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EN
Disturbances in the antioxidant system could play a role in pathogenesis of chronic liver disease. The aim of our study was to evaluate the levels/activities of antioxidants in blood of patients with chronic liver disease. We estimated selenium and glutathione concentrations and glutathione peroxidase activities in blood of 59 patients with chronic hepatitis B or C virus infection (group 1) and 64 patients with alcoholic, autoimmune or cryptogenic chronic liver disease (group 2). The results were compared with 50 healthy controls. Whole blood and plasma selenium and red cell glutathione concentrations were significantly lower in the patients compared with the controls. Red cell glutathione peroxidase activity was slightly reduced in both subgroups of group 1 and in group 2 with normal alanine aminotransferase values. Plasma glutathione peroxidase activity was slightly but significantly higher in patients with elevated aminotransferase values. The findings suggest that disturbances in antioxidant parameters in blood of patients with chronic liver disease may be the cause of the peroxidative damage of cells.
EN
Hepatitis C virus (HCV) is an enveloped, single-stranded RNA virus, belonging to the Flaviviridae family. HCV infection is a major cause of chronic hepatitis worldwide, leading to steatosis, liver cirrosis and hepatocellular carcinoma. Significant advances in understanding the mechanisms of HCV infection have been made since the development of a cell culture system reproducing the complete HCV cell cycle in vitro. HCV represents a new paradigm in interactions between the virus and its target cell, the human hepatocyte, due to the central role of lipoproteins in the HCV life cycle. Very low density lipoproteins are required for virus particle assembly and secretion. Upon the release, the infectious virus circulates in the blood as triglyceride-rich particles and infects cells using lipoprotein-receptor dependent mechanisms. HCV cell entry is a multi-step process: heparan sulphate and/or low-density lipoprotein receptor are cell surface factors mediating an initial virus attachment; subsequent virus interaction with tetraspanin CD81 and the human scavenger receptor SR-BI, the main HCV receptors, triggers virus movement to the tight junctions and its uptake via Claudin-1 and occludin. Another originality of HCV is that initiation of productive infection requires dynamic microtubules. Whereas other viruses use kinesin or dynein-dependent transport, HCV exploits mechanisms driven by microtubule polymerization to efficiently infect its target cell, in which virus nucleocapsid protein might play a particular role. An improved of understanding of the cellular-events involved in HCV cell entry and transport, leading to the initiation of productive HCV infection, may reveal novel targets for anti-viral interventions.
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tom 54
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nr 4
703-715
EN
Hepatitis C virus (HCV) is a causative agent of chronic liver disease leading tocirrhosis, liver failure and hepatocellular carcinoma. The prevalence of HCV is estimated as 3% of the world population and the virus is a major public health problem all over the world. For over 16 years, since HCV had been discovered, studies of the mechanisms of the viral life cycle and virus-host interactions have been hampered by the lack of a cell culture system allowing the virus to be grown in laboratory conditions. However, in recent years some new model systems to study HCV have been developed. The major breakthrough of the last two years was the cell culture system for maintaining the virus in an adapted hepatocyte-derived cell line. This review describes the techniques and applications of most of the in vitrosystems and animal models currently used for working with hepatitis C virus
EN
Literature data indicate an association between the presence of Helicobacter spp. in the liver and the development of hepatocellular carcinoma (HCC). However, the role of H. pylori infections in chronic liver diseases (CLD) remains controversial. The aim of this study was to detect Helicobacter spp. DNA in patients with CLD, and to investigate the host response to the presence of the bacterium in the liver. Helicobacter spp. DNA was detected in 59% samples. H.pylori was the most prevalent species (94%). We estimated the expression level of IL-1 and IL-8 genes. The presence of Helicobacter spp. did not have a significant effect on the gene expression of IL-8 and IL-1.
10
Content available remote Gas exchange abnormalities in patients listed for liver transplantation
72%
EN
Abnormalities of pulmonary gas exchange are common in patients with advanced liver disease. Since arterial blood hypoxemia is an important issue in the preoperative evaluation of liver transplant candidates, the study was undertaken to determine the incidence and severity of lung function impairment with a special emphasis on pulmonary gas exchange abnormalities in this group of patients. 104 consecutive patients (47 F and 57 M, mean age 46 ±11 yr) listed for orthotopic liver transplantation participated in this prospective study. All patients underwent evaluation including: clinical assessment (Child-Pough and MELD classification), chest X-ray, chest sonography, lung function tests, arterial blood gases measurement, and transthoracic contrast enhanced echocardiography. There were 2 patients with acute hepatic failure, 6 patients with primary or metastatic liver carcinoma, and 96 patients with chronic liver disease. The mean PaO2 and lung function parameters for the entire group were within normal limits. There were 29 hypoxemic patients (PaO2< 80 mmHg) and 40 patients with widened (>20 mmHg) P(A-a)O2. DLCO was significantly lower in cirrhotic vs. non-cirrhotic patients (76.5 ±19.3 vs. 92.4 ±19.0% predicted; P<0.001). Hepatopulmonary syndrome (HPS) was recognized in 23 (24%) patients. 91% of patients with HPS showed mild to moderate stage of disease. There were significant difference between differences HPS patients and non-HPS patients in DLCO (69.0 ±14.5 vs. 83.5 ±20.7, P<0.01). In conclusion, all patients referred for OLT should be screened for gas exchange abnormalities. Such a workup should include not only PAO2 but also DLCO and P(A-a)O2 measurement together with contrast enhanced echocardiography.
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