Browsing by Author "Dopsaj, V. (6507795892)"
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Publication Evaluation of derived coulter red blood cell parameters for the assessment of iron deficiency in adults with congenital heart disease(2012) ;Dopsaj, V. (6507795892) ;Mikovic-Golubovic, G. (55135898800) ;Martinovic, J. (57210017185)Kalimanovska-Ostric, D. (6603414966)Introduction: The aim of our study was to evaluate derived red blood cell parameters in determining the presence of iron depletion and iron-deficient erythropoiesis, as states that precede iron deficiency anemia, in adults with congenital heart disease. Methods: Eighty-eight adults who were diagnosed with congenital heart disease were divided into two groups (cyanotic and acyanotic). In both groups, congenital heart disease patients were then divided into three subgroups: with iron depletion, with iron-deficient erythropoiesis, and a control group. The following parameters were measured: complete blood count, reticulocytes, ferritin, soluble transferrin receptor, haptoglobin, lactate dehydrogenase, and calculated parameters: low hemoglobin density (LHD), red cell size factor (RSF), and microcytic anemia factor (MAF). Results: Discriminant analysis indicated statistically significant differences in the first discriminant function: Function 1 - body iron, LHD, MAF, sTfR, and RSF (P<0.001) in patients with acyanotic congenital heart disease and significant differences in both discriminant functions in patients with cyanotic congenital heart disease: Function 1 - body iron, soluble transferrin receptor, LHD, RSF, MAF, lactate dehydrogenase, and haptoglobin (P=0.008) and Function 2 - reticulocytes (#), immature reticulocyte fraction and reticulocytes (%) (P=0.049). Conclusions: Beside parameters that describe iron metabolism dynamics (body iron and soluble transferrin receptor), LHD, indicator of hypochromia, have the highest potential to differentiate and classify iron deficiency in patients with congenital heart disease. © 2012 Blackwell Publishing Ltd. - Some of the metrics are blocked by yourconsent settings
Publication Evaluation of derived coulter red blood cell parameters for the assessment of iron deficiency in adults with congenital heart disease(2012) ;Dopsaj, V. (6507795892) ;Mikovic-Golubovic, G. (55135898800) ;Martinovic, J. (57210017185)Kalimanovska-Ostric, D. (6603414966)Introduction: The aim of our study was to evaluate derived red blood cell parameters in determining the presence of iron depletion and iron-deficient erythropoiesis, as states that precede iron deficiency anemia, in adults with congenital heart disease. Methods: Eighty-eight adults who were diagnosed with congenital heart disease were divided into two groups (cyanotic and acyanotic). In both groups, congenital heart disease patients were then divided into three subgroups: with iron depletion, with iron-deficient erythropoiesis, and a control group. The following parameters were measured: complete blood count, reticulocytes, ferritin, soluble transferrin receptor, haptoglobin, lactate dehydrogenase, and calculated parameters: low hemoglobin density (LHD), red cell size factor (RSF), and microcytic anemia factor (MAF). Results: Discriminant analysis indicated statistically significant differences in the first discriminant function: Function 1 - body iron, LHD, MAF, sTfR, and RSF (P<0.001) in patients with acyanotic congenital heart disease and significant differences in both discriminant functions in patients with cyanotic congenital heart disease: Function 1 - body iron, soluble transferrin receptor, LHD, RSF, MAF, lactate dehydrogenase, and haptoglobin (P=0.008) and Function 2 - reticulocytes (#), immature reticulocyte fraction and reticulocytes (%) (P=0.049). Conclusions: Beside parameters that describe iron metabolism dynamics (body iron and soluble transferrin receptor), LHD, indicator of hypochromia, have the highest potential to differentiate and classify iron deficiency in patients with congenital heart disease. © 2012 Blackwell Publishing Ltd. - Some of the metrics are blocked by yourconsent settings
Publication Lipid peroxidation as risk factor for endothelial dysfunction in antiphospholipid syndrome patients(2016) ;Stanisavljevic, Natasa (36163559700) ;Stojanovich, L. (55917563000) ;Marisavljevic, D. (55945359700) ;Djokovic, A. (42661226500) ;Dopsaj, V. (6507795892) ;Kotur-Stevuljevic, J. (6506416348) ;Martinovic, J. (57210017185) ;Memon, L. (13007465900) ;Radovanovic, S. (24492602300) ;Todic, B. (57190843532)Lisulov, D. (57190839259)The aim of this study was to evaluate oxidative stress markers and it relations to endothelial damage as risk factor for thrombosis in patients with primary (PAPS) and secondary (SAPS) antiphospholipid syndrome (APS) in correlation to traditional risk factors. Flow-mediated (FMD) and nitroglycerine (NMD)-induced dilation of the brachial artery were studied in 140 APS patients (90 PAPS, 50 SAPS) and 40 controls matched by age, sex, and conventional risk factors for atherosclerosis. Markers of oxidative stress, lipid hydroperoxydes (LOOH), advanced oxidation protein products (AOPP), total sulfhydryl groups (tSHG), and paraoxonase 1 activity (PON1) were determined by spectrophotometric method. Oxidative stress dominates in APS patients. LOOH and AOPP correlate to lipid fractions (p < 0.05), unlike PON1, tSHG that correlated to antiphospholipid antibody positivity (p < 0.05). FMD was lower in APS patients comparing to controls (p < 0.001). Cholesterol is independent variable for FMD impairment in control group (p = 0.011); LOOH in PAPS (p = 0.004); LOOH, aCL, and triglycerides in SAPS patients (p = 0.009, p = 0.049, and p = 0.012, respectively). Combined predictive of aCL and LOOH is better for FMD impairment than LOOH alone in both PAPS and SAPS patients (AUC 0.727, p = 0.001, 95 % CI 0.616–0.837 and AUC 0.824, p˂0.001, 95 % CI 0.690–0.957, respectively). Lipid peroxidation is independent predictor for endothelial dysfunction in APS patients. We demonstrated synergistic effect of aCL and LOOH as risk for endothelial impairment in both PAPS and SAPS patients. © 2016, International League of Associations for Rheumatology (ILAR).