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Background: Anticardiolipin (aCL) antibodies are associated with thrombosis and have an important role in the etiology of diseases such as stroke and myocardial infarction whose etiologies were based on thrombosis. H. pylori has been proposed to be responsible for the pathophysiology of some diseases including stroke, myocardial infarction, thrombosis, and autoimmune diseases. From this point of view, we hypothesized a possible relationship between H. pylori infection and aCL antibodies and initially aimed to determine the prevalence of aCL antibody positivity in children with H. pylori infection. Materials and Methods: Anticardiolipin antibodies were studied in 84 patients before and after eradication therapy and in a control group including 40 children. Results: The pretreatment aCL IgA (median 12.78 APL/mL), aCL IgM (median 21.60 MPL/mL), and aCL IgG antibody levels (median 14.22 GPL/mL) were significantly higher than those of post-treatment results (median 5.38 APL/mL, 7.02 MPL/mL, and 6.64 GPL/mL, respectively) and controls (median 5.90 APL/mL, 4.80 MPL/mL, and 4.81 GPL/mL, respectively). Anticardiolipin antibodies revealed no significant differences between the study group after therapy and the control group. Conclusions: In our particular experience, H. pylori can cause aCL antibody positivity in children and eradication of H. pylori provides the disappearance of these antibodies. [ABSTRACT FROM AUTHOR]

Objective: In our study, using echocardiography measurements, patients Will i acute lymphoblastic leukemia receiving anthracycline therapy have been evaluated as for the presence of anthracycline-induced cardiac dysfunction, and it has been carried out to determine the statistically significant predictive echocardiography parameters. Methods: Thirty cases (mean age 9.87±3.92 years, 13 males and 17 females) with acute lymphoblastic leukemia receiving anthracycline therapy were enrolled in the study, along with 30 ageniatehed controls. Their cardiac functions were evaluated echocardiographically with two dimensional, M-mode, PW Doppler and PW tissue Doppler methods. Results: Left ventricular cardiac functions were significantly reduced in the study group. The fractional shortening (FS) was 36.09±3.17 in the study group as opposed to 39.65±3.21 in controls (p=0.03). Diastolic functions (E/A ratio) weren't significantly altered in the study group. Right ventricular (RV) flow E/A was 1.36±0.29 and 1.34±0.69, respectively (p>0.05). Left ventricular (LV) flow E/A was 1.53±0.31 and 1.58±0.35, respectively (p>0.05). Myocardial performance index (MPI) was calculated in the study subjects using both PW Doppler and PW tissue Doppler methods, and compared to controls. RV flow MPI was 0.39±0.02. and 0.33±0.03. respectively (p<0.01). LV flow MPI was 0.41±0.08 and 0.34±0.04, respectively (pcO.Ol). RV tissue MPI was 0.44±0.04, and 0.39±0.0S, respectively (p<0.01). LV tissue MPI was 0.42±0.02 and 0.36±0.01, respectively (pcO.Ol). Conclusion: The results of our study show that MPI and systolic functional changes are better indicators of anthracycline cardioloxicity than diastolic functions. We suggest that RV and LV tissue MPI be primarily used in the search for anthracycline cardiotoxicity. [ABSTRACT FROM AUTHOR]

Captopril and enalapril are the most commonly used angiotensin converting enzyme inhibitors in several cardiac diseases in children. On the other hand, the intrinsic renin-angiotensin system in the bone marrow might affect the growth of hematopoietic colonies and cellular production, proliferation and differentiation in physiological and pathological states. Starting with the hypothesis that inhibition of the renin-angiotensin system may have some effects on the hematopoietic system, including morphological changes within the granulocytes, we thus aimed to investigate prospectively whether the use of angiotensin converting enzyme inhibitors has any effect on the morphology, and especially segmentation, of neutrophils in peripheral blood. A total of 40 children with various heart diseases receiving either of two angiotensin converting enzyme inhibitors (captopril or enalapril) aged between 2 to 16 years were enrolled, and 40 healthy age- and sex-matched children were enrolled as controls. Complete blood count, peripheral blood smear, liver and renal function tests, and measurement of serum alkaline phosphatase, ferritin, vitamin B12 and folate levels were performed in all cases. Peripheral blood smears were viewed by two pediatric hematologists in a blinded manner. Neutrophil hypersegmentation was described as presence of five or more neutrophils with five well-separated lobes or at least one neutrophil with six or more lobes among 100 segmented neutrophils. The number of patients with neutrophil hypersegmentation in the study group was significantly higher than in the control group, and the mean lobe count in the study group was significantly higher than in the control group. Neutrophil hypersegmentation, as detected in patients using angiotensin converting enzyme inhibitors in the present study, has not been reported previously. Further studies aiming to explain the pathophysiological mechanism(s) underlying neutrophil hypersegmentation in patients receiving angiotensin converting enzyme inhibitors are needed. [ABSTRACT FROM AUTHOR]

The objective in this study was to determine whether there was any relation between leptin and vascular endothelial growth factor (VEGF) in children with cyanotic and acyanotic heart anomalies. The study group consisted of 18 children with cyanotic congenital heart disease (CHD) and 20 age-adjusted children with acyanotic CHD as controls. Serum VEGF and leptin levels were determined by enzyme-linked immunosorbent assay (ELISA). The mean VEGF level was 149.25±42.93 pg/ml (range 80.66-217.00) in the cyanotic group and 88.18±20.94 pg/ml (range 48.44-112.71) in the acyanotic group (p<0.001). The mean leptin level was 7.55±1.46 ng/ml (range 4.08-10.25) in the cyanotic group and 6.89±1.43 ng/ml (range 2.67-8.57) in the acyanotic group (p=0.168). There was a significant positive correlation (r=0.723, p<0.001) between VEGF and leptin levels in the cyanotic group while there was no correlation (r=0.235, p=0.348) in the acyanotic group. Arterial oxygen saturation (SaO2) was negatively correlated (r= -0.625, p<0.001) with VEGF, but not correlated with leptin (r= -0.207, p=0.211) in the cyanotic group. There was no correlation between VEGF, leptin and SaO2 in the acyanotic group. We conclude that it is likely that both VEGF and leptin have a role in the pathogenesis of angiogenesis in cyanotic CHD. [ABSTRACT FROM AUTHOR]

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