Prevalence of Dio2 T92A polymorphism and its association with thyroid autoimmunity

The 3, 5, 3′-L-triiodothyronine (T3) partly derives by the deiodination of the prohormone 3, 5, 3′, 5′-L-tetraiodothyronine (T4) by the type 2 iodothyronine deiodinase (D2). The single-nucleotide polymorphism in the D2 gene at position 92 (Dio2 T92A ), generates an enzyme with a reduced T4 to T3 conversion velocity. Because thyroid hormones can modulate the immune response, we hypothesized a pathophysiological role for Dio2 T92A polymorphism in autoimmunity. The objective of this study was to investigate the Dio2 T92A polymorphism in relation to thyroid autoimmunity (TA). We compared the prevalence of Dio2 T92A polymorphism and serum thyroid hormone levels in healthy subjects and subjects with TA. A total of 110 subjects with TA and 106 controls were genotypized for Dio2 T92A polymorphism. Free T3 (FT3), free T4 (FT4) and TSH were measured and compared with the Dio2 T92A polymorphism. Dio2 92T/A , Dio2 92A/A , and Dio2 92T/T healthy subjects were 40.9%, 46.4%, and 12.7%, respectively. These prevalences were similar to those of some European countries whilst significantly different from that of Brazil. In the two groups of healthy subjects and TA subjects, Dio2 T92A polymorphism had a similar distribution with nonsignificant differences. Similarly, no significant differences were observed in the serum concentration of FT3, FT4, and TSH between subjects with different Dio2 T92A polymorphism. The FT4/FT3, and TSH/FT3 ratios were higher in Dio2 92T/T than in Dio2 92T/A and Dio2 92A/A subjects in both TA and healthy groups, but these differences were not significant. In conclusion, the distribution of Dio2 T92A polymorphism may reflect geographical and ethnic differences, and it is not associated with TA.