Kuriyama M, Mizuma A, Yokomine R, Igata A, Otuji Y
Clin Chim Acta. 1980 Dec 8;108(2):169-77. doi: 10.1016/0009-8981(80)90002-9.
We performed a study concerning the activity of erythrocyte transketolase and thiamine metabolism in 73 uremic patients with or without neuropathy and 67 normal control subjects. Although the total vitamin B1 level in whole blood was high in the uremic patients, the transketolase activity in the hemolysate and the thiamine pyrophosphate effect on it were lower than those of normal subjects. The values of the transketolase activity of the two groups were statistically correlated with the levels of the thiamine pyrophosphate effect and the vitamin B1 content of the blood. Inhibition of transketolase activity was apparent in the uremic patients. However, this inhibition did not seem to be the only cause for the development of uremic neuropathy since no significant difference in these activities was observed among uremic patients with and without neuropathy. Moreover, a direct correlation could not be confirmed between transketolase activity and motor nerve conduction velocity.
我们对73例有或无神经病变的尿毒症患者以及67名正常对照者进行了一项关于红细胞转酮醇酶活性和硫胺素代谢的研究。尽管尿毒症患者全血中总维生素B1水平较高，但溶血产物中转酮醇酶活性及其硫胺素焦磷酸效应低于正常受试者。两组转酮醇酶活性值与硫胺素焦磷酸效应水平及血液中维生素B1含量具有统计学相关性。尿毒症患者中转酮醇酶活性受到明显抑制。然而，这种抑制似乎并非尿毒症神经病变发生的唯一原因，因为在有神经病变和无神经病变的尿毒症患者之间，这些活性未观察到显著差异。此外，转酮醇酶活性与运动神经传导速度之间未能证实存在直接相关性。
