Further comparison of thyroid function in patients with different genotypes showed that the frequency of the G-allele was significantly higher among hypothyroid patients (P < 0·05). Interestingly, among 25 hypothyroid patients NVP-AUY922 chemical structure with both elevated thyroid peroxidase antibody and thyroglobulin antibody concentrations, 14 presented with the AG genotype and 11 with the GG genotype, while no AA genotype was found in this group. Evaluating the independent effect of different genetic and non-genetic factors on thyroid function with multiple regression analysis, we established a strong contribution

of thyroid peroxidase antibodies (P < 0·0002) and an insignificant contribution of thyroglobulin antibodies, CT60 genotype, age, family history and smoking. After elimination of the thyroid autoantibody effect, the contribution of the CT60 genotype reached the level of significance (P < 0·05). This study of patients with two different forms of thyroid

autoimmune disease, HT and PPT, demonstrates a strong contribution of CT60 CTLA-4 SNP to thyroid autoantibody production. The significant increase of thyroid peroxidase antibody concentration and slight increase of thyroglobulin antibody concentration found in patients carrying the polymorphous CT60 CTLA-4 allele is consistent with our previous report on HT patients, where exon 1 and promoter CTLA-4 polymorphisms were studied [6]. Exon 1 SNP has also been shown to influence higher thyroid learn more autoantibody production in Graves’ disease [9]. Nevertheless, no data are available in the literature on association of TCL CT60 SNP with thyroid autoantibody production. Similarly, the data on genetic susceptibility in PPT are scarce in spite of the relatively high prevalence of 8% in the postpartum period [10]. A few earlier reports suggested an association with human leucocyte antigen (HLA) status, which was not confirmed afterwards [11]. The first report referring to the CTLA-4 gene in PPT

was published a decade ago, describing no association between PPT and microsatellite CTLA-4 polymorphism [12]. The second report was our recent case–control study, where we were not able to demonstrate a link between CT60 CTLA-4 SNP and PPT [13]. However, the strong influence of thyroid peroxidase antibodies on development, thyroid function and prognosis of PPT was reported, as patients with higher thyroid peroxidase antibodies in the postpartum period developed PPT more often, presented with hypothyroidism more often and developed permanent hypothyroidism more often [2,11,14,15]. The current study also showed that thyroid peroxidase antibody concentrations were significantly higher in the hypothyroid form of PPT and the frequency of patients positive for thyroid autoantibodies was also significantly higher among hypothyroid patients.