ICAM1 K469E and E-selectin S128R polymorphisms could predispose to increased autoantibody production and TSH suppression in Graves' disease.

The etiopathogenesis of Graves' disease (GD) has not been clearly elucidated although the role of chronical inflammation and endothelial dysfunction has been established. Adhesion molecules such as intercellular adhesion molecule 1 (ICAM1), vascular cell adhesion molecule 1 (VCAM1), and E-selectin are secreted from vascular endothelium and promote accumulation of leukocytes in damaged endothelial areas. This study examined the possible association of ICAM1 (G241R and K469E), VCAM1 (T-1591C and T-833C), and E-selectin (S128R) single nucleotide polymorphisms (SNPs) with the occurrence of GD. ICAM1 (G241R and K469E), VCAM1 (T-1591C and T-833C), and E-selectin (S128R) SNPs in DNA from peripheral blood leukocytes of 171 patients with GD and 259 healthy controls were investigated by real-time PCR combined with melting curve analysis using fluorescence-labeled hybridization probes. We did not find significant differences in the distributions of studied polymorphisms, nor in the haplotype frequencies between patients with GD and healthy control. However, the anti-TPO levels in E-selectin 128R allele carrying subjects (SR + RR) were higher than S128S genotype (p < 0.05). In addition, the decline of TSH levels was more prominent in ICAM1 469 E carrying subjects (KE + EE) in comparison with wild homozygotes (p < 0.05). Although there is not association between ICAM1 (G241R and K469E), VCAM1 (T-1591C and T-833C), and E-selectin (S128R) SNPs and susceptibility to GD, higher anti-TPO in E-selectin 128 SR + RR, and lower TSH in ICAM1 469 KE + EE subjects suspect that these genotypes are prone to increased antithyroid autoantibody production with more accentuated TSH suppression in GD. Further studies with a larger cohort, analyzing other polymorphisms in ICAM, VCAM1 and E-selectin genes are necessary to support our observations.

G241R and K469E polymorphisms of intercellular adhesion molecule 1 (ICAM-1) could predispose to Hashimoto thyroiditis.

This study examined firstly the possible association of G241R and K469E single nucleotide polymorphisms (SNPs) of ICAM-1 gene with the occurrence of Hashimoto thyroiditis (HT). G241R and K469E SNPs in DNA from peripheral blood leukocytes of 190 HT and 247 healthy controls were investigated by real-time PCR combined with melting curve analysis using fluorescence-labeled hybridization probes. There was a significant increase of ICAM-1 241R allele frequency in patients with HT compared with healthy controls (P = 0.04, OR = 1.84, 95 % CI = 1.00-3.37). Regarding ICAM-1 K469E polymorphism, patients homozygous for E allele had 1.73-fold increased risk for developing HT according to KK homozygotes (P = 0.04, 95 % CI = 1.00-3.01). The 469E allele frequency was higher in HT patients according to controls, however the difference was at borderline significance (P = 0.05, OR = 1.30, 95 % CI = 1.00-1.70). No associations between polymorphisms and HT phenotypes were observed. We suggest that the G241R and K469E SNPs of ICAM-1 gene may be related to occurrence of HT. However, more studies with larger sample size including other loci of the ICAM-1 gene are necessary to support our findings before any definite statement can be made about the relationship between HT and ICAM-1 polymorphism.

The 8-oxoguanine DNA N-glycosylase 1 (hOGG1) Ser326Cys variant affects the susceptibility to Graves' disease.

Oxidative DNA damage, caused by either endogenous or exogenous sources of reactive oxygen species (ROS), has been linked several diseases including Graves' disease (GD). 7,8-Dihydro-8-oxoguanine (8-oxoG) is a major lesion produced by ROS and is considered a key biomarker of oxidative DNA damage. In humans, 8-oxoG is mainly repaired by 8-oxoguanine DNA N-glycosylase-1 (hOGG1), which is an essential component of the base excision repair (BER) pathway. The functional studies showed that hOGG1 Ser326Cys polymorphism is associated with the reduced DNA repair activity and increased risk for some oxidative stress-related diseases. In this study, we firstly investigated hOGG1 Ser326Cys polymorphism in GD. According to our results, Cys/Cys genotype frequency in the GD patients (23.4%) was significantly higher than the controls (9.2%). Cys/Cys genotype had an 3.5-fold [95% CI (confidence interval): 2.10-6.01, p < 0.001] the Cys allele had 1.83-fold (95% CI: 1.43-2.34, p < 0.001) increase in the risk for developing GD. Our results suggest that Ser326Cys polymorphism of the hOGG1 gene is associated with GD risk.

