The impact of liver steatosis on early and sustained treatment response in chronic hepatitis C patients.

Steatosis is a frequent feature of hepatitis C virus (HCV) infection. Steatosis may be an important cofactor in both accelerating fibrosis and increasing liver necroinflammatory activity in chronic hepatitis C. The main objective of this study was the evaluation of biological response rates, early viral response, sustained viral response in patients with chronic hepatitis C treated with Interferon-alpha (IFN-α), Pegylated (PEG)-IFN-α2a or -α2b plus Ribavirin and to relate it to the presence of hepatic steatosis. There were selected to take part to the research 210 patients with chronic hepatitis C who have fulfilled all inclusion and exclusion criteria and were treated with PEG-IFN plus Ribavirin. Patients' progress has been monitored by determining next parameters: age, gender; biochemical tests - alanine aminotransferase (ALT), aspartate aminotransferase (AST); serological assays - detect antibody to hepatitis C virus (anti-HCV); molecular assays - detect, quantify and/or characterize HCV-RNA; liver histopathological examination. Steatosis was graded using the Brunt system. These parameters were included in an area under curve (AUC) analysis. Purpose is to estimate their degree of influence on getting early viral response (EVR) and sustained viral response (SVR). Based on the obtained results, it appears that initial value of HCV-RNA, dVL parameter value (low relative percentage of viral load during the first 12 weeks of treatment), histological scores steatosis may be predictive in the viral response in chronic hepatitis C. Our research demonstrates that a high degree of liver steatosis impairs both EVR and SVR in chronic hepatitis C treated with standard PEG-IFN and Ribavirin for 48 weeks and that a steatosis score of ≤3 predicts EVR with a sensibility of 91.03% with specificity of 21.54%.

Rare case of single coronary artery in a patient with liver cirrhosis.

We report here the case of a 58-year-old male presented with atypical chest pain, dyspnea and fatigue, with a medical history of liver cirrhosis and undergoing treatment with beta-blocker. The clinical exam was normal. The 12-lead electrocardiogram (ECG) showed normal heart rate, without repolarization changes. Transthoracic echocardiography revealed no wall motion abnormalities of the left ventricle, moderate tricuspid regurgitation with mild pulmonary hypertension and left ventricular hypertrophy. The biochemical markers for myocardial infarction were negative. He underwent coronary angiography that revealed a single coronary artery originating from the right coronary sinus of Valsalva.

The cadherin switch assessment in the epithelial-mesenchymal transition of urothelial bladder carcinomas.

INTRODUCTION: The epithelial-mesenchymal transition (EMT) process is a complex molecular mechanism that is involved in the acquisition of an aggressive, invasive and metastatic phenotype by carcinomas. The cadherin switch consists in the alteration of E-cadherin and N-cadherin expression and is specific for the EMT process. MATERIALS AND METHODS: This study included 35 cases of primitive urothelial carcinomas investigated in relation with clinicopathological prognostic parameters and expression of E- and N-cadherins in the advancing edge and intratumoral compartments. RESULTS: In both compartments, the immunoexpression of E-cadherin decreased, while that of N-cadherin increased in high grade, deeply invasive, or those cases with lymph node metastases and advanced stages carcinomas, with a negative linear correlation observed between their expression percentage values. In this study, it was observed the presence of cadherin switch in urothelial carcinomas, the variation of the two proteins' immunostaining patterns being higher at the advancing edge. The presence of N-cadherin in intratumoral compartment designated it as actively involved in EMT process. CONCLUSIONS: The analysis of cadherins switch can be used to identify superficial urothelial carcinoma with invasion and metastasis potential.

Histochemical and immunohistochemical evidence of tumor heterogeneity in colorectal cancer.

INTRODUCTION: Intratumoral heterogeneity implies the existence of differences between tumor cells, which can best be shown by histochemical and immunohistochemical techniques. The histological study is a mandatory step in any research aimed at characterizing tumor heterogeneity. Immunohistochemistry (IHC) also plays an important role in the differentiation of tumor types, assessing aggressiveness. MATERIALS AND METHODS: Investigated group consisted of 50 patients with colorectal adenocarcinoma, for each were recorded clinicopathological data and harvested samples intraoperatively, which were included in paraffin blocks. We perform Hematoxylin-Eosin staining for histological grade and other indices. IHC study used Avidin-Biotin-Peroxidase (ABC), with the markers: CK7, CK20, MUC1, MUC2, Ki-67, PCNA, p53, KRAS, BCL2, PTEN, EGFR. The resulting data were analyzed by statistical methods. RESULTS: Most of colorectal adenocarcinoma studied had no special histological features and had G2 grade. IHC detected in most cases the CK20+÷CK7- phenotype (78%) and MUC1 (74%) protein expression. The proliferation markers (Ki-67 and PCNA) were present in all tumor mass with a variable index, which shows high intratumoral heterogeneity, but p53 and KRAS were distributed more uniformly, showing low intratumoral heterogeneity. PTEN was expressed nuclearly in 86% of the cases and EGFR in 42%. CONCLUSIONS: The expression profiles of cytokeratins and mucins in the colorectal adenocarcinomas are useful in defining tumor phenotypes with different prognosis and therapy. We found a significant positive correlation between KRAS protein expression and BCL2 and TP53 expression. The study demonstrated the intratumoral and intertumoral heterogeneity, expressed at phenotypic level.