of 20 mg or more [3–5]. This risk was similar for men and women, but varied with age. Fracture rates in women rose exponentially with advancing age in both con- trol group and glucocorticoid users, however in both men and women the incidence rates tended to be greater among those on higher doses of oral glucocorticoids [5]. Interest- ingly, patients aged 70–79 years were using oral glucocor- ticoids most frequently, and tended to use them for longer periods of time than younger patients. Likewise, patients on higher doses of oral glucocorticoids were more likely to continue treatment for longer periods of time. Based on this study, however, the concomitant use of bone-active treat- ments during glucocorticoid treatment was found to be very low, ranging from 4.0 to 5.5% [5]. Bone loss occurs rapidly within the first 6–12 months of starting glucocorticoid therapy [6] Fig. 1, and is the 0960-0760/$ – see front matter © 2004 Elsevier Ltd. All rights reserved. doi:10.1016/j.jsbmb.2004.01.003