Sustained Vertebral Fracture Risk Reduction After Withdrawal of Teriparatide in Women With Osteoporosis following Menopause

Updated: Jun 18, 2020

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Teriparatide (recombinant human parathyroid hormone) is a hormone therapy used by post-menopause women suffering from osteoporosis after menopause. The Fracture Prevention Trial (FPT), a randomized, placebo-controlled investigation involving 1637 women with postmenopause osteoporosis, showed that a dosage of 20 or 40 µg of teriparatide each day significantly lowered the risk of vertebral fracture in postmenopause women during an average of18 months of therapy. The investigation detailed below assesses the safety and frequency of new vertebral fractures once post-menopause women have ended teriparatide therapy.

Postmenopause women in the FPT were asked to go back for follow-up visits to give statistics on fracture reduction after ending teriparatide hormone therapy. Few studies have analyzed the degree to which the antifracture value of osteoporosis drugs is maintained in postmenopause females after hormone therapy has finished. This research pays particular attention to whether or not the decline in vertebral fracture risk observed in post-menopause women during the FPT continued right through to the 18-month follow-up visit.

Findings showed that during the follow-up, protection against new vertebral fractures was related to prior teriparatide hormone therapy use and to the fewer vertebral fractures that happened during the FPT in postmenopause women using this kind of hormone therapy.

It was reported that teriparatide hormone therapy use by post-menopause women also safeguarded against later fracture during follow-up, suggesting that it could halt the cycle of increasing risk fracture, which is typical of advanced osteoporosis, and obvious in a follow-up survey in postmenopause women who had previously taken placebo.

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Variation in vertebral T-score during hormone therapy is a highly associated effect of postmenopause women's treatment with teripararide hormone therapy. This could have also perhaps explained a large section of the constant reduction in fracture risk in postmenopause women throughout the follow-up study.

Dempster and colleagues reported improvements in bone microarchitecture in paired biopsy samples from postmenopause women with osteoporosis using human parathyroid hormone therapy for 3 years. Parathyroid hormone therapy increased trabecular connectivity and cortical thickness and eliminated deficiencies in microarchitecture associated with increased skeletal frailty. These improvements might affect fracture risk in postmenopause women after parathyroid hormone therapy has been stopped.

The study outlined above demonstrates that vertebral fracture risk reduction in postmenopause women by teriparatide therapy continues for at least 18 months after therapy has finished. Throughout the follow-up study there were no signs of possible unknown adverse effects of previous teriparatide therapy or side effects associated with stopping the therapy in postmenopause women. This appears to be the first large-scale osteoporosis trial offering statistics on vertebral fracture occurrence in postmenopause women after osteoporosis drug treatment has ended. However, as is so often the case with studies of this nature, there are restrictions and thus more randomized controlled trials are needed to confirm the extent to which sequential hormone therapy with other agents may reduce vertebral fracture risk in postmenopause women.