Comparative analysis of HLA II allele and genotype frequency distribution in patients with type 1 diabetes mellitus and autoimmune thyroiditis

Aim.  To compare HLA II allele and genotype frequency distribution in type 1 diabetes mellitus (T1DM) and autoimmune thyroiditis (AIT) with that in isolated T1DM. Materials and Methods. A total of 92 T1DM patients were subdivided into two groups. The first group comprised 54 patients with estab...

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Bibliographic Details
Main Authors: Ekaterina Alexandrovna Repina, Tatiana Mikhailovna Atamanova, Yana Stanislavovna Zvereva, Yulia Vladimirovna Tishina, Sergey Alexandrovich Prokof'ev
Format: Article
Language:English
Published: Endocrinology Research Centre 2013-12-01
Series:Сахарный диабет
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Online Access:https://dia-endojournals.ru/dia/article/viewFile/6268/4150
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Summary:Aim.  To compare HLA II allele and genotype frequency distribution in type 1 diabetes mellitus (T1DM) and autoimmune thyroiditis (AIT) with that in isolated T1DM. Materials and Methods. A total of 92 T1DM patients were subdivided into two groups. The first group comprised 54 patients with established AIT comorbidity or elevation of anti-thyroid autoantibodies (ATA). Patients with isolated T1DM (ATA-negative) formed the second group. HLA-genotyping was performed by multiprimer PCR set for the three following genes: DRB1, DQA1 and DQВ1. Results.  Prevalence of alleles DRB1*01, *03(017), *04, *07, *11 and genotypes 01/03, 01/04, 03/04 tends to be higher among patients with AIT comorbidity. The comorbidity group was also characterized by the trend towards higher prevalence of ?marker/marker? and ?marker/non-marker? combinations favouring the former variant. Conversely, ATA-negative patients exhibited trend for higher prevalence of ?non-marker/non-marker? combination. Conclusion. Statistically insignificant difference between HLA II alleles and genotypes in the two studied groups suggests that primary genetic factors are common in these two diseases. Plausibly, genes other than DRB1, DQA1 and DQВ1 determine the localization of the autoimmune process.
ISSN:2072-0351
2072-0378