Enhancement of bone mass in osteoporotic women with parathyroid hormone followed by alendronate

Treatment of osteoporosis with PTH causes a marked increase in vertebral bo ne mineral density (BMD). However, this effect is rapidly reversed when the treatment is stopped. The purpose of the present study was to determine wh ether the bisphosphonate alendronate could preserve or enhance bone density in patients previously treated with PTH. Sixty-six postmenopausal osteopor otic women were treated for 1 yr with 50, 75, or 100 mu g recombinant human PTH-(1-84) or placebo, and then were given 10 mg alendronate daily for an additional year. BRID was measured in the femoral neck, lumbar spine, and w hole body. Markers of bone turnover included skeletal alkaline phosphatase, osteocalcin, and N-telopeptide. During the first year, changes in BMD (mean +/- SD) in women receiving PTH tall doses combined) were 7.1 +/- 5.6% (spine), 0.3 +/- 6.2% (femoral neck) , and -2.3 +/- 3.3% (total body). After switching to alendronate for 1 yr i n women who previously had received PTH, mean changes in BMD were 13.4 +/- 6.4% (spine), 4.4 +/- 7.2% (femoral neck), and 2.6 +/- 3.1% (whole body). I n the subgroup of patients who had received the highest dose of PTH, the me an increase in vertebral BMD was 14.6 +/- 7.9%. All markers of bone turnove r increased during treatment with PTH and decreased to below baseline after 1 yr of alendronate. In conclusion, sequential treatment of osteoporosis with PTH and alendronat e results in an increase in vertebral bone density that is considerably mor e than has been reported with alendronate or estrogens alone. This combinat ion of drugs may be a useful approach to maximizing bone density in women w ith vertebral osteoporosis.