[Diabetic neuropathy: clinical and experimental progress in its pathogenesis and treatment]

Diabetic symmetrical polyneuropathy have been known to arise from metabolic alteration such as accelerated polyol pathway and/or from neurovascular deficit. Recently, two other hypotheses were confirmed. Decreased neurotrophic supports were reported in diabetic neuropathy. Subcutaneous injection of recombinant human nerve growth factor ameliorated sensory symptoms and cooling detection threshold. The most common adverse effect was injection site hyperalagesia. Brain-derived neurotrophic factor, neurotrophin-3 and insulin-like growth factors are under clinical trials. The excessive oxidative stresses are also associated with diabetic neuropathy. Increased production and decreased scavenge system of free radicals enhance their cytotoxic effects. Alpha-lipoic acid, gliclazide and troglitazone have been reported to be effective for diabetic neuropathy.