[Pathogenesis and treatment of diabetic neuropathy]

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.