ABSTRACT
This study was done to investigate the role of some risk factors for development of peripheral neuropathy in children and young adolescents with type I diabetes mellitus [type I DM]. Diabetic patients were divided into three groups: Group I included 10 diabetic patients with clinically and electrophysiologically evident peripheral neuropathy. Group II included 20 diabetic patients with subcIinicaI peripheral neuropathy evident only by measuring the motor nerve conduction velocity [MCV], and Group III included 30 diabetic patients with neither clinical nor subclinical peripheral neuropathy. The patients included were 33 females and 27 males, their age ranged from 5-20 years. Ten normal healthy individuals of matched age and sex served as a control group [Group IV]. All the studied groups were subjected to full clinical and neurological examination, measuring [MCV] of the common peroneaI and median nerves, estimation of egcosyIated hemoglobin level [HbA1c], assay of erythrocyte superoxide dismutase [SOD] as well as molecular genetic study of the manganese superoxide dismutase [MnSOD] gene polymorphism. Our results showed a significant increase in HbA1c level and a significant decrease' In SOD level as well as MCV of common peroneaI and median nerves in group I and group II as compared with group III and group IV. There were significant negative correlations between HbA1c when compared with SOD and MCV as well as signiticant positive correlations between SOD levels and MCV in all the diabetic groups. The frequencies of Ala allele and the AIa/Ala genotype of the Mn-SOD gene were significantly lower in neuropathic diabetic patients. In contrast, the Val allele and VaWaI genotype were significantly more frequent in neuropathic diabetic patients than in diabetic subjects without peripheral neuropathy
Conclusion: EIectrophysioIogicaI studies should be done in all type-I diabetic patients regardless their age or duration of the disease for early diagnosis and following the progression of diabetic neuropathy before start of clinical manifestations [subcIinicaI peripheral neuropathy]. Poor glycemic control, low levels of the key antioxidant enzyme SOD, and the Val allele with Ala/ VaI genotype of the Mn-SOD gene Were signiticant risk factors for the development of diabetic neuropathy in type 1 diabetic patients which may necessitate appropriate support for enhancing antioxidant supply to act against the rapid onset and progression of diabetic neuropathy, by reducing the excess of oxygen free radicals [OFR] and peroxide