Calculation of Biological Variation Components and Reference Change Value for Serum Copper and Zinc.

BACKGROUND: Zinc and copper are among the most important trace elements. Deficiencies of these trace elements cause a wide variety of disorders. The present study aims to report the definitive assessment of biological variation (BV) parameters for these elements as within-subject BV (CVI), between subject BV (CVG), index of individuality (II), and reference change value (RCV) in a Turkish cohort study group. METHODS: Ten blood specimens were collected weekly from 20 healthy volunteers (13 women, 7 men) for 10 weeks. Collected sera were stored at -80°C until the time of analysis. Serum zinc and copper levels were analyzed with atomic absorption spectrometry and ANOVA test was used to calculate the variations. RESULTS: The CVI and CVG for zinc were 6.26% and 23.27%, respectively. Analytical variation (CVA) was calculated as 4.24%. II and RCV for zinc were calculated as 0.26 and 21.51%, respectively. The CVI and CVG for copper were 6.05% and 19.64%, respectively. CVA was calculated as 4.24%. II and RCV for copper were calculated as 0.31 and 20.47%, respectively. CONCLUSIONS: Since II values were less than 0.6 for both analytes, the reference values will be of little use. RCV might be preferred for better evaluation instead.

Impact of low- or high-flux haemodialysis and online haemodiafiltration on inflammatory markers and lipid profile in chronic haemodialysis patients.

BACKGROUND/AIMS: We aimed to evaluate the impact of low- or high-flux haemodialysis (HD) and online haemodiafiltration (OL-HDF) on inflammation and the lipid profile in HD patients. METHODS: 50 HD patients were assigned to two groups for HD with low-flux (n = 25) or high-flux (n = 25) polysulphone dialysers for 6 weeks. Subsequently, all patients were haemodialysed with a low-flux polysulphone dialyser for 6 weeks, then transferred to OL-HDF for another 6 weeks. Blood samples for lipids and inflammatory markers (IL-6, IL-8, TNF-α, hs-CRP) were obtained at baseline and every 6 weeks. RESULTS: Changes in inflammatory markers and lipids from baseline to the 6-week dialysis period did not differ between low- and high-flux groups. When patients were transferred from low-flux HD to OL-HDF, IL-6, IL-8, and TNF-α levels significantly decreased whereas HDL and LDL cholesterol significantly increased. CONCLUSION: Low- and high-flux polysulphone membranes had similar effects on lipids and inflammatory markers, whereas OL-HDF potently reduced pro-inflammatory cytokines.

Monocyte heterogeneity in myocardial infarction with and without ST elevation and its association with angiographic findings.

OBJECTIVES: Monocytes and mature macrophages play significant roles after myocardial infarction. Here, our aim is to investigate the monocyte heterogeneity in acute ST elevation myocardial infarction (STEMI) and non-STEMI separately and determine any possible relationships between monocyte heterogeneity and coronary angiographic characteristics. METHODS: Thirty STEMI, 30 non-STEMI, and 25 stable angina pectoris patients were enrolled. Blood samples were taken immediately at admission, and on days 2, 3, 4, 5, and 7 after STEMI or non-STEMI for cytometric analysis to determine monocyte heterogeneity. Peak creatine kinase (CK) and CK-myocardial band (CK-MB) levels were used to determine the severity of myocardial infarction. Coronary angiographic findings, such as the Gensini score, the presence of acute total occlusion, and development of no reflow after stenting, were noted. RESULTS: The peak levels of CD14++CD16- monocytes were higher and were reached later in the STEMI group (631.6±116.7 vs. 539.6±103.0/mm, P=0.003; day 2.73±0.64 vs. 2.27±0.74, P=0.011). Peak CK and CK-MB levels were correlated positively with CD14++CD16- monocytes in the non-STEMI group. The Gensini score was found to be correlated with the peak CD14+CD16+ monocyte levels in the non-STEMI and stable angina pectoris groups. Patients with total occlusion of the culprit artery had significantly higher levels of CD14++CD16- monocytes (642.3±113.2 vs. 532.5±98.2/mm, P<0.001). The peak levels of CD14++CD16- monocytes were higher in patients with no reflow compared with the patients with thrombolysis in myocardial infarction grade 3 flow after percutaneous coronary intervention of the culprit lesion (688.1±104.6 vs. 565.1±111.0, P=0.002). In patients with no reflow, we also found higher peak CD14+CD16+ monocyte levels (82.3±12.1 vs. 71.2±10.6, P=0.02). CONCLUSION: Monocyte heterogeneity differs in STEMI and non-STEMI. Peak levels of CD14++CD16- monocytes were higher and were reached later in the STEMI group compared with the non-STEMI group. More importantly, worse angiographic characteristics related to prognosis are associated with monocyte heterogeneity in both STEMI and non-STEMI patients.

High frequency of aspirin resistance in patients with nephrotic syndrome.

BACKGROUND: Aspirin has a beneficial role in prevention of cardiovascular and thromboembolic events. Patients may experience thromboembolic events despite aspirin treatment, a phenomenon called aspirin resistance. We evaluated the frequency of aspirin resistance and its correlation with clinical and biochemical parameters among patients with nephrotic syndrome (NS). METHODS: A total of 83 patients (50 males, 33 females, age range 18-79 years) with NS using aspirin 100 mg/day were included in the study. Demographic information and aetiology of NS based on the histology of a renal biopsy were recorded for each patient. Blood samples were drawn to investigate the association of aspirin resistance with inflammation and thrombotic risk factors. Aspirin resistance was defined as a normal collagen/epinephrine closure time<159 s using a platelet function analyzer (PFA-100). RESULTS: Aspirin resistance was determined in 51 patients (61.4%). The number of patients exposed to azathioprine therapy was significantly higher in the aspirin-sensitive group (P=0.043), whereas patients exposed to cyclosporine therapy were significantly higher in the aspirin-resistant group (P=0.017). More patients in the aspirin-resistant group were on angiotensin-converting enzyme inhibitor therapy compared with the aspirin-sensitive group (P=0.024). The aspirin-resistant group showed significantly higher serum low-density lipoprotein cholesterol (LDL-C) (151±47 versus 104±21 mg/dL; P<0.001), triglyceride levels (192±116 versus 134±82 mg/dL; P=0.015) and glomerular filtration rates (91.8±43.0 versus 74.0±35.6 mL/min/1.73 m2; P=0.044) compared with the aspirin-sensitive group. In multivariate analysis, LDL-C was the only parameter associated independently with aspirin resistance [odds ratio (OR) 1.04, 95% confidence interval (CI) 1.02-1.06; P=0.004]. CONCLUSIONS: A significant number of patients with NS are resistant to aspirin therapy. Serum LDL-C level is closely associated with aspirin resistance in NS.