Shilpashree Y. D1, Devaki R. N2
INTRODUCTION: Oxidative stress due to enhanced free-radical generation and/or a decrease in antioxidant defense mechanisms has been implicated in the pathogenesis of diabetic neuropathy. This study was conducted to study the impact of glycemic control on oxidative stress and antioxidant balance in diabetic neuropathy.
METHODS: fifty patients with diabetic neuropathy and fifty age matched healthy controls were included in the study. Glycosylated hemoglobin (HbA1c) was estimated to assess the severity of diabetes and the glycemic control. Serum malondiaaldehyde (MDA) levels were assessed as a marker of lipid peroxidation and hence oxidative stress. Superoxide Dismutase (SOD) levels were assessed for antioxidant status.
RESULTS: Significant positive correlation was found between serum MDA levels and hba1c (r = 0.276, p < 0.0001) in patients with diabetic neuropathy. There was statistically significant reduction in the Glutathione peroxidase levels. Further, SOD levels were inversely correlated with HbA1c (r= -0.603, p<0.0001) levels.
CONCLUSION AND SUMMARY: oxidative stress is greatly increased in patients suffering from diabetic neuropathy and is inversely related to glycemic control. This may be due to depressed antioxidant enzyme levels and may also be responsible for further depletion of antioxidant enzyme GPx. This worsens the oxidative stress and creates a vicious cycle of imbalance of free radical generation and deficit of antioxidant status in these patients which may lead to nervous system damage causing diabetic neuropathy. A good glycemic control is essential for prevention of diabetic neuropathy.
