Midregional pro-atrial natriuretic peptide: a novel marker of myocardial fibrosis in patients with hypertrophic cardiomyopathy

We aimed to determine the diagnostic performance of biomarkers in predicting myocardial fibrosis assessed by late gadolinium enhancement (LGE) cardiovascular magnetic resonance imaging (CMR) in patients with hypertrophic cardiomyopathy (HCM). LGE CMR was performed in 40 consecutive patients with HCM. Left and right ventricular parameters, as well as the extent of LGE were determined and correlated to the plasma levels of midregional pro-atrial natriuretic peptide (MR-proANP), midregional pro-adrenomedullin (MR-proADM), carboxy-terminal pro-endothelin-1 (CT-proET-1), carboxy-terminal pro-vasopressin (CT-proAVP), matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase-1 (TIMP-1) and interleukin-8 (IL-8). Myocardial fibrosis was assumed positive, if CMR indicated LGE. LGE was present in 26 of 40 patients with HCM (65%) with variable extent (mean: 14%, range: 1.3–42%). The extent of LGE was positively associated with MR-proANP (r = 0.4; P = 0.01). No correlations were found between LGE and MR-proADM (r = 0.1; P = 0.5), CT-proET-1 (r = 0.07; P = 0.66), CT-proAVP (r = 0.16; P = 0.3), MMP-9 (r = 0.01; P = 0.9), TIMP-1 (r = 0.02; P = 0.85), and IL-8 (r = 0.02; P = 0.89). After adjustment for confounding factors, MR-proANP was the only independent predictor associated with the presence of LGE (P = 0.007) in multivariate analysis. The area under the ROC curve (AUC) indicated good predictive performance (AUC = 0.882) of MR-proANP with respect to LGE. The odds ratio was 1.268 (95% confidence interval 1.066–1.508). The sensitivity of MR-proANP at a cut-off value of 207 pmol/L was 69%, the specificity 94%, the positive predictive value 90% and the negative predictive value 80%. The results imply that MR-proANP serves as a novel marker of myocardial fibrosis assessed by LGE CMR in patients with HCM.     

Role of contrast-enhanced 3D magnetic resonance portography in evaluating portal venous system compared with color Doppler ultrasonography

Aim The purpose of this study was to evaluate the capability of contrast-enhanced three-dimensional (3D) MR portography in detecting abnormal findings associated with the portal venous system compared with the results of color Doppler ultrasonography (CDUS). Materials and methods MR portography findings were retrospectively compared with the results of CDUS examinations in 161 patients, who were suspected of having portal venous system abnormalities. Portal venous vessels were divided into main 5 groups including the main portal vein, its left and right intrahepatic branches, splenic vein and superior mesenteric vein. Imaging findings were classified as normal, occluded, or partially thrombosed. Results of clinical and imaging follow-up examinations including CDUS, MR portography or angiography, if available, were used as a proof of final diagnosis. The potential sites of varicose veins and collateral vessels were also examined by both imaging methods. Results Vascular abnormalities were identified in 79 of 161 patients. There was a statistically significant agreement between the results of MR portography and CDUS in evaluating portal venous system (κ = 0.871, P < 0.05). The sensitivity of MR portography was slightly superior to CDUS in detecting partially thrombosis and occlusion in the main portal venous vessels. In addition, MR portograms were superior to CDUS in the management of patients with portal hypertension by identifying portosystemic collaterals more adequately, and clearly demonstrated portal venous vessels that cannot be visualized at CDUS. Conclusion Results of present study indicates that contrast-enhanced 3D MR portography is well suited and superior to CDUS in the management of patients with portal hypertension.     

Hemophagocytosis associated with leukemia: a striking association with juvenile myelomonocytic leukemia

The aim of this study was to describe the characteristics and outcome in a group of pediatric patients with hematological malignancies who developed hemophagocytosis at diagnosis or during the disease course. Eight patients with hematological malignancy and associated hemophagocytosis were included. The initial diagnosis was juvenile myelomonocytic leukemia (JMML) in five, nonlymphoblastic leukemia (ANLL) in two, and T-cell lymphoma associated with myeloproliferative syndrome in one patient. Hemophagocytosis was concomitantly present at the time of diagnosis of the primary disease in four of the five patients with JMML and in the two patients with ANLL. Three had abnormalities related to chromosome 8 [(trisomy 8, monosomy 8, and t (8;13) (p11; p12)], and one had inversion 16. Multiple chromosomal losses were present in one patient, including both chromosomes 8 and 16. Bone marrow karyotyping revealed 46, XX; 47, XXX mosaicism in one patient. Two patients had PTPN11 mutation and one patient k-RAS mutation. The patients with JMML and neurofibromatosis (n = 2), the patient with lymphoma and t (8;13) positive AML, and a fourth patient with PTPN11 mutation did not remit and had unfavorable outcomes.     

The effects of allopurinol on rat liver and spleen tissues in a chronic hyperammonemia animal model

OBJECTIVE: To investigate whether hyperammonemia can lead to any structural change in liver and spleen tissues or biochemical changes in blood and if allopurinol (ALLO) has a protective effect in hyperammonemia. METHODS: This study was conducted between April and May 2006. Thirty-six females Wistar Albino rats were randomly divided into 3 equal groups: Controls, administered with ammonia (NH3) and administered with NH3 + ALLO groups. Ammonium acetate (2.5 mmole/kg/day) was injected to NH3 group intraperitoneally (IP) for 28 days. The other group received ammonium acetate (2.5 mmole/kg) plus ALLO (50 mg/kg) IP for 28 days. After finishing the study, blood and tissue samples were collected to perform histopathological and biochemical analysis. RESULTS: Liver and spleen tissues were normal in the control group. In NH3 group, liver tissues were minimally vacuolar and granular degenerations and moderate mononuclear cell infiltration. However, there was no histopathological change in NH3 + ALLO group. Spleen tissues were normal in NH3 group. In biochemical analysis, there was no significant difference between the groups (p>0.05). CONCLUSION: The ammonium acetate may cause minimal structural changes in rat liver and ALLO can prevent this. We found that biochemical parameters do not necessarily correlate with the histopathological findings.     

Chemoprotective effect of ascorbic acid, α-tocopherol,and selenium on cyclophosphamide-induced toxicity in the rat ovarium

ObjectiveThe aim of the study was to evaluate the protective efficacy of ascorbic acid, α-tocopherol, and selenium by measuring the glutathione (GSH) levels and proliferating cell nuclear antigen (PCNA) and growth differentiation factor-9 (GDF-9) expression in the ovarian tissues of rats treated with cyclophosphamide (CP) therapy.MethodsFemale Wistar rats were divided into 5 groups of 6 rats each: (I) control, (II) only CP, (III) CP + ascorbic acid, (IV) CP + α-tocopherol, and (V) CP + selenium. Immunohistochemical stainings and GSH protocol were then applied.ResultsFollowing CP administration, the rats exhibited significantly lower GDF-9 expression in oocytes and PCNA expression in granulosa cells of follicles in all stages of development (P < 0.05). In CP + antioxidant groups (Groups III, IV, V), GDF-9 immunoreaction in oocytes and PCNA immunoreaction in granulosa cells of the developing follicles were found to show an increase towards the levels observed in the control group (P < 0.05).ConclusionsCP was found to cause remarkable degenerative effects in normal ovarian tissue, and we believe that this damage can be reduced and ovarian tissue can be spared from the toxic effects of CP by using antioxidants such as ascorbic acid, α-tocopherol, and selenium.