ABSTRACT
INTRODUCTION: Many studies support the role of vitamin D in the pathogenesis of both types of diabetes. Pancreatic tissues express the vitamin D receptor (VDR) and vitamin D-binding protein; some allelic variations in genes involved in vitamin D metabolism and VDR are associated with glucose intolerance, defective insulin secretion, and sensitivity. Epidemiological links have been established between type 2 diabetes mellitus (DM) and hepatitis C virus (HCV) infection. AIM: To explore the possible therapeutic potential of pharmacologic doses of 1-α-hydroxy vitamin D therapy in improving pancreatic ß-cell function in HCV seropositive hemodialysis (HD) patients. PATIENTS AND METHODS: Twenty HCV seropositive HD patients and 20 HCV seronegative patients as control group were randomly selected from HD units. 1-α-Hydroxy vitamin D therapy was administrated in the dose ranged from 0.25 to 0.5 µg/day for 3 months. Corrected total serum calcium, phosphorus, intact parathyroid hormone (iPTH), 25-hydroxy vitamin D [25(OH) vitamin D], 1,25-dihydroxy vitamin D, and glucoparameters [fasting blood glucose, glycohemoglobin test (HbA1c%), homeostatic model assessment (HOMA)-insulin resistance, and HOMA-ß-cell function% (B%)] were measured under basal conditions and after 3 months of therapy. RESULTS: There was highly significant improvement in the concentrations of fetal bovine serum (FBS), serum insulin, HbA1c%, 25(OH) vitamin D, and HOMA-ß-cell function in HCV seropositive and HCV seronegative groups after oral 1-alphacalcidiol therapy (p < 0.001). Positive correlation exists between the percentage increase in serum insulin and that in HOMA-ß-cell function versus 25(OH) vitamin D (p < 0.021 and p < 0.027, respectively) in HCV negative group. CONCLUSION: 1-α-Hydroxy vitamin D oral therapy may improve glycemic control in HCV seropositive and HCV seronegative HD patients.
