Abstract
Aims: The present study was undertaken to explore the relationship of plasma homocysteine in the pathogenesis of neuropathy in diabetic patients.Subjects and Methods: Forty two type 2 diabetic patients [22 with neuropathy (DN group) and 20 without neuropathy (DNN group)], age range between 35-70 years had relatively controlled glycemia and duration of diabetes 7-15 years, were studied. Motor and sensory nerve conduction velocities and action potential amplitudes of peripheral nerves were determined by following standard protocol. HbA1c was estimated by modified HPLC (BIO-RAD Variant, USA). Serum C-peptide was measured by enzyme linked immunosorbentassay (ELISA), plasma total homocysteine by Fluorescent Polarization Immunoassay (FPIA). Results: Age, BMI and blood pressure of the study subjects were. Duration of diabetes between DN and DNN groups was comparable. DN group had significantly higher fasting glucose levels (9.8±3.8, mmol/l) compared to the DNN group (6.9±1.8, p=0.004). This trend was also reflected in the HbA1c level: 8.7± 2.1 vs 7.2±1.6 in DN group and DNN group respectively (p=0.009). The two diabetic groups had relatively higher absolute C-peptide level compared to the controls (p=ns). DN and DNN groups had significantly higher plasma homocysteine level compared to the Controls. But between the two diabetic groups no significant difference was observed. Ulnar and peroneal motor nerve conduction velocities and compound muscle action potentials in the diabetic neuropathy group significantly lower compared to diabetic counterpart and the controls. Ulnar and sural sensory nerve conduction velocities and action potentials were significantly lower in the diabetic neuropathy group compared to the diabetic counterpart and the controls. Plasma homocysteine did not show any correlation with nerve conduction velocities and action potential amplitudes.Conclusions: The data concluded that (i) Diabetic neuropathy may not be related to hyperhomocysteinemia in type 2 diabetic patients of Bangladeshi origin; (ii) Hyperglycemia, even at milder level, is related to neuronal dysfunction in these subjects; and (ii) Hyperinsulinemia don't seem to be prerequisite for neuropathy in these subjects. DOI: http://dx.doi.org/10.3329/bjms.v11i4.12607 Bangladesh Journal of Medical Science Vol. 11 No. 04 Oct12
Highlights
Diabetes mellitus is an increasingly prevalent disorder all over the world 1
Fasting glucose was significantly higher in the DN group compared to the DNN group (9.7 3.8 vs 7.1 1.8, p=0.006)
Diabetic neuropathy group had significantly higher HbA1c level compared to the nondiabetic counterpart (p=0.009) (Table)
Summary
Diabetes mellitus is an increasingly prevalent disorder all over the world 1. Of the two major diabetic classes type 2 diabetes mellitus is linked with more aggressive complications. Most common chronic complications of T2DM include retinopathy, nephropathy, neuropathy, acute myocardial infarction and peripheral vascular disease. Diabetic peripheral neuropathy (DPN) found to occur in up to. 50% of diabetic patients and causes sensory-motor and/or autonomic dysfunction 2. Several pathogenic mechanisms have been suggested to contribute the pathogenesis and severity of diabetic peripheral neuropathy which include microangiopathy, oxidative stress, polyol flux, insulin deficiency, glycemic control and advanced glycation end products .3-5. The course and severity of DPN found to be further affected by a wide range of comorbid conditions Several pathogenic mechanisms have been suggested to contribute the pathogenesis and severity of diabetic peripheral neuropathy which include microangiopathy, oxidative stress, polyol flux, insulin deficiency, glycemic control and advanced glycation end products .3-5 The course and severity of DPN found to be further affected by a wide range of comorbid conditions
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