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透析性骨软化症中甲状旁腺对急性低钙血症的反应性

Parathyroid gland responsiveness to acute hypocalcemia in dialysis osteomalacia.

作者信息

Kraut J A, Shinaberger J H, Singer F R, Sherrard D J, Saxton J, Miller J H, Kurokawa K, Coburn J W

出版信息

Kidney Int. 1983 May;23(5):725-30. doi: 10.1038/ki.1983.85.

Abstract

The majority of chronic hemodialysis patients have elevated serum iPTH levels and bone disease characterized by osteitis fibrosa. However, a small group of patients develop osteomalacic bone disease associated with normal or slightly elevated iPTH values and a tendency to hypercalcemia which occurs either spontaneously or after treatment with small doses of vitamin D sterols. To examine the causes of the relatively low iPTH levels, we evaluated the change in serum iPTH levels that occurred in response to acute hypocalcemia, produced by dialysis using a low calcium dialysate, in 11 patients with osteomalacia and 8 control hemodialysis patients. Dialysis against a dialysate free of calcium for 60 to 90 min led to a fall in serum calcium to 7.5 +/- 0.2 and 7.2 +/- 0.2 mg/dl in the osteomalacic and control patients, respectively. Serum iPTH rose in controls from 1380 +/- 287 to 1960 +/- 287 pg/ml (P less than 0.01), whereas in patients with osteomalacia it rose from 360 +/- 58 to 507 +/- 104 pg/ml (P less than 0.05), a value only slightly above normal for this PTH assay. These data suggest that the relatively low basal levels of serum iPTH do not arise as a consequence of physiologic suppression of parathyroid gland function. This reduction in parathyroid function could contribute to the pathogenesis of low turnover osteomalacia.

摘要

大多数慢性血液透析患者血清iPTH水平升高,并患有以纤维性骨炎为特征的骨病。然而,一小部分患者会发展为骨软化性骨病,其iPTH值正常或略有升高,且有高钙血症倾向,这种高钙血症可自发出现,或在小剂量维生素D甾醇治疗后出现。为了研究iPTH水平相对较低的原因,我们评估了11例骨软化症患者和8例对照血液透析患者在使用低钙透析液进行透析导致急性低钙血症时血清iPTH水平的变化。用无钙透析液透析60至90分钟后,骨软化症患者和对照患者的血清钙分别降至7.5±0.2和7.2±0.2mg/dl。对照组血清iPTH从1380±287pg/ml升至1960±287pg/ml(P<0.01),而骨软化症患者血清iPTH从360±58pg/ml升至507±104pg/ml(P<0.05),该值仅略高于此PTH检测的正常范围。这些数据表明,血清iPTH相对较低的基础水平并非甲状旁腺功能生理抑制的结果。甲状旁腺功能的这种降低可能有助于低转换型骨软化症的发病机制。

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