Objective: Vascular endothelial growth factor (VEGF) plays a pivotal role in the pathogenesis of autoimmune chronic inflammatory conditions and papillary thyroid carcinoma (PTC). Design: We hypothesized that, as VEGF expression is increased both in PTC and in lymphocytic thyroiditis (LT), it may stimulate the development of PTC in patients with LT. To evaluate this, we examined both tumor and adjacent non-tumoral tissues of PTC patients with and without LT. Methods: A total of 50 patients with PTC (52.50±7.41 years) and 17 patients with nodular goiter (NG) (50.47±10.38 years) were included in the study. According to the presence of LT, patients with PTC were further divided into two groups. Immunohistochemical analyses of VEGF were conducted in all patients and for PTC patients, both tumor tissue and adjacent non-tumoral tissue were evaluated. Results: The scores for intensity of staining and percentage of labeled thyrocytes for VEGF were found to be significantly higher in the PTC patients than in the NG patients (p<0.001, p<0.001, respectively). The tumor tissue revealed similar scores for PTC patients with LT and without LT. However, the scores in adjacent non-tumoral tissue were higher in PTC patients with LT than in patients without LT (p=0.004, p=0.01, respectively). Conclusions: To the best of our knowledge, our results are the first to demonstrate that the expression of VEGF in adjacent non-tumoral tissue were higher in PTC patients with LT than in those without, which shows a possible role of VEGF expression in the progression of PTC in the presence of LT.

ABSTRACT Background: Obesity and overweight are significant public health problems due to higher risk for coronary artery disease (CAD). It is very important to determine new predictive markers to identify the CAD risk in obese and overweight. To this aim, we analyzed HDL-C subclass and their paraoxonase-1 (PON-1) activity in obese, overweight and normal weight subjects. Method: 71 newly diagnosed obese, 40 overweight and 30 healthy subjects as a control group were enrolled the study. Serum lipids levels were determined with enzymatic colorimetric method. PON-1 activities and HDL-3 levels were determined by spectrophotometric methods. Non-HDL3-C concentrations were calculated with the subtraction of HDL3-C from total HDL-C. Results: The mean serum levels of total HDL-C, HDL3-C, Non-HDL3-C -C and ApoA1 were higher in control group than obese and overweight groups. There were a statistically significant difference between obese and control group in terms of Lp(a), hsCRP and HOMA index. Higher total PON-1, non-HDL3 PON-1 and HDL3 PON-1 activities were found in the control group compared to obese and overweight groups. Total HDL was weakly negative correlated with the HOMA index, BMI and waist circumference. There was a weak negative correlation between non-HDL3-C and waist circumstance. Conclusion: Abnormal HDL-subgroups pattern and decreased PON-1 activities causes increased risk for CVD in obese and overweight individuals. Therefore determination of HDL subgroups and their PON-1 activity improves risk prediction compared with measuring total HDL-C levels and its PON-1 activity alone. Body weight and insulin resistance appear to have a role in the decreased HDL-C levels and PON-1activity in obese.