Cyclical etidronate therapy for prevention of postmenopausal bone loss: A 1-year open-label follow-up study

The objective of this study was to evaluate whether the pharmacological act ivity of cyclical etidronate therapy is sustained beyond the dosing period. A group of 121 postmenopausal women who had completed a 2-year, double-bli nd, placebo-controled parallel study with etidronate or placebo (400 mg/day for 14 days every 3 months) and calcium agreed to participate in a 1-year open-label follow-up study to evaluate the effect of discontinuing etidrona te treatment. Fifty-nine subjects in the former etidronate group and 62 in the placebo group received 500 mg/day of elemental calcium; 54/59 and 58/62 subjects, respectively, completed the study. Outcomes of the study were bo ne mineral density (BMD) measured by dual energy Xray absorptiometry (DXA), and biochemical markers of bone turnover (urinary deoxypyridinoline/creati nine and serum osteocalcin). To determine whether there was a residual effe ct of previous therapy we compared mean percentage changes from baseline (y ear 0) to year 3 for both spinal and femoral neck BMD and markers of bone t urnover in the former cyclical etidronate and placebo groups. To evaluate t he carryover effect of treatment we compared the percent change from year 2 to year 3 for the same variables. Mean percentage change (SEM) from year 2 to year 3 for spinal BMD in the former cyclical etidronate group was -2.87 % (0.48%) versus -0.99% (0.36%) in the placebo group (P = 0.0022). in the f emoral neck, the BMD changes were -0.86% (0.42%) versus -1.01% (0.41%) (NS) . Biochemical markers increased within 6 months toward baseline levels. Mea n percentage changes from baseline (year 0) in both spinal and femoral neck BMD were significantly different between groups 1 year after treatment dis continuation. No differences between groups were maintained in deoxypyridin oline and osteocalcin. It is concluded that following withdrawal of cyclica l etidronate therapy bone loss resumes at a normal and moderately accelerat ed rate in the proximal femur and lumbar spine, respectively. A positive ef fect on BMD at both cortical and trabecular sites is maintained for 1 year after treatment withdrawal.