Decreased Thyroid Peroxidase Antibody Titer in Response to Selenium Supplementation in Autoimmune Thyroiditis and the Influence of a SEPP Gene Polymorphism: A Prospective, Multicenter study in China.
Nyckelord
Abstrakt
Background Recent intervention studies have suggested selenium(Se) as an effective treatment in autoimmune thyroiditis (AIT). However, the exact mechanism is still unclear. The aim of the present study was to explore the effect of Se on thyroid peroxidase antibody (TPOAb) titers in patients with AIT and to analyze a potential impact of the genetic background on the effect of Se supplementation Methods Randomized, placebo-controlled, double-blind trial. 364 patients with elevated TPOAb (>300 IU/mL) were recruited and randomized to receive Se yeast 200 μg/day supplementation or placebo. Urinary iodine concentration (UIC), serum thyroid-stimulating hormone (TSH), free thyroxine (FT4), TPOAb, Se, malondialdehyde (MDA), and serum glutathione peroxidase (GPX3) activity were measured at baseline and follow-up. 96 patients were genotyped for SNP r25191g/a. Results The median UIC was 182 μg/L. Serum Se increased significantly (p<0.001) after Se treatment. TPOAb titer decreased by 10.0% at 3 months and by 10.7% at 6 months after se supplementation while there was a moderate increase in TPOAb titer over the follow-up period in patients receiving placebo. GPX3 activity significantly increased (p<0.001), and MDA significantly decreased (p<0.001) after 6 months of Se supplementation. TPOAb titer decreased to different extents in patients with different genotypes of SNP r25191g/a after Se supplementation. Serum TPOAb titer in patients with the AA genotype had a more significant decrease (by 46.2%) than those with the GA and GG genotypes (by 14.5 and 9.8% respectively) at 3 months of Se supplementation (P=0.070). Conclusions Se supplementation significantly reduced TPOAb titer in patients with AIT, and there may be an important genetic component influencing interindividual differences in the decrease in TPOAb titer.