Increases in bone mineral density after discontinuation of daily human parathyroid hormone and gonadotropin-releasing hormone analog administration in women with endometriosis
Increases in bone mineral density after discontinuation of daily human parathyroid hormone and gonadotropin-releasing hormone analog administration in women with endometriosis
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DOI：
10.1210/jc.84.4.1214
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发表时间：
1999-04-01
影响因子：
5.8
通讯作者：
Arnold, AL
中科院分区：
文献类型：
--
作者：
Finkelstein, JS;Arnold, AL
间歇性PTH给药可增加年轻女性接受长效GnRH类似物治疗子宫内膜异位症的脊柱骨密度（BMD），防止髋部和全身骨质流失。为了确定停止给药后对骨密度的有益影响是否持续，我们重新测量了38名子宫内膜异位症患者的骨密度和骨转化生化指标，这些患者分别接受GnRH类似物（醋酸纳伐林，200 μ g，鼻内，每天两次；n = 23；组I）或接受纳伐林加人PTH-(1-34) （40 μ g/天，sc; n = 15；组2）治疗6-12个月，治疗结束后1年。停止纳伐林治疗后，月经周期功能迅速恢复。在第1组中，除桡骨近端（P = 0.065）和全身骨密度（P = 0.069）停止纳伐林治疗外，所有部位的骨密度均显著增加[前后路（API和侧棘）P < 0.001；股骨颈P = 0.014；粗隆P = 0.004]。2组停止纳伐林治疗后，股骨颈（P = 0.002）、股骨粗隆（P = 0.029）、前棘（P < 0.001）、侧棘（P = 0.012）、股骨颈（P = 0.002）的骨密度显著升高。治疗结束后，治疗组2和治疗组1脊柱骨密度增高较多（P = 0.045）。尽管停止纳伐林治疗后这些增加，BR；ID在美联社脊柱仍大大低于基线值(P < 0.001),股骨颈(P = 0.006),往往低于基线值在转子(P = 0.057)和全身(P = 0.101)结束时在组1 1年随访期间,相比之下,在美联社BMD显著高于基线值和脊柱侧(P < 0.001)网站和类似于基线值的其他骨骼咬最后1年随访期间在2组,停止治疗后，两组的骨周转率均恢复到基线值。我们得出结论，甲状旁腺激素对骨骼的有益作用持续存在于恢复月经周期功能的妇女中。尽管骨密度增加的部分原因可能是由于卵巢功能的恢复，但骨密度的额外增加很可能代表甲状旁腺激素对骨骼的进一步合成代谢作用，直到停止给药后才会被检测到。
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 these beneficial effects on BMD persist after PTH administration is discontinued, we remeasured BMD and biochemical markers of bone turnover in 38 women with 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 received 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, BMD increased significantly at all sites [P < 0.001 for the anterior-posterior (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 density (P = 0.069 after nafarelin therapy was stopped. In group 2, BMD increased 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 therapy was stopped. BMD of the spine in the AP projection increased more in group 2 and than in group 1 after therapy was stopped (P = 0.045). Despite these increases after discontinuation of nafarelin therapy, BR;ID was still significantly below baseline values at the AP spine (P < 0.001) and femoral neck (P = 0.006) and tended to be lower than baseline values at the trochanter (P = 0.057) and total body (P = 0.101) at the end of the 1-yr follow-up period 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 values at the other skeletal Bites at the end of the 1-yr follow-up period in group 2, Bone turnover returned to baseline values in both groups when therapy was stopped. We conclude that the beneficial effects of PTH on bone persist in women who regain cyclic menstrual function. Although part of the increases in BMD are probably due to restoration of ovarian function, additional increases in BMD most likely represent a further anabolic effect of PTH on bone that is not detected until after PTH administration is stopped.