Lack of association between intercellular adhesion molecule-1 (ICAM-1) polymorphisms and polycystic ovary syndrome.

PURPOSE: This study examined the possible association of G241R and K469E single nucleotide polymorphisms (SNPs) of ICAM-1 gene with the occurrence and clinical/biochemical characteristics of polycystic ovary syndrome (PCOS). METHODS: G241R and K469E SNPs in DNA from peripheral blood leukocytes of 169 PCOS and 259 healthy control women were investigated by real-time PCR combined with melting curve analysis using fluorescence-labeled hybridization probes. RESULTS: We did not find significant differences in the distributions of G241R and K469E polymorphisms, nor in the haplotype frequencies between PCOS and control women. None of the studied polymorphisms were found to affect insulin resistance indices significantly. CONCLUSIONS: These preliminary results suggest that the 241 and 469 SNPs of ICAM-1 gene may not be risk factors for PCOS. Further studies with a larger cohort, analyzing other ICAM-1 polymorphisms are necessary to support our observations before any statement can be made about the relationship between PCOS and ICAM-1 polymorphisms.

Polymorphisms of DNA base-excision repair genes APE/Ref-1 and XRCC1 are not associated with the risk for Graves' disease.

Oxidative stress has been implicated in etiopathogenesis of Graves' disease (GD). Increased lipid peroxidation and oxidative DNA damage have been found in GD patients. Oxidative DNA damage is mainly repaired by the base-excision repair (BER) pathway. Polymorphisms in DNA-repair genes have been associated with the increased risk of various diseases and could also be related to the etiology of GD. Therefore, we conducted a study including 197 patients with GD and age- and sex-matched 303 healthy subjects to examine the role of single-nucleotide polymorphisms of BER genes, APE/Ref-1 (codon 148) and XRCC1 (codons 194 and 399) as a risk factor for GD. These polymorphisms were determined by quantitative real-time PCR and melting curve analysis using LightCycler. No significant association was observed between the variant alleles of APE/Ref-1 codon 148 [odds ratio (OR) = 0.89, 95% confidence interval (CI) = 0.69-1.17], XRCC1 codon 194 (OR = 1.24, 95% CI = 0.79-1.94), and XRCC1 codon 399 (OR = 1.12, 95% CI = 0.86-1.46) and GD. These preliminary results suggest that APE/Ref-1 (codon 148) and XRCC1 (codons 194 and 399) polymorphisms are not significant risk factors for developing GD.

Single nucleotide polymorphisms in base-excision repair genes hOGG1, APE1 and XRCC1 do not alter risk of Alzheimer's disease.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder with a poorly understood etiology. There is considerable evidence that oxidative stress occurs in AD and increased DNA damage has been found in brain tissues and leukocytes of AD patients. Base excision repair (BER) is the major pathway responsible for removing oxidative DNA damage. Polymorphisms in DNA-repair genes have been associated with the increased risk of several age-related disorders including various types of cancer and could also be related to the etiology of AD. We conducted a case-control study including 91 patients with AD and age- and sex-matched 93 control subjects to examine the role of single nucleotide polymorphisms of BER genes, hOGG1 (Ser326Cys), APE1 (Asp148Glu) and XRCC1 (Arg280His and Arg399Gln) as a risk factor for AD. The frequencies of the hOGG1-Ser326Cys, APE1-Asp148Glu and XRCC1-Arg280His and XRCC1-Arg399Gln variant alleles in our control group were 0.23, 0.31, 0.10 and 0.33, respectively. No significant association was observed between the variant alleles of hOGG1-Ser326Cys (OR=1.32, 95% CI=0.83-2.11), APE1-Asp148Glu (OR=1.08, 95% CI=0.70-1.68), XRCC1-Arg280His (OR=0.53, 95% CI=0.24-1.14) and XRCC1-Arg399Gln (OR=1.05, 95% CI=0.68-1.63) and AD. Our results suggest that the polymorphic variants of these BER genes are not independent risk factors for AD.

