Evaluation of the efficacy of etidronate therapy in preventing glucocorticoid-induced bone loss in patients with inflammatory rheumatic diseases - A randomized study

The prevention and treatment of glucocorticoid-induced osteoporosis is a ma jor concern for rheumatologists since inflammatory joint disease is among t he most common reasons for long-term glucocorticoid therapy. We used a rand omized placebo-controlled design to evaluate the efficacy of one-year cycli cal etidronate therapy in preventing bone loss in 83 glucocorticoid-treated patients with rheumatoid arthritis, polymyalgia rheumatics, or Giant cell arteritis. Glucocorticoid treatment duration was shorter than three months, and the starting dose was greater than 7.5 mg of prednisone-equivalent per day, Etidronate was given according to the standard cyclical schedule, i.e . 400 mg/d for periods of 14 days separated by 76-day intervals during whic h patients took 500 mg of supplemental calcium per day. The primary evaluat ion criterion was the change in lumbar spine hone mineral density after one year of etidronate therapy. Bone mineral density decreased by 1.94+/-0.61% in the placebo group and increased by 0.86+/-0.6% in the etidronate group, yielding a between-group difference of 2.8+/-0.86% (P=0.002). The differen ce was largest in postmenopausal women (3.38+/-1.11%; P=0.004). At the femo ral neck, there was a smaller bone mineral density decrease: in the etidron ate than In the placebo group, but the difference (1.11+/-1.13%] was not st atistically significant. The most common side effects were gastrointestinal symptoms and showed no difference between the two groups. Four fractures ( Including one vertebral fracture] occurred in the placebo group versus two [including one vertebral) in the etidronate group. Etidronate prevents gluc ocorticoid-induced lumbar spine hone loss in patients with rheumatoid arthr itis, polymyalgia rheumatica, or giant cell arteritis.