Abstract
Background: Diabetic peripheral neuropathy (DPN) is one of the major chronic complications of diabetes and leading high-risk factor of foot ulcers/amputations. Its early detection/management is therefore of primary importance. About 60-70% of diabetic patients will eventually develop DPN. The cause of diabetic neuropathy is multifactorial, including poor diabetes control, diabetes duration, metabolic/vascular factors, etc. Vitamin D (VitD) deficiency is a common global public health problem. VitD deficiency contributes significantly to pathogenesis of both types of diabetes by impairing insulin secretion and increasing insulin resistance. Aim: Our aim was to assess correlation between serum levels of 25(OH) VitD and DPN in Georgian patients with type 2 diabetes mellitus (T2DM). Method: Patients supervised and treated at our Center were selected; 80 T2DM patients (35 males and 45 females) with previously diagnosed DPN and VitD deficiency were enrolled in this study and comprised the Study Group/SG; their mean age was 45±5 yrs and diabetes duration varied from 5 to 10 yrs. Age and diabetes duration match 50 patients (22 males and 33 females ), without previously diagnosed DPN and normal VitD level were used as controls (CG). HbA1c in SG was 8.3±1.5% and in CG – 7.4±1.4%. Neurological tests and examinations with Sudoscan (a non–invasive method for the assessment of the small fiber function, Impeto Medical, France) were performed in all the patients. In the SG results of all neurological tests (monofilament test, tip-term/temperature test, vibration test) were positive, Sudoscan examination revealed presence of small fiber neuropathy in these patients. In CG patients all neurological tests were performed and all, except Sudoscan, were negative; while Sudoscan revealed presence of small fiber neuropathy in this group as well. Vitamin D was measured in both groups. Results: Comparison of the data obtained for the SG and CG showed that VitD concentration was significantly lower in T2DM patients with DPN (both large and small fiber), than in patients with only small fiber DPN and normal VitD levels. In 76 out of 80 SG patients the levels of 25(OH) VitD were low (<20 ng/ml); while in 44 out of 50 patients in the CG they were within the normal range (30-50 ng/ml). Discussion: This study showed that VitD deficiency is present in Georgian patients with DPN; it may play significant role in development of DPN; normalization and control of VitD level may prevent progression of the peripheral nerve damage. Thus, it is relevant to regularly check VitD levels and maintain them within the normal range. Observations will continue.
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