Blood pressure profile is associated with microalbuminuria and retinopathy in hypertensive nondiabetic patients.

BACKGROUND: Target organ damage is important for global cardiovascular risk assessment. The aim of this study was to explore the association between the blood pressure profile and end-organ damage in a hypertensive non-diabetic cohort. METHODS: A total of 560 consecutive hypertensive nondiabetic patients (mean age: 58.2 ± 13.3 years, 221 men) were included in the study. All patients underwent thorough physical examination including fundoscopic examination. First morning urine samples were obtained from each patient and measurement of the albumin-to-creatinine ratio in first morning urine collection samples was used for diagnosis of microalbuminuria. All patients underwent a 24-h ambulatory blood pressure monitoring and were grouped as dippers and non-dippers according to the presence or absence of >10% decrease in blood pressure during the night, respectively. RESULTS: The non-dipper group consisted of 247 patients with a non-dipper blood pressure profile, 31 patients with reverse dipping and 4 patients with extreme dipping. Non-dipper patients were significantly older. Coronary artery disease, cerebrovascular disease, hypertensive retinopathy and microalbuminuria were significantly more prevalent in the non-dipper patients. Non-dipping hypertension increased the risk of hypertensive retinopathy by 1.89 times (95% confidence interval, CI:1.35-2.65, p < 0.001) and the risk of microalbuminuria by 2.23 times (95% CI:1.49-3.33, p < 0.001). Non-dipping hypertension was still significantly associated with hypertensive retinopathy and microalbuminuria when adjusted by age and sex. CONCLUSION: Non-dipping hypertension was associated with increased risk of hypertensive retinopathy and microalbuminuria. Blood pressure profiles should also be considered in assessing the risk for hypertensive patients.

Polymorphisms in the DNA repair genes XPD (ERCC2) and XPF (ERCC4) are not associated with sporadic late-onset Alzheimer's disease.

Nucleotide excision repair (NER) is the most versatile mechanism of DNA repair, recognizing and dealing a variety of helix-distorting lesions. Xeroderma pigmentosum group D (XPD) and group F (XPF) are essential participants in NER pathway. There is evidence that two common polymorphisms of XPD gene (g.22541C>A; exon 6 and g.35931A>C; Lys>Gln; exon 23) may be associated with differential DNA repair activities. Alzheimer's disease (AD) is characterized by progressive neuronal loss correlated in time with the symptoms of disease considered. Although deficient DNA repair was proposed in the etiology of AD by several researchers, polymorphisms of DNA repair genes have not been studied in AD yet. We conducted a case-control study including 97 patients with AD and age- and sex-matched 101 control subjects to examine the role of genetic polymorphisms of XPD and XPF (g.30028T>C; exon 11) as a risk factor for AD. The frequencies of the XPD/exon 6, XPD/exon 23, and XPF/exon 11 variant alleles in our control group were 0.41, 0.35, and 0.35, respectively. No significant association was observed between the variant alleles of XPD/exon 6 (OR=0.94, 95% CI=0.63-1.41), XPD/exon 23 (OR=1.24, 95% CI=0.82-1.86) and XPF/exon 11 (OR=1.08, 95% CI=0.72-1.64) and AD. Our results suggest that the polymorphic variants of these NER genes do not contribute to the risk of developing AD.

Three dimensional left atrial volume index is correlated with P wave dispersion in elderly patients with sinus rhythm.

