ALENDRONATE FOR THE PREVENTION AND TREATMENT OF GLUCOCORTICOID-INDUCED OSTEOPOROSIS

Background Osteoporosis is a common complication of long-term glucocor ticoid therapy for which there is no well-proved preventive or restora tive treatment. Methods We carried out two 48-week, randomized, placeb o-controlled studies of two doses of alendronate in 477 men and women, 17 to 83 years of age, who were receiving glucocorticoid therapy. The primary end point was the difference in the mean percent change in lu mbar-spine bone density from base line to week 48 between the groups. Secondary outcomes included changes in bone density of the hip, bioche mical markers of bone turnover, and the incidence of new vertebral fra ctures. Results The mean (+/-SE) bone density of the lumbar spine incr eased by 2.1+/-0.3 percent and 2.9+/-0.3 percent, respectively, in the groups that received 5 and 10 mg of alendronate per day (P<0.001) and decreased by 0.4+/-0.3 percent in the placebo group. The femoral-neck bone density increased by 1.2+/-0.4 percent and 1.0+/-0.4 percent in the respective alendronate groups (P<0.01) and decreased by 1.2+/-0.4 percent in the placebo group (P<0.01). The bone density of the trochan ter and total body also increased significantly in the patients treate d with alendronate. There were proportionally fewer new vertebral frac tures in the alendronate groups (overall incidence, 2.3 percent) than in the placebo group (3.7 percent) (relative risk, 0.6; 95 percent con fidence interval, 0.1 to 4.4). Markers of bone turnover decreased sign ificantly in the alendronate groups (P<0.001). There were no differenc es in serious adverse effects among the three groups, but there was a small increase in nonserious upper gastrointestinal effects in the gro up receiving 10 mg of alendronate. Conclusions Alendronate increases b one density in patients receiving glucocorticoid therapy. (N Engl J Me d 1998;339:292-9.) (C)1998, Massachusetts Medical Society.