SELENIUM STATUS IN LATVIAN PATIENTS WITH AUTOIMMUNE THYROID DISEASES

Introduction. Selenium deficiency, along with genetic predisposition and environmental triggers, may play a role in the pathogenesis of Hashimoto’s thyroiditis (HT) and Graves’ disease (GD). Objective. We aimed to assess selenium status in Latvian patients with newly diagnosed, treatment-naïve GD and HT. Methods. Eleven hyperthyroid GD patients, 40 HT patients (32 euthyroid and 8 hypothyroid), and 21 age- and sex-matched healthy subjects were recruited into this study. Plasma selenium concentration was determined fluorometrically by using fluorescence spectrophotometer. Results. Median plasma selenium levels were 85.03 (60.09–116.60) µg/L for HT patients, 71.33 (59.05–104.42) µg/L for GD patients and 80.35 (67.15–113.67) µg/L for the controls. Selenium concentrations did not differ significantly among the three groups (p=0.763). Likewise, no differences were observed in selenium levels between euthyroid and hypothyroid HT patients (85.03 (60.09–116.56) and 94.78 (47.46–117.02) µg/L, respectively; p=0.886). We found a significantly lower selenium concentrations in HT patients with higher TPOAb levels (≥400 IU/mL) in comparison to patients with lower antibody titers (<400 IU/mL) (72.75 (52.10–88.43) vs. 89.04 (65.53–117.51) µg/L, respectively; p=0.05). In addition, levels of selenium failed to correlate with other characteristics such as age, titers of TPOAb, TgAb, and TSHRAb, TSH, FT3, FT4 (all p>0.05). Conclusions. Selenium status in Latvian patients with newly diagnosed GD and HT is at suboptimal level, although no difference in selenium levels between autoimmune thyroid disease patients and controls was observed. Interestingly, HT patients with higher TPOAb levels had a lower selenium concentration, suggesting that these patients might benefit from selenium supplementation.