Vitamin-D Receptor (VDR) Gene Polymorphisms (TaqI, FokI) in Turkish Patients with Hashimoto's Thyroiditis: Relationship to the Levels of Vit-D and Cytokines.

Abstract

Hashimoto's thyroiditis (HT) is a common autoimmune disease. Vitamin D is an important regulator of immune system. It has been shown in several studies that vitamin D prevents the development of lots of autoimmune diseases. There are some studies that prove vitamin D receptor (VDR) gene polymorphism increases the risk of Hashimoto's thyroiditis. In this study, we aimed to investigate the association between HT and level of 25(OH)D3, IL-2, IL-4, IL-5, TNF-α and IFN-γ and VDR FokI and TaqI gene polymorphism. Moreover, to find out whether low levels of vitamin D affect HT pathogenesis over inflammatory parameters. We performed a case-control study that included 136 cases with HT (49 euthyroid, 49 subclinical hypothyroid, 38 hypothyroid patients) and 50 healthy control. Serum levels of 25(OH)D3, glucose, insulin, parathyroid hormone, calcium, phosphorus, alkaline phosphatase were measured and IL-4, IL-5, TNF-α, IFN-γ analysis were performed with ELISA kits in all 186 subjects. Genetic analysis for VDR FokI and TaqI gene polymorphisms were done by RFLP in all subjects. Mean serum 25(OH)D levels were 14.88±8.23 ng/ml in patient with HT and 15.52±1.34 ng/ml in healthy controls. There were no statically significant differences between the groups in terms of vitamin D levels (P=0.977). Prevalence of vitamin D insufficiency in HT cases was significantly higher than controls (p=0.02). Although serum IL-2, IL-4, TNF-α and IFN-γ were significantly higher in HT patients, there were no significant differences regarding IL-5 levels. Significant differences were observed between the groups regarding the genotype of TaqI but no differences regarding FokI genotype. Vitamin D insufficiency is associated with HT. There is a relationship between VDR TaqI gene polymorphism and HT. Although vitamin D levels are low in both patient and control group, detection of high level of inflammatory parameters in HT group makes us think that low level of vitamin D does not affect HT pathogenesis over these parameters.