BACKGROUND: P wave dispersion is a noninvasive electrocardiographic predictor for atrial fibrillation. The aim of the study was to explore relation between left atrial volume index assessed by 3-dimensional echocardiography and P wave dispersion in elderly patients. METHODS: Seventy-three consecutive patients over the age of 65 (mean age: 75 ± 7 years, 17 men) were included. P wave dispersion is calculated as the difference between maximum and minimum P wave durations. Left atrial volume index was measured by both 2-dimensional and 3-dimensional echocardiography and categorized as normal (≤ 34 mL/m(2)) or increased (mild, 35-41 mL/m(2); moderate, 42-48 mL/m(2); severe, ≥ 49 mL/m(2)). RESULTS: Thirty-one patients had normal left atrium while 24 patients had mildly enlarged, nine had moderately enlarged, and nine had severely enlarged left atrium. Prolongation of P wave dispersion was more prevalent in patients with dilated left atrium. P wave dispersion was significantly correlated with both 2-dimensional (r = 0.600, p < 0.001) and 3-dimensional left atrial volume index (r = 0.688, p < 0.001). Both left atrial volume indexes were associated with prolonged P wave dispersion when adjusted for age, sex, presence of hypertension, and left ventricular mass index. Receiver-operator characteristic (ROC) analysis revealed that a 3-dimensional left atrial volume index ≥ 25 mL/m(2) separated patients with prolonged P wave dispersion with a sensitivity of 82.2 %, specificity of 67.9 %, positive predictive value of 80.4 %, and negative predictive value of 70.4 %. CONCLUSION: In elderly patients, 3-dimensional left atrial volume index showed a better correlation with P wave dispersion and might be helpful in discriminating patients with prolonged P wave dispersion, who might be prone to atrial fibrillation.

Arg25Pro (c.915G>C) polymorphism of transforming growth factor ß1 gene suggests an association with increased risk for Hashimoto's thyroiditis.

BACKGROUND: The etiopathogenesis of Hashimoto's thyroiditis (HT) - has not been clearly elucidated although the role of chronic inflammation, endothelial dysfunction, and imbalance between pro- and anti-inflammatory cytokines has been established. Transforming growth factor ß1 (TGFß1) is required to maintain immune homeostasis, and is implicated in lymphocyte infiltration, production of autoantibodies and thyrocyte destruction seen in patients with HT. AIM: The aim of the present study was to investigate the possible association of Leu10Pro (c.869T>C) and Arg25Pro (c.915G>C) single nucleotide polymorphisms (SNPs) of TGFß1 gene with the occurrence of HT. METHODS: We analyzed the genotype and allele frequencies of polymorphisms at codon 10 and 25 in 178 patients who had been diagnosed as having HT and 197 healthy controls using PCR-restriction fragment length polymorphism (RFLP). RESULTS: There was no notable risk for HT afflicted by Leu10Pro (c.869T>C) polymorphism of TGFß1 gene. However, there was a significant increase of Arg25Pro (c.915G>C) C allele frequency in patients with HT compared with healthy controls (p=0.003, OR=1.87, 95% CI=1.23-2.84). Moreover, heterozygous (CG) subjects had a 2.53-fold increased risk for developing HT with respect to wild (GG) homozygotes (p<0.001, 95% CI=1.57-4.05). TSH levels in CG heterozygous patients were increased in comparison with wild homozygotes (p=0.006). CONCLUSION: This study indicates that the Arg25Pro (c.915G>C) polymorphism of TGFß1 gene may be related to increased risk for HT.

Effects of smoking on healthy young men's hematologic parameters.

OBJECTIVE: Cigarette smoking carries higher risks for most of the chronic diseases. It also has chronic and acute effects on the hematologic system. This study explores the effects of cigarette smoking on some blood values of the healthy young male smokers. METHODS: In this study, cigarette smoking and usage of substance, additional diseases, birth places, and education levels of 171 healthy male subjects between the ages of 20 and 30 years were investigated. Anthropometric measurements of the cases were obtained. Thyroid function tests, vitamin B12, folic acid, ferritin, ferrous/iron, total iron binding capacity, leucocytes, platelets, hemoglobin, hematocrit, mean corpuscular volume (MCV), mean platelet volume (MPV), HBs AG, Anti-HBs and Anti-HIV were evaluated. Groups of smokers and nonsmokers were compared. The group of smokers was also sorted into subgroups of "2 year-smokers", "5 year-smokers" and "10 year-smokers" according to their pack-years of smoking. The effects of pack-years of smoking on the blood values were also investigated. RESULTS: The MCV values of the group of smokers were higher than the values of nonsmokers, which were statistically significant (p<0.05). As a result of the subgroup analyses of smokers, the white blood cell (WBC) counts of the individuals smoking for 5 or more years were significantly higher than those with a history of smoking less than 5 years, (p<0.05). CONCLUSION: This study supports the idea that cigarette smoking and especially longer durations of smoking have adverse effects on the hematologic parameters.

