Martin R A
Postgrad Med. 1987 Sep 1;82(3):183-7. doi: 10.1080/00325481.1987.11699961.
Peripheral neuropathy in diabetes begins as a physiologic aberration related to hyperglycemia and its subsequent effects of endoneurial hypoxia, elevated sorbitol levels, and decreased myoinositol levels. Resultant decreases in sodium-potassium-adenosine triphosphatase levels ultimately lead to structural alterations at the nodes of Ranvier. Aldose reductase inhibitors and dietary myoinositol supplementation are being used in long-term clinical studies to monitor the possibility that they may prevent or reverse these abnormalities. In the meantime, symptomatic treatment remains the mainstay of management.
糖尿病性周围神经病变始于一种与高血糖及其随后的神经内膜缺氧、山梨醇水平升高和肌醇水平降低相关的生理异常。钠钾三磷酸腺苷水平的降低最终导致郎飞结处的结构改变。醛糖还原酶抑制剂和膳食肌醇补充剂正在长期临床研究中使用，以监测它们预防或逆转这些异常的可能性。与此同时，对症治疗仍然是主要的治疗方法。
