D'Amour M L, Bruneau J, Butterworth R F
Neurology Service, André-Viallet Clinical Research Center, Hôpital Saint-Luc University of Montreal.
Can J Neurol Sci. 1991 May;18(2):126-8. doi: 10.1017/s0317167100031565.
Thiamine status was evaluated using the erythrocyte transketolase activation assay in 20 alcoholic patients admitted on a voluntary basis to a Detoxification Unit. Electromyographic evaluation revealed significant reductions of motor and sensory conduction velocities in the alcoholic group. 38% of alcoholic patients showed significant erythrocyte transketolase activation deficits indicative of severe thiamine deficiency. In the case of peroneal nerve, reduced conduction velocities were negatively correlated with abnormal transketolase parameters. These findings are consistent with a contributory (but not exclusive) role of thiamine deficiency in the pathogenesis of alcoholic peripheral neuropathy. Deficiencies of other vitamins as well as direct neurotoxic effects of alcohol could also be involved in this phenomenon.
采用红细胞转酮醇酶激活试验,对20名自愿入住戒毒所的酒精性患者的硫胺素状态进行了评估。肌电图评估显示,酒精组患者的运动和感觉传导速度显著降低。38%的酒精性患者表现出显著的红细胞转酮醇酶激活缺陷,表明存在严重的硫胺素缺乏。在腓总神经方面,传导速度降低与转酮醇酶参数异常呈负相关。这些发现与硫胺素缺乏在酒精性周围神经病发病机制中所起的作用(但非唯一作用)相一致。其他维生素缺乏以及酒精的直接神经毒性作用也可能与这一现象有关。