Arg25Pro (c.915G>C) polymorphism of transforming growth factor ß1 gene increases the risk of developing Graves' disease.

BACKGROUND: Graves' disease (GD) arises due to complex interactions between genetic and environmental factors. Transforming growth factor ß1 (TGFß1) is required to maintain immune homeostasis, and is implicated in lymphocyte infiltration, thyroid follicular cell hyperplasia, and production of autoantibody in the thyroid gland of patients with GD. AIM: The aim of the present study was to investigate the possible association of Leu10Pro (c.869T>C) and Arg25Pro (c.915G>C) single nucleotide polymorphisms (SNPs) of TGFß1 gene with the occurrence of GD. METHODS: We analyzed the genotype and allele frequencies of these SNPs in 171 patients with GD and 197 healthy controls using PCR-restriction fragment length polymorphism (RFLP). RESULTS: The distribution of Leu10Pro (c.869T>C) genotype and allele frequencies in the control and GD groups were not significantly different. However, there was a significant increase of Arg25Pro (c.915G>C) C allele frequency in patients with GD compared with healthy controls (p<0.0001, OR=4.77, 95% CI=3.32-7.03). In addition, C allele carrying subjects (CG+CC) had 5.31-fold increased risk for developing GD according to GG homozygotes (p<0.0001, 95% CI=3.43-8.44). No association between polymorphisms and GD phenotypes was observed. CONCLUSION: This study indicates that the Arg25Pro (c.915G>C) polymorphism of TGFß1 gene may be related to occurrence of GD.

The evaluation of endothelin 1 (EDN1) and endothelin receptor type A (EDNRA) gene polymorphisms in Hashimoto's thyroiditis.

PURPOSE: Endothelin1 (EDN1) is well established marker of inflammation. The functions of EDN1 are mediated mainly by endothelin receptors type A (EDNRA). The etiopathogenesis of Hashimoto's thyroiditis (HT) remains still elusive although the role of chronic inflammation and subsequent endothelial dysfunction has been established. This study examined firstly the possible association of EDN1 (G5665Tand T-1370G) and EDNRA (C+70G and G-231A) single nucleotide polymorphisms (SNPs) with the occurrence of HT, and evaluates the relationship between genotypes and clinical/laboratory manifestation of HT. MATERIALS AND METHODS: We analyzed genotype and allele distributions of above mentioned polymorphisms in 163 patients with HT and 181 healthy controls by real-time PCR combined with melting curve analysis. RESULTS: No significant associations between HT and variant alleles of EDN1 5665 and -1370, as well as EDNRA +70 and -231 SNPs were found. Haplotype analysis demonstrated that there was a strong (D'=0.76, r(2)=0.487) and weak (D'=0.403, r(2)=0.086) linkage disequilibrium (LD) between EDN1 -1370 and 5665, and between EDNRA -231 and +70 SNPs, respectively. However, haplotype frequencies in patients were similar to those in controls. In addition, it was observed that the EDNRA +70 G allele had protective effect against early (at age before 40 years) disease onset of HT (OR: 0.51, 95% CI=0.32-0.79, p=0.003). CONCLUSION: Although no significant associations between susceptibility to HT with EDN1 5665 and -1370, as well as with EDNRA+70 and -231 SNPs were found, EDNRA +70 polymorphism was related with decreased risk for early onset HT.

Polymorphisms of endothelin 1 (G5665T and T-1370G) and endothelin receptor type A (C+70G and G-231A) in Graves' disease.

