ABSTRACT
Introduction Glucocorticoid-induced osteoporosis was discovered more than 60 years ago when Cushing first described the tendency of patients with excess endogenous glucocorti coids (GCs) to develop bone fractures |l|. Many cross-sectional studies have found that patients using oral GCs have reduced bone mineral density (BMD) and longitu dinal studies have reported a rapid onset of this BMD loss. In the only two randomized trials available, the loss o f lumbar spine BMD at 3 to 5 months was statistically signifi cantly greater in patients using on average 7.5 mg prednisolone per day compared with randomly selected controls |2,3|. Several epidemiological studies reported increased risks of fractures, including vertebral and hip, in patients using oral GCs |4,5|.
