THE ROLE OF PARATHYROID-HORMONE IN THE PATHOGENESIS, PREVENTION AND TREATMENT OF POSTMENOPAUSAL OSTEOPOROSIS

Parathyroid hormone (PTH) is the principal regulator of bone remodelin g in the adult skeleton. The acute in vivo effect of: PTH is to increa se bone resorption, although sustained increases in its circulating le vels accelerate both formation and resorption, These divergent effects have focused attention on PTH as a factor contributing to bone loss i n some postmenopausal women, as well as interest in its role as therap y for the disease. Sustained increases in PTH are classically seen in primary hyperparathyroidism. While still controversial, increasing evi dence suggests that primary hyperparathyroidism is associated with inc reased rates of bone loss, particularly from cortical sites in the ske leton. It is clear that the remodeling space is increased in primary h yperparathyroidism, and that surgical correction of the disease leads to substantial increases in bone mass in patients with osteoporosis, R ecently, secondary hyperparathyroidism has emerged as an important con tributor to increased rates of bone turnover and bone loss in postmeno pausal women. The etiology of secondary hyperparathyroidism in postmen opausal women is complex, and is probably related to alterations in vi tamin D metabolism and tissue responsiveness to 1,25(OH)(2)vitamin D. PTH has emerged at the forefront of anabolic therapies for the treatme nt of postmenopausal osteoporosis. When given as a single agent, inter mittent daily subcutaneous administration of PTH induces consistent ga ins in trabecular bone mass with more varying effects on the cortical envelope. However, recent therapeutic trials employing a second agent, most notably estrogen, give hope that this approach may provide the f irst truly efficacious anabolic therapy for this devastating disease. (C) 1998, Editrice Kurtis.