PURPOSE: Endothelin 1 (EDN1) is a strong angiogenic and mitogenic factor, playing a key role in hypervascularization, thyroid follicle cell hyperplasia, and lymphocyte infiltration in the thyroid gland of patients with Graves' disease (GD). EDN1 induces angiogenesis and mitogenesis via endothelin receptor type A (EDNRA). This study examined the possible association of EDN1 (G5665T and T-1370G) and EDNRA (C+70G and G-231A) single nucleotide polymorphisms (SNPs) with the occurrence of GD, and evaluates the relationship between genotypes and clinical/laboratory manifestations of GD. MATERIALS AND METHODS: We analyzed genotype and allele distributions of EDN1 and EDNRA polymorphisms in 165 patients with GD and 181 healthy controls by real-time PCR combined with melting curve analysis. RESULTS: No significant associations between GD and variant alleles of the studied polymorphisms were observed. However, the anti-thyroid peroxidase (anti-TPO) and anti-thyroglobulin (anti-TG) levels in EDN1 G5665T GG genotype were higher than those in T allele carriers (GT+TT) (p=0.001 and p=0.026, respectively). In addition, anti-TPO levels in EDN1 T-1370G wild-type homozygous patients were found to be higher than in mutant gene carrying patients (GT+GG) (p=0.006). The presence of EDNRA+70G allele was associated with 3.37-fold increased risk for development of ophthalmopathy in GD patients (p=0.009). CONCLUSION: Although there were no associations between EDN1 (G5665T and T-1370G) and EDNRA (C+70G and G-231A) SNPs and susceptibility to GD, EDN1 G5665T and T-1370G polymorphisms were related to alterations of autoantibody production and EDNRA C+70G polymorphism is related with increased risk for ophthalmopathy in GD patients.

Metabolic syndrome and glucose tolerance status.

AIM: To determine justifiability of oral glucose tolerance test (OGTT) in non diabetic patients with metabolic syndrome (MetS). METHODS: It was included 398 patients attended to Outpatient Clinics of Sisli Etfal Training and Research Hospital. Eligible patients were assigned as patients with MetS according to International Diabetes Federation (IDF) criteria. RESULTS: After OGTT, there were 7 (2%) diabetic patients, 119 (30%) patients had impaired glucose tolerance (IGT) and 272 (68%) were normal. Height, weight, waist circumference, fasting glycemia, high density cholesterol were not different between IGT and non IGT group. CONCLUSION: OGTT is necessary in MetS non diabetic situation for detection early prediabetic patients.

Relationship between left atrial volume index and cognitive decline in elderly patients with sinus rhythm.

Left atrial (LA) enlargement is a predictor of cardiovascular outcomes such as atrial fibrillation (AF), stroke, and death. The aim of this study was to explore the relationship between LA size and cognitive function in elderly patients without any signs of clinical dementia, AF or previous stroke. We assessed the cognitive status and LA volume (LAV) of 108 consecutive patients (27 males; mean age, 74.8 ± 6.9 years) with sinus rhythm. Cognitive status was assessed by the Mini Mental State Examination (MMSE). Patients with a MMSE score of ≤25 were considered to have cognitive impairment. LAV was measured with two-dimensional echocardiography. LAV index (LAVI) was obtained by indexing LAV to body surface area. Thirty-five patients (32.4%) had cognitive impairment. The patients with cognitive impairment had significantly larger left atria than the patients with normal cognitive function. Receiver operating characteristic analysis revealed a cut-off point of ≥ 34 mL/m(2) for LAVI to predict patients with cognitive impairment (sensitivity, 97.1%; specificity, 52.1%; positive predictive value, 49.3%; negative predictive value, 97.4%). LAVI ≥34 mL/m(2) was significantly associated with cognitive impairment (p = 0.001, odds ratio = 36.91, 95% confidence interval = 4.8-284.2). Logistic regression analysis revealed that LAVI ≥ 34 mL/m(2) and age were independently associated with cognitive impairment. Increased LAVI is associated with cognitive impairment. Assessment of cognitive function may be recommended in elderly patients with enlarged left atria.

Use of knee height for the estimation of stature in elderly Turkish people and their relationship with cardiometabolic risk factors.

