Grzelec H
Kliniki Neurologii Instytutu Neurologiczo-Psychiatrycznego Pomorskiej Akademii Medycznej, Szczecinie.
Neurol Neurochir Pol. 1991 Jul-Aug;25(4):477-84.
The pathogenesis of neuropathy and other late, degenerative complications of diabetes remains largely unresolved. Metabolic derangements thought to be responsible for their development are induced by chronic hyperglycaemia. The present studies concern as follows: sorbitol accumulation due to increased polyol pathway activity, altered myoinositol metabolism in diabetic nerve, followed by diminished sodium-potassium ATPase activity, nonenzymatic glycosylation of structural proteins and rheologic changes in microcirculation. These processes impair nerve metabolism, function and structure directly or indirectly, due to primary vascular alternations and endoneural hypoxia. Partial elucidation of the mechanism involved in pathogenesis of diabetic neuropathy has provoked emergence of new therapeutic approaches. So far their results are equivocal and require further studies. At present, improved glycaemia control is undoubtedly the most important factor in prevention and treatment of neuropathy and other late complications of diabetes.
糖尿病性神经病变及其他晚期退行性并发症的发病机制在很大程度上仍未得到解决。被认为是导致其发生的代谢紊乱是由慢性高血糖引起的。目前的研究涉及以下方面：多元醇途径活性增加导致山梨醇积累、糖尿病神经中肌醇代谢改变，继而钠钾ATP酶活性降低、结构蛋白的非酶糖基化以及微循环中的流变学变化。由于原发性血管改变和神经内膜缺氧，这些过程直接或间接损害神经代谢、功能和结构。对糖尿病性神经病变发病机制所涉及机制的部分阐明引发了新治疗方法的出现。到目前为止，其结果尚无定论，需要进一步研究。目前，改善血糖控制无疑是预防和治疗糖尿病性神经病变及其他晚期并发症的最重要因素。
