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.

Oxidative stress may be an effective risk factor in the development of overt hypothyroidism in HT.

Objective: Although several studies reported increased oxidative stress in Hashimoto's thyroiditis (HT), the effect of levothyroxine treatment on oxidative status is not studied extensively. Therefore, we conducted this study to investigate the effects of levothyroxine replacement on oxidative stress in HT. Design and methods: Thirty-six patients recently diagnosed with HT-related hypothyroidism and 36 healthy controls were included in the study. Levothyroxine replacement was started to patients with hypothyroidism, and had been followed-up for 6 months. Results: Mean basal serum total antioxidant status (TAS), total thiol, arylesterase, and paraoxonase 1 (PON1) levels were significantly lower, and serum total oxidant status (TOS) and oxidative stress index (OSI) were significantly higher in the patients with hypothyroid than the controls. In the hypothyroid group serum TAS, total thiol, arylesterase, and PON1 levels increased and serum TOS and OSI levels decreased significantly after levothyroxine treatment. Pretreatment serum TAS, total thiol, PON1, and arylesterase levels were positively correlated with free levothyroxine (fT 4 ) and negatively correlated with thyroid-stimulating hormone (TSH), antithyroid peroxidase (anti-TPO), and antithyroglobulin (anti-TG) levels. Also, pretreatment serum TOS and OSI levels were negatively correlated with fT 4 levels and positively correlated with TSH, anti-TPO, and anti-TG. We have also found that the fT 4 and anti-TPO levels are independent predictors of the oxidative stress parameters in stepwise multivariable linear regression analysis. Conclusion: This study suggests that levothyroxine replacement decreases oxidant status and increases antioxidant status following the 6 months of levothyroxine replacement in hypothyroidism that develops in accordance with the HT.

Objective. Th e aim of the present study was to determine the irisin levels in patients with the type 1 diabetes mellitus (T1DM) and to examine the relation of irisin levels with the infl ammation and autoimmunity.Methods. Th is study included 35 cases diagnosed with T1DM and 36 healthy volunteers. Antiglutamic acid decarboxylase (anti-GAD), islet cell antibody (ICA), and insulin autoantibody levels were measured in patients at the time when they were included into the study and recorded from the patient fi les. Serum irisin levels were measured by ELISA kit.Results. Th e median irisin levels were determined higher in T1DM group compared to the control one (6.8 ng/ml vs. 4.8 ng/ml, p=0.022; respectively). Median irisin levels were higher in anti-GAD (p=0.022) and ICA (p=0.044) positive groups compared to negative groups. In T1DM group, irisin levels displayed positive correlation with glycosylated hemoglobin (HbA1c) (r=0.377, p<0.001) and anti-GAD (r=0.392, p=0.020) and negative correlation with creatinine (r=-0390, p=0.021). In multivariate regression model, HbA1c (B±SE: 2.76±17683, p<0.001), and anti-GAD (B±SE: 2.311±0.610, p=0.001) were determined as independent predictors for predicting the irisin levels.Conclusion. In patients with T1DM, which chronic infl ammation and autoimmunity take part in their etiopathogenesis, anti-GAD levels were an independent risk factor for the irisin. Th is may suggest that factors such as infl ammation and autoimmunity can be eff ective in the synthesis of irisin.