Increases in bone mineral density after discontinuation of daily human parathyroid hormone and gonadotropin-releasing hormone analog administration in women with endometriosis

Intermittent PTH administration increases spinal bone mineral density (BMD) and prevents bone loss from the hip and total body in young women treated with a long acting GnRH analog for endometriosis. To establish whether thes e beneficial effects on BMD persist after PTH administration is discontinue d, we remeasured BMD and biochemical markers of bone turnover in 38 women w ith endometriosis who had been treated with a GnRH analog alone (nafarelin acetate; 200 mu g, intranasally, twice daily; n = 23; group I) or who had r eceived nafarelin plus human PTH-(1-34) (40 mu g/day, sc; n = 15; group 2) for 6-12 months 1 yr after therapy was completed. Cyclic menstrual function returned promptly after nafarelin therapy was discontinued. In group 1, BM D increased significantly at all sites [P < 0.001 for the anterior-posterio r (API and lateral spine; P = 0.014 for the femoral neck; P = 0.004 for the trochanter], except the proximal radius (P = 0.065) and total body bone de nsity (P = 0.069 after nafarelin therapy was stopped. In group 2, BMD incre ased significantly at the AP spine (P < 0.001), lateral spine (P = 0.012), femoral neck (P = 0.002), and trochanter (P = 0.029) after nafarelin therap y was stopped. BMD of the spine in the AP projection increased more in grou p 2 and than in group 1 after therapy was stopped (P = 0.045). Despite thes e increases after discontinuation of nafarelin therapy, BR;ID was still sig nificantly below baseline values at the AP spine (P < 0.001) and femoral ne ck (P = 0.006) and tended to be lower than baseline values at the trochante r (P = 0.057) and total body (P = 0.101) at the end of the 1-yr follow-up p eriod in group 1, In contrast, BMD was significantly above baseline values at the AP and lateral spine (P < 0.001) sites and was similar to baseline v alues at the other skeletal Bites at the end of the 1-yr follow-up period i n group 2, Bone turnover returned to baseline values in both groups when th erapy was stopped. We conclude that the beneficial effects of PTH on bone p ersist in women who regain cyclic menstrual function. Although part of the increases in BMD are probably due to restoration of ovarian function, addit ional increases in BMD most likely represent a further anabolic effect of P TH on bone that is not detected until after PTH administration is stopped.