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许多糖尿病性神经病损的病因假说提示血清葡萄糖浓度对神经传导系统有一些直接影响,动物实验支持神经组织损害的代谢假说,然而在人的糖尿病性神经病损的发生和发展中,还未获得代谢控制作用的直接证据.本研究目的是评估胰岛素依赖型的Ⅰ型糖尿病儿童的外周神经功能,探讨代谢情况与神经传导损害的关系.作者研究了30名胰岛素依赖型糖尿病患者,男14例,女16例,年龄2～18岁(平均7.9±3.5岁),平均病程32.1月(最短1月,最长180月),均无肾或眼并发症及外周神经病损的主客观体征.所有病例一直接受混合的中、速效M C 胰岛素治疗,日行2次,根据每日尿糖量和空腹、餐后血糖量变
The etiological hypothesis of many diabetic neuropathy suggests that serum glucose concentration has some direct effects on the nervous system and that animal experiments support the metabolic hypothesis of nerve tissue damage. However, metabolic control has not yet been achieved in the development and progression of human diabetic neuropathy The purpose of this study was to evaluate peripheral nerve function in children with insulin-dependent type 1 diabetes mellitus and to explore the relationship between metabolic status and nerve conduction impairment.The authors studied 30 insulin-dependent diabetes mellitus patients, 14 males and 16 females Cases, aged 2 to 18 years (average 7.9 ± 3.5 years), the average duration of 32.1 months (the shortest January, up to 180 months), no subjective and objective signs of renal or eye complications and peripheral neuropathy all cases have been accepted Mixed, quick-acting MC insulin treatment, 2 times a day, according to the daily amount of urine sugar and fasting, postprandial blood glucose changes