Objective: We have aimed to study the relation between Hashimoto's thyroiditis (HT) and thyroid autoantibodies and oxidative stress parameters in euthyroid, subclinical and overt hypothyroid stages. Design and methods: A total of 124 patients were included in the study; 93 of whom were newly diagnosed with HT (31 patients in each of the euthyroid, subclinical hypothyroid and overt hypothyroid subgroups), aged over 18 and had not received any prior treatment and 31 of whom were healthy volunteers. Results: Total oxidant status (TOS) and oxidative stress index (OSI) levels were higher, and total antioxidant status (TAS) and total thiol and arylesterase levels were lower in the overt hypothyroid group compared to other groups. TOS and OSI levels increased, and TAS levels decreased significantly in each phase from euthyroid, subclinical hypothyroid, to overt hypothyroid subgroups among HT patients. There was a negative correlation between TAS, log (paraoxonase1) and paraoxonase1/HDL and anti-thyroid peroxidase and a negative correlation between anti-thyroglobulin and total thiol. It was also determined that overt hypothroidism was an individual predictor that effects all of the oxidative stress parameters, but not total thiol, levels. Conclusion: Our results suggest that oxidative stress increases continuously during the development of subclinical hypothyroidism and overt hypothyroidism in patients with HT. To determine whether this is a cause or result, randomized, controlled trials that study the effect of antioxidant treatment on the development of overt hypothyroidism and its consequences, e.g., increase in total cholesterol levels, may be performed in euthyroid and/or subclinical hypothyroid patients with HT.

In this study, we aimed to examine dynamic thiol/disulfide homeostasis in type 1 diabetes mellitus (T1DM) and identify the factors associated with thiol oxidation. Thirty-eight subjects (18 male, 20 female) diagnosed with T1DM and 38 (17 male, 21 female) healthy volunteers without any known diseases were included in the study. Thiol/disulfide homeostasis concentrations were measured by a newly developed method (Erel & Neselioglu) in this study. After native thiol, total thiol and disulfide levels were determined; measures such as disulfide/native thiol, disulfide/total thiol, and native thiol/total thiol were calculated. In T1DM patients, compared to the control group, disulfide (p = 0.024), disulfide/native thiol (p < 0.001), and disulfide/total thiol (p < 0.001) were determined higher, while native thiol (p = 0.004) and total thiol (p < 0.001) levels were much lower. In the patient group, a positive correlation was determined between c-reactive protein (r = 325, p = 0.007; r = 316, p = 0.010, respectively), fasting blood glucose (r = 279, p = 0.018; r = 251, p = 0.035, respectively), and glycosylated hemoglobin (r = 341, p = 0.004; r = 332, p = 0.005, respectively) and rates of disulfide/native thiol and disulfide/total thiol. We determined that thiol oxidation increase in T1DM patients compared to the control group. We thought that hyperglycemia and chronic inflammation might be the major cause of increase in oxide thiol form. In order to determine the relationship between the status of autoimmunity and dynamic thiol/disulfide in T1DM, dynamic thiol/disulfide homeostasis in newly diagnosed-antibody positive-T1DM patients is required to be investigated.

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This study aimed to examine the relationship between the ratio of monocyte frequency to high-density lipoprotein (HDL) cholesterol level (the monocyte/HDL ratio (MHR)) and asymptomatic organ damage (AOD) in primary hypertension (PHT). A total of 366 participants were enrolled in the study, including 275 cases currently being followed up after a diagnosis of PHT in our clinic and 91 healthy volunteers. The MHR was higher in patients with PHT than in individuals in the control group. In the PHT group, the MHR was higher in patients with AOD (AOD+) than in patients without AOD (AOD-). In the correlation analyses performed in the PHT group, there were positive correlations between the MHR and the following AOD indicators: carotid intima media thickness, left ventricular mass index, urinary protein levels and urinary albumin levels. In a multivariate linear regression analysis, the MHR was found to be an independent risk factor associated with these indicators of AOD. In conclusion, our study shows that MHR is associated with AOD in patients with PHT.