Abstract

Selenium (Se) supplementation has been used to help prevent the progression of Graves' ophthalmopathy (GO) and autoimmune thyroid diseases (AITD) patients. We investigated Se serum and selenoprotein P (SePP) levels in Graves' disease (GD) with and without GO, Hashimoto's thyroiditis (HT) patients and in 27 control individuals (C). We studied 54 female and 19 male patients: 19 with GD without GO, 21 GD with GO, 14 with HT and 19 with HT+LT4. Se values were measured using graphite furnace atomic absorption spectrophotometry. Serum SePP levels were measured by ELISA. Median Se levels were similar among all groups; GD patients: 54.2 (46.5-61.1 μg/L), GO: 53.6 (43.5-60.0 μg/L), HT: 51.9 (44.6-58.5 μg/L), HT+LT4 54.4 (44-63.4) and C group patients: 56.0 (52.4-61.5 μg/L); P = 0.48. However, serum SePP was lower in GO patients: 0.30 (0.15-1.05 μg/mL) and in HT patients: 0.35 (0.2-1.17 μg/mL) compared to C group patients: 1.00 (0.564.21 μg/mL) as well as to GD patients: 1.19 (0.62-2.5 μg/mL) and HT+LT4 patients: 0.7 (0,25-1.95); P = 0.002. Linear regression analysis showed a significant relationship between SePP and TPOAb values (r = 0.445, R2 = 0.293; P < 0.0001). Multiple regression analysis found no independent variables related to Se or SePP. A serum Se concentration was lower than in some other countries, but not significantly among AITD patients. The low serum SePP levels in GO and HT patients seems to express inflammatory reactions with a subsequent increase in Se-dependent protein consumption remains unclear.

Highlights

  • Selenium (Se) is fundamental to cell metabolism as it is incorporated by a group of important proteins known as selenoproteins, each of which plays a critical role in thyroid metabolism

  • A possible explanation may be the presence of patients with elevated serum thyroid peroxidase antibody (TPOAb) values compared with our patients, which could lead to follicular thyroid cell damage, and increased Se-dependent protein depletion resulting in low Se serum concentrations [31]

  • The serum Se concentrations obtained in Graves’ disease (GD) patients were similar to those reported by Zagrodzki and cols. [32], but lower than values obtained by Pedersen and cols. [12] in newly diagnosed GD patients, which pointed out that inflammatory activity could be responsible for the low serum Se levels

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Summary

Introduction

Selenium (Se) is fundamental to cell metabolism as it is incorporated by a group of important proteins known as selenoproteins, each of which plays a critical role in thyroid metabolism. Se is transported in the circulation mainly by SePP, which is produced in the liver, and is considered the best nutritional biomarker for Se [1,5] SePP has an antioxidant activity [2,7]. It can reduce hydroperoxides, protecting plasma proteins and endothelial cells against oxidative damage [5]. In Se deficiency situations the thyroid gland appears to maintain high concentrations of Se, suggesting that there is a retention mechanism that allows maintaining normal thyroid function at the detriment of other cells and tissues [1,12].

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