Prevention of bone loss with risedronate in glucocorticoid-treated rheumatoid arthritis patients

The aim of the study was to assess risedronate's effect on bone mineral den sity in postmenopausal women with rheumatoid arthritis receiving glucocorti coids. We carried out a two center, 2 year, double-masked, placebo-controll ed trial with a third year of nontreatment follow-up. We studied 120 women requiring long-term glucocorticoid therapy at > 2.5 mg/ day prednisolone ra ndomized to treatment with daily placebo; daily 2.5 mg risedronate; or cycl ical 15 mg risedronate (2 out of 12 weeks). At 97 weeks, bone mineral densi ty was maintained at the lumbar spine (+1.4%) and trochanter (+0.3%) in the daily 2.5 mg risedronate group, while significant bone loss occurred in th e placebo group (-1.6%, p = 0.03; and 4.0%, p<0.005, respectively). At the femoral neck, there was a nonsignificant bone loss in the daily 2.5 mg rise dronate group (-1.0%) while in the placebo group bone mass decreased signif icantly (-3.6%, p<0.001). The difference between placebo and daily 2.5 mg r isedronate groups was significant at the lumbar spine (p = 0.009) and troch anter (p = 0.02) but did not reach statistical significance at the femoral neck. Although not significantly different from placebo at the lumbar spine , the overall effect of the cyclical regimen was similar to that of the dai ly 2.5 mg risedronate regimen. Treatment withdrawal led to bone loss in the risedronate groups that was significant at the lumbar spine. A similar num ber of patients experienced adverse events (including upper gastrointestina l events) across treatment groups and risedronate was generally well tolera ted. Thus risedronate preserves bone mass in postmenopausal women with rheu matoid arthritis receiving glucocorticoids while patients receiving a place bo have significant bone loss.