Hashimoto Tiroiditinde Selenyum ve Selenoprotein Düzeyleri ile Oksidatif Stres Biyogöstergelerinin Değerlendirilmesi
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Hashimoto's thyroiditis (HT) is an autoimmune disease of thyroid gland. In the course of the disease, thyroid gland is attacked by a variety of cell- and antibody-mediated immune processes. It is reported that high iodine intake, selenium (Se) deficiency, smoking, infectious diseases, environmental triggers and some drugs may contribute the development of autoimmune thyroiditis. It is considered that oxidative events may increase in immune diseases like HT, and thyroid gland could not give an adequate response against oxidative stress depending on alterations in the antioxidant defense system. Se has a critical role in antioxidant defense system, thyroid hormone metabolism and regulation, and immune processes. Se deficiency may contribute oxidative stress and infectious diseases. It is considered that oxidative stress may increase with the contribution of Se deficiency in autoimmune diseases like HT. The objective of this study was to evaluate the parameters of thyroid hormones and oxidant/antioxidant status including selenium and selenoproteins in the children newly diagnosed by HT. The study group was composed of 29 patients with HT admitted to Keçiören Training and Research Hospital Pediatric Endocrinology Department (age=8-16 years). Concentrations of thyroid hormones and antibodies (serum thyroid stimulating hormone, TSH; free thyroxin, sT4; free triiodothyronine, sT3 and thyroperoxidase antibodies, anti-TPO), urinary iodine levels, erythrocyte antioxidant enzyme activities (glutathione peroxidase 1, GPx1; catalase, CAT, superoxide dismutase, SOD); plasma GPx3 activities and selenoprotein P (SePP) levels, erthyrocyte total glutathione (GSH), plasma malondialdehyde (MDA) and serum zinc (Zn) concentrations were determined. The results were compared with those of a healthy control group (n=29) who were matched for age and gender with HT group. The children in the study groups had no chronic, endocrine or genetic disease and were not taking any regular medication or supplementation. Iodine deficiency (mild or moderate) was observed in 62 % of HT children. Significant elevations in TSH and anti-TPO concentrations and significant decreases in sT3 levels were determined in HT group compared to control and a significant correlation was found between urinary iodine and anti-TPO levels. The activities of SOD (24 %) and GPx1 (45,5 %) were decreased significantly in patient group. GPx3 activities of HT patients were found to be higher significantly (15,6 %). Total GSH concentrations decreased in HT group compared to control (23,6 %), but the differences were not significant. Significant correlations between GSH and GPx3, sT3 and TSH were also observed. However, we did not observe any significant differences in MDA levels and CAT activities between HT and control groups (p>0.05). Our results suggest an imbalance between oxidant and antioxidant status and the presence of oxidative stress and overall findings indicate the importance of antioxidant defense system including selenoenzymes in HT. However, future studies are needed to determine whether elevated oxidative stress is the result or the cause of chronic inflammation and autoimmunity observed in HT.