The determination of the approximately truest value in height measurement is important in many fields, but it is difficult to perform true measurements, especially in the elderly individuals. We planned to investigate the following items in geriatric Turkish population: to calculate the decrease in height with advancing age by using the standing height measurement and estimated height derived from the knee height; to evaluate the significance of difference between the two measurement methods in the calculation of body mass index (BMI) and waist/height ratio (WHtR); to determine the cut-off value of WHtR according to estimated height in elderly individuals. We studied 551 cases aged between 19 and 97 years. Knee height was measured using a sliding caliper in a sitting position. Linear regression analysis was carried out to derive predictive equations for the estimation of stature with adults (≤ 50 years of age) according to the gender. This equation was then used to estimate height among elderly subjects. Of the cases, 60.3% were <60 years (mean: 48.75 ± 7.50); 39.7% of the cases were >60 years (mean: 69.51 ± 7.12). Estimated BMI (EBMI) measurements in the females and males >60 years were in average 1.23 kg/m(2) and 0.92 kg/m(2) higher than their real BMIs, respectively. EBMI measurements in the females <60 years were 0.32 kg/m(2) higher than their real BMIs (p<0.01). There is a statistically significant difference between WHtR in the females of both age groups, and in the males >60 years, as compared to our estimated WHtR (EWHtR) measurements (p<0.01). The cut-off point of WHtR was 0.61 and 0.58 in the female and male cases of >60 years in our study, respectively. WHtR seemed to be a better anthropometric index that could predict most cardiometabolic risk factors in our study. EWHtR emerged to be a better cardiometabolic risk index especially in the elderly group.

Vascular endothelial growth factor polymorphisms increase the risk of developing Graves' disease.

BACKGROUND: Graves' disease (GD) is a consequence of genetic and environmental factors. Vascular endothelial growth factor (VEGF) is a strong angiogenic and mitogenic factor, which plays a key role in lymphocyte infiltration, and hypervascularization in the thyroid gland of patients with GD. AIM: The aim of this study is to investigate the relationship between GD and A-2578C, T-460C and G+405C single nucleotide polymorphisms (SNPs) of VEGF gene, as well as to evaluate whether there are any relationships between genotypes and some clinical/laboratory parameters of GD. METHODS: We analyzed the genotype and allele distributions of the above mentioned SNPs in 167 patients with established GD diagnosis and 203 healthy controls by real-time PCR combined with melting curve analysis using fluorescence-labeled hybridization probes. RESULTS: The distribution of VEGF A-2578C and T-460C genotypes and allele frequencies in control and GD groups were not significantly different. With regard to the +405 polymorphism, the frequency of C allele was 1.8-fold increased in GD patients compared to controls, and the CC genotype was associated with a 4.6-fold increased disease risk. There was no relationship between some clinical/laboratory parameters with G+405C polymorphism. However, in -2578C allele carrying GD patients the anti-thyroid antibody levels were increased according to wild homozygous. Additionally, -2578C and -460T alleles were related with early (at age before 40) disease onset. CONCLUSION: VEGF +405 polymorphism may be a risk factor for GD, while the -2578 SNP is related with increased autoantibody production.

Oxidative stress parameters in serum and low density lipoproteins of Hashimoto's thyroiditis patients with subclinical and overt hypothyroidism.

BACKGROUND: Although prooxidant and antioxidant status were reported to be changed in clinical and experimental hypothyroidism, obtained results are conflicting. In addition, in subclinical hypothyroidism, scarced and controversial data are available about oxidative stress. Therefore, we aimed to investigate prooxidant-antioxidant status only in Hashimoto's thyroiditis (HT) patients with subclinical (sHT) and overt hypothyroidism (oHT). SUBJECTS AND METHODS: Thirty sHT and 18 oHT patients and 30 healthy control subjects were included in the study. Endogenous and prooxidant 2,2'-azobis-(2-amidinopropane) hydrochloride (AAPH)-induced malondialdehyde (MDA), diene conjugate (DC), protein carbonyl (PC) and nitrotyrosine (NT) levels as well as ferric reducing antioxidant power (FRAP) were determined in serum. In addition, endogenous DC and copper-induced MDA levels were measured in low density lipoprotein (LDL) fraction. RESULTS: Although there were no significant difference in serum endogenous MDA and DC levels, AAPH-induced MDA levels were significantly increased in sHT patients. All these parameters increased in oHT patients. Serum PC levels were detected to be increased in both sHT and oHT patients. Serum FRAP values did not alter in sHT patients, but they lowered in oHT patients. Endogenous DC and copper-induced MDA levels in LDL fraction did not change in sHT patients. However, these parameters were detected to be increased significantly in oHT patients as compared to controls and sHT patients. CONCLUSION: In conclusion, there were significant increases in oxidative stress parameters in serum and LDL-fraction in oHT patients. However, oxidative stress was detected to stimulate partly in serum, but not LDL fraction in sHT patients.