Objective: Increased QT interval dispersion (QTd) is an electrocardiographic parameter shown to be associated with malignant ventricular arrhythmias and sudden death, and QT dispersion corrected for heart rate (QTc) has emerged as a potentially important predictor of cardiac death. Increased QTd has been detected to be directly related to thyroid-stimulating hormone (TSH) levels in overt hypothyroidism, however not much is known about subclinical hypothyroidism (SH). This study was conducted to investigate the QTc in SH and determine the changes following normalization of TSH levels with L-thyroxine. Subjects and Methods: Fifty-eight women with naive SH due to Hashimoto’s thyroiditis, mean age 39.37 ± 10.43 years, and 54 age-, sex- and weight-matched controls with normal TSH were included after exclusion of any factor that might interfere with cardiac conductibility. Electrocardiographic measurements were performed with a magnifier and Bazett’s formula was used to calculate QTc. The patients were separated into two groups regarding basal TSH levels (subgroup A: 5 > TSH > 10 mIU/l, n = 36; subgroup B: TSH > 10 mIU/l, n = 22). L-Thyroxine 1–2 µg/kg/day was administered to subgroup B. Results: Mean QTc interval of the study group was significantly longer than that of the control group (100 ± 30 vs. 76 ± 30 ms, p = 0.000). It was also longer in subgroup A (5 > TSH > 10 mIU/l, n = 36) and subgroup B (p = 0.001, p = 0.000, respectively). In subgroup B, following normalization of serum TSH, mean post-treatment QTc measurement was similar to that of the control group (75 ± 40 vs. 76 ± 30 ms, p > 0.05). Conclusion: We detected prolonged QTc among SH cases. Prolongation remained significant for the whole group as well as the two subgroups. The differences in QTc were corrected when TSH levels of >10 mIU/l returned to normal.

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IgG4 levels are evidently increased in patients with GD, and there is a possible relationship between IgG4 and GO. Our results suggest that IgG4 may be helpful in screening GD patients with high risk for GO and may well become a good indicator for the selection of right medication in the future.

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Acute rheumatic fever (ARF) is a systemic inflammatory disease that develops as a consequence of an exaggerated immune response to group A beta-haemolytic streptococci, which causes pharyngitis. Major manifestations of ARF include carditis, arthritis and chorea. Several investigators have attempted to establish a relation between ARF and human leucocyte antigens (HLA). Heterogeneity in various studies has been found, although associations with certain antigens were reported. The aim of this study was to analyse whether HLA-DR alleles play a role in the resistance or susceptibility to streptococci-related disorders including rheumatic heart disease (RHD) as a sequela of ARF and recurrent streptococcal pharyngitis in Turkish patients. The study included 102 patients with RHD, 71 persons with recurrent streptococcal pharyngitis and 130 healthy controls. HLA-DR alleles were typed by using polymerase chain reaction (PCR)-sequence-specific primers. Positive association with HLA-DRB1*07 allele was found for RHD when compared with healthy controls [29.4% vs 13.1%; P < 0.01, P-corrected: P < 0.01, odds ratio (OR) 2.78, 95% confidence interval (CI) 1.43-5.26] and also for recurrent streptococcal pharyngitis (26.8% vs 13.1%; P < 0.05, P-corrected: P < 0.05, OR 2.44, 95% CI 1.17-3.56). The frequency of HLA-DRB1*11 allele was decreased in patients with RHD (23.5% vs 42.3%; P < 0.01, P-corrected: P < 0.01, OR 0.42, 95% CI 0.24-0.75). Data suggest that HLA-DRB1*07 allele may be a genetic factor in increasing the susceptibility to develop RHD and recurrent streptococcal pharyngitis. HLA-DRB1*11 allele seems to be a protective factor against RHD.