Endocrine Abstracts

Introduction: Hashimoto’s thyroiditis (HT) is caused by a variety of genes, cytokines, receptors, and environmental factors. A series of enzymes known as type 1 and type 2 deiodinases (D1, D2) are in charge of converting thyroxine (T4) into triiodothyronine (T3). It is believed that the low free T3 (fT3) levels caused by D2 polymorphism may result in thyroid autoimmunity through the induction of inflammation. However, iodothyronine deiodinase (DIO) gene polymorphism and HT in conjunction with fT3 levels have not been thoroughly investigated. In this study, we aimed to examine the relationship between HT and DIO polymorphisms (D1 rs11206244, D2 rs225014, and D2 rs12885300) as well as the effect of DIO gene polymorphisms on fT3 and autoantibody levels (anti-thyroid peroxidase, anti-thyroglobulin, thyroid receptor antibody).

Methods: Participants aged 18-65 years are included in this cross-sectional study. Among 183 participants, 87 is diagnosed with HT, and 96 are healthy subjects. We measured autoantibody levels and thyroid ultrasonography to determine the diagnosis of HT. Peripheral blood samples were collected from all participants for genetic analysis and to measure thyroid function tests. All participant’s genomes were analyzed for DIO polymorphisms by PCR-RFLP method. We included only euthyroid HT patients with or without levothyroxine treatment for the evaluation of DIO gene polymorphisms on fT3 levels.

Results: HT patients were found to have D2 rs225014 ‘TC’ and ‘CC’ alleles more frequently (P= 0.025) than in healthy controls. Free T3 levels were shown significantly lower in euthyroid HT patients compared to healthy subjects (P= 0.007). In addition, HT patients with D2 rs225014 ‘TC and CC’ alleles were found to have significantly decreased fT3 levels (P=0.005) compared to the healthy subjects. No association was found in the D1 rs11206244, D2 rs12885300 polymorphisms, HT and fT3 levels. None of the DIO gene polymorphisms was associated with the autoantibody levels.

Conclusions: We demonstrated that the D2 rs225014 ‘TC’ and ‘CC’ alleles were associated with HT. HT patients with D2 rs225014 polymorphism ‘TC and CC’ alleles exhibited lower fT3 levels compared to the healthy subjects. Our findings support D2 rs225014 polymorphism is linked to HT and that fT3 may function as a potential mediating factor in this connection.