Avram M M, Feinfeld D A, Huatuco A H
N Engl J Med. 1978 May 4;298(18):1000-3. doi: 10.1056/NEJM197805042981805.
In a retrospective analysis to determine whether secondary hyperparathyroidism in uremia has a role in uremic peripheral neuropathy, we simultaneously measured motor-nerve conduction velocity and serum parathormone level in 42 uremic patients. We compared age-matched groups of nondiabetic uremic patients, divided into three groups according to serum parathyroid hormone, for degree of impairment of motor-nerve conduction velocity, and 12 diabetic patients with uremia. The group with highest levels had a significantly (P less than 0.01) lower conduction velocity (25.3 +/- 4.9 m per second) than the group with normal or slightly elevated parathyroid hormone, who had only mild depression of nerve conduction (45.1 +/- 1.3 m per second). Mean serum calcium and creatinine were not significantly different between groups. Nerve conduction velocity was similarly depressed in 17 patients on additional dialysis studied prospectively and divided into groups according to parathyroid hormone levels. These results suggest a relation between high parathormone levels and uremic neuropathy and implicate parathyroid hormone as a uremic toxin.
在一项旨在确定尿毒症继发性甲状旁腺功能亢进是否在尿毒症周围神经病变中起作用的回顾性分析中,我们同时测量了42例尿毒症患者的运动神经传导速度和血清甲状旁腺激素水平。我们将年龄匹配的非糖尿病尿毒症患者根据血清甲状旁腺激素分为三组,比较其运动神经传导速度的受损程度,并与12例尿毒症糖尿病患者进行比较。甲状旁腺激素水平最高的组,其传导速度(25.3±4.9米/秒)显著低于(P<0.01)甲状旁腺激素正常或轻度升高的组,后者仅存在轻度神经传导抑制(45.1±1.3米/秒)。各组间的平均血清钙和肌酐无显著差异。对17例接受额外透析的患者进行前瞻性研究,并根据甲状旁腺激素水平分组,其神经传导速度同样受到抑制。这些结果表明甲状旁腺激素水平升高与尿毒症神经病变之间存在关联,并提示甲状旁腺激素是一种尿毒症毒素。