Asymmetric dimethylarginine is not a good predictor of ischemia using myocardial perfusion scintigraphy.

BACKGROUND/AIM: Asymmetric dimethylarginine (ADMA) plays role in the pathogenesis of coronary artery disease and related mortality and morbidity through a number of mechanisms. We hypothesized that plasma ADMA levels would be increased in the presence of reversible ischemia as measured by GATED single photon emission computed tomography (SPECT) myocardial perfusion scintigraphy (MPS). MATERIALS AND METHODS: Fasting i.v. blood samples were drawn before testing. All patients underwent 99mTc-sestamibi GATED SPECT MPS with a one-day stress-rest protocol; the images were visually analyzed. Post-stress GATED parameters, including ejection fraction, end systolic and end diastolic volumes, and automatic stress defect scores, were recorded. RESULTS: The plasma ADMA levels were higher in the ischemic group than in the non-ischemic group (0.46 ± 0.19 vs. 0.40 ± 0.15; P = 0.016). Plasma ADMA levels (odds ratio [OR] = 13.5; 95% confidence interval [CI] = 1.7-109.01; P = 0.015) and sex (OR = 2.49, 95% CI = 1.18-5.26; P = 0.017) were independent predictors of ischemia. There was no linear correlation between plasma ADMA levels and both the GATED SPECT and stress test parameters. CONCLUSION: Our data support the hypothesis that increased baseline ADMA levels are independently related with the presence of reversible ischemia.

Serum visfatin and omentin levels in slow coronary flow.

OBJECTIVE: The adipocytokines visfatin and omentin have a direct effect on inflammation and endothelial injury. The expression of visfatin is closely associated with the expression of proinflammatory cytokines. Omentin has an anti-inflammatory effect and is inversely associated with coronary artery disease (CAD). The slow coronary flow phenomenon is an angiographic finding characterized by delayed distal vessel opacification in the absence of significant epicardial coronary disease. The pathophysiology of SCF has not been clearly identified, although multiple abnormalities including endothelial dysfunction, atherothrombosis and inflammation have been reported. However, the relationship between visfatin, omentin and SCF is still unknown. In this study, we aimed to investigate the relationship of these adipocytokines with SCF. METHODS: The study included slow coronary flow (n=45) and normal coronary flow (n=55) subjects, according to the corrected TIMI frame count, who underwent angiography in the catheterization laboratory of Duzce University. Statistical analyses were performed with SPSS version 12. RESULTS: Visfatin levels were significantly higher in patients with SCF than in controls (p<0.001). Plasma omentin levels were lower in the SCF group than in controls, although without statistical significance. Visfatin, gender and platelet count were significant predictors of SCF in multivariate logistic regression analysis (OR 0.748, 95% CI 0.632-0.886, p=0.01; OR 30.016, 95% CI 4.355-206.8, p=0.01; OR1.028, 95% CI 1.006-1.050, p=0.011, respectively). CONCLUSION: Adipocytokines such as visfatin and omentin may play a role in the pathogenesis of coronary slow flow.

Omentin serum levels and omentin gene Val109Asp polymorphism in patients with psoriasis.

BACKGROUND: Psoriasis is a chronic inflammatory disease of uncertain pathogenesis. Omentin is a new adipokine with anti-inflammatory properties; however, the relationship between psoriasis and omentin has not been fully established yet. OBJECTIVES: This study was designed to evaluate the relationship between psoriasis and omentin serum levels and Val109Asp polymorphism in exon 4 of the omentin gene. METHODS: Forty-nine patients with plaque-type psoriasis and 39 healthy subjects were included in the study. Omentin concentrations were determined by using enzyme-linked immunosorbent assay. Val109Asp polymorphism in exon 4 of the omentin gene was assessed by the polymerase chain reaction-restriction fragment length polymorphism method. Genotypes were determined according to the bands formed in agarose electrophoresis gels. In the statistical analysis, the level of significance was set at P < 0.05. RESULTS: The serum omentin levels of the patients with psoriasis (354.2 ± 152.0) were found to be significantly lower than those in the control group (488.7 ± 190.3) (P = 0.001). A moderate level negative correlation was determined between serum omentin level and body mass index and waist circumference. No significant differences were observed between the patient and control groups in terms of the genotype and allele frequency of Val109Asp polymorphism in exon 4 of the omentin gene (P > 0.05). CONCLUSIONS: Omentin serum levels were determined to be low in patients with psoriasis. No significant difference was found regarding Val109Asp polymorphism of the omentin gene. To the best of our knowledge, our study is the first clinical study to examine the relationship between psoriasis and omentin in terms of serum and genomic levels.

Does MBL2 codon 54 polymorphism play a role in the pathogenesis of psoriasis?

