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Clinical and Developmental Immunology
Volume 2012 (2012), Article ID 340542, 5 pages
http://dx.doi.org/10.1155/2012/340542
Research Article

Thr92Ala Polymorphism of Human Type 2 Deiodinase Gene (hD2) Affects the Development of Graves' Disease, Treatment Efficiency, and Rate of Remission

1Institute of Endocrinology, Almazov Federal Heart, Blood and Endocrinology Centre, 2 Akkuratova Street, Saint-Petersburg 197541, Russia
2Institute of Molecular Biology and Genetics, Almazov Federal Heart, Blood and Endocrinology Centre, 2 Akkuratova Street, Saint-Petersburg 197541, Russia
3Department of Mathematical Modeling, Almazov Federal Heart, Blood and Endocrinology Centre, 2 Akkuratova street, Saint-Petersburg 197541, Russia

Received 14 June 2012; Revised 7 October 2012; Accepted 18 October 2012

Academic Editor: Shervin Assassi

Copyright © 2012 Babenko Alina et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Clinical symptoms vary in thyrotoxicosis, and severity of these depends on many factors. Over the last years, impact of genetic factors upon the development and clinical significance of thyrotoxic symptoms became evident. It is known that a production of T3 in various tissues is limited by deiodinase 2 (D2). Recent studies revealed that certain single nucleotide polymorphisms (including threonine (Thr) to alanine (Ala) replacement in D2 gene codon 92, D2 Thr92Ala) affect T3 levels in tissues and in serum. Individuals with Ala92Ala genotype have lower D2 activity in tissues, compared with that in individuals with other genotypes. In our study, we have assessed an association of D2 Thr92Ala polymorphism with (1) frequency of disease development, (2) severity of clinical symptoms of thyrotoxicosis, and (3) rate of remissions, in Graves' disease patients.