The role of oxidative stress and endothelial injury in diabetic neuropathy and neuropathic pain.

OBJECTIVE: The roles of endothelin-1 (ET-1) and oxidative stress causing vascular injury in the pathogenesis of diabetic neuropathy are debatable. The present study was undertaken to clarify the possible effects of oxidative stress and ET-1 in diabetic patients with and without peripheric neuropathy.

METHODS: We studied plasma ET-1, nitric oxide (NO), catalase, glutathione (GSH) levels of fifty (22 females, 28 males) patients with Type 2 diabetes in order to evaluate endothelial dysfunction and oxidative stress. The neuropathy types (motor, sensorial and sensorimotor), comorbid diseases, antidiabetic treatments, smoking, diabetes duration were also considered. Short McGill Pain Questionnaire (SF-MPQ) was also performed for patients with neuropathy.

RESULTS: There were no significant differences between patients with (n=23) and without (n=27) neuropathy with regards to demographic features except diabetic disease duration. The statistical analysis was done considering this difference. Although NO and ET-1 levels were higher, and catalase and GSH levels were decreased in neuropathic patients, no statistical significancy was found. We also couldn't find any correlations between the parameters and SF-MPQ scores.

CONCLUSIONS: Although there were no relationships between neuropathy and the studied parameters, we found lower levels of catalase and GSH as intracelluler antioxidants and higher NO and ET-1 as markers of endothelial injury in patients with neuropathy. Our data suggest that there is a need of further studies with larger study groups in order to clear out the role of endothelial injury and oxidative status in the pathogenesis of diabetic neuropathy.

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