BACKGROUND: Psoriasis is a T cell-mediated immune disease in which various cytokines, primarily tumor necrosis factor-α (TNF-α), are complexly involved. Mannose-binding lectin (MBL) gene polymorphisms decrease MBL serum levels, thereby increasing the synthesis of proinflammatory cytokines such as TNF-α. OBJECTIVES: This trial was designed to evaluate the role of the MBL2 codon 54 polymorphism in the pathogenesis of psoriasis. METHODS: Fifty patients diagnosed with psoriasis vulgaris and 53 healthy subjects were included in the trial. The polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method was applied to determine the MBL2 codon 54 polymorphism. Genotypes were determined according to the bands formed in agarose electrophoresis gels. For the statistical analysis, the level of significance was set at P < 0.05. RESULTS: A total of 33 (66.0%) of the 50 psoriasis patients were detected to have A/A genotype and 17 (34.0%) had B/B genotype. Of the control subjects, 44 (83.0%) had A/A genotype and nine (17.0%) had B/B genotype. There was a statistically significant difference between the groups (P = 0.047). The analysis of allele frequencies revealed A allele prevalences to be 79 (79.0%) and 95 (89.6%), and B allele prevalences to be 21 (21.0%) and 11 (10.4%), in the patient and control groups, respectively. A statistically significant difference between allele frequencies was detected (P = 0.031). CONCLUSIONS: This study suggests that the MBL2 codon 54 polymorphism may have an association with psoriasis in the Turkish population.

Resistin predicts ischemia in myocardial perfusion scintigraphy.

UNLABELLED: Aim: Resistin plays a role in the pathogenesis of coronary artery disease and is related to mortality and morbidity through a number of mechanisms. We hypothesize that plasma resistin levels are increased in the presence of ischemia, as measured by GATED single- photon emission computed tomography myocardial perfusion scintigraphy (SPECT MPS), in comparison with nonischemic subjects. MATERIALS AND METHODS: Fasting intravenous blood samples of patients were drawn before a stress test. An ELISA kit was used for the assays. All patients underwent a technetium 99m-sestamibi GATED SPECT MPS study with a 1-day stress-rest protocol. Images were analyzed visually and patients were assessed as ischemic or nonischemic. Resistin levels were presented as medians (25th-75th percentiles) and were compared using the Mann-Whitney U test. RESULTS: Plasma resistin levels were higher in the ischemic group (n = 47) than in the nonischemic group (n = 67) [9.04 pmol/L (6.27-11.8 µmol/L) vs. 3.56 µmol/L (0.39-7.93 pnol/L), respectively; P < 0.001). We showed that plasma resistin levels (OR = 1.26, 95% CI: 1.13-1.41; P < 0.001) and METs (OR = 0.82, 95% CI: 0.70-0.92; P = 0.021) were independent predictors ofischemia. No linear correlation was found between plasma resistin levels and GATED SPECT or stress test parameters. CONCLUSION: Increased baseline resistin levels are independently related to presence of ischemia but are not related to the extent or severity of ischemia, or other functional parameters such as poststress ejection fraction, end systolic, and end diastolic volumes.

Association of vitamin B12 with obesity, overweight, insulin resistance and metabolic syndrome, and body fat composition; primary care-based study.

AIM: To investigate correlation of vitamin B12 with obesity insulin resistance, metabolic syndrome. METHODS: The cross-sectional and primary care-based study was carried out. Anthropometric, blood pressure measurements and bioelectric impedance analysis (BIA) were recorded. Vitamin B12, folic acid, hemogram, insulin, ferritin, iron, total iron binding capacity and other biochemical tests were assayed. The subjects were grouped as obesity, overweight, control, metabolic syndrome (MetS) and insulin resistance (IR). Correlation of vitamin B12 with body mass index (BMI), IR, age, and BIA was evaluated. RESULTS: The study enrolled 976 patients (obesity: 414, overweight: 212, and control: 351). The mean age in groups of obesity, overweight and control were 35.9 ± 8.7, 28.9 ± 6.3 and 33.1 ± 8.7, respectively (p = 0.142). Vitamin B12 level was significantly lower in patients with obesity and overweight than healthy individuals (178.9 ± 25.2; 219.8 ± 78.5, and 328.5 ± 120.5, p less than 0.001, respectively). Vitamin B12 level was lower in patients with MetS (+/-) and IR (+/-), but insignificant (p = 0.075 and 0.058, respectively). Significant and negative correlation was observed between vitamin B12 and BMI (r =-0.221, p=0.001). No significant difference was observed between obese male and female patients (247.8 ± 89.1 versus 235.5 ± 89.3 pg/mL, respectively, p=0.090). CONCLUSION: Low Vitamin B12 level was associated with obesity and overweight, but not with insulin resistance, metabolic syndrome and gender. Vitamin B12 was negatively correlated only with body mass index.

Normal range of mean platelet volume in healthy subjects: Insight from a large epidemiologic study.

AIM: Mean platelet volume (MPV) in the healthy population has not been studied before. Therefore, the aim of the study was to measure MPV in normal subjects in a large cohort of Turkish adults. METHODS: A total of 2298 subjects with a mean age of 50 (age range 18 to 92) were interviewed. Subjects who had smoking habit, diabetes, hypertension, coronary artery disease, dyslipidemia, chronic obstructive pulmonary disease, cancer, chronic use of any drugs including antiplatelets, heavy drinkers, metabolic syndrome, ejection fraction <55%, creatinine >1.4 in men and >1.1 in women, abnormal liver function tests and an abnormal TSH were excluded in a in a stepwise manner. Complete blood counts were done on the same day within 6 hours by a CELL-DYN 3700 SL analyzer (Abbott Diagnostics). RESULTS: Three hundred twenty-six participants (204 females (63%) and 122 males (37%) with a mean age of 41 ± 16) constituted the final healthy cohort. Mean MPV of the cohort was 8.9 ± 1.4 fL. There was no significant difference among age groups regarding MPV. CONCLUSION: Ninety-five percent of the individuals had a MPV between 7.2 and 11.7 fL. A patient having a MPV beyond this range should be evaluated carefully especially for occlusive arterial diseases.