Liver Cirrhosis in Chronic Hepatitis B Patients Is Associated with Genetic Variations in DNA Repair Pathway Genes.

Liver cirrhosis (LC), contributing to more than 1 million of deaths annually, is a major healthcare concern worldwide. Hepatitis B virus (HBV) is a major LC etiological factor, and 15% of patients with chronic HBV infection (CHB) develop LC within 5 years. Recently, novel host genetic determinants were shown to influence HBV lifecycle and CHB course.

Genetic variation in IL-10 influences the progression of hepatitis B infection.

Objectives: The outcomes of hepatitis B virus (HBV) infection vary substantially among affected individuals, providing evidence of the role of host genetic background in the susceptibility to HBV persistence and the dynamics of liver injury progression to cirrhosis and hepatocellular carcinoma (HCC).

Methods: Six single-nucleotide polymorphisms within the interleukin 10 gene (IL10) were genotyped by MALDI-TOF mass spectrometry in 857 patients with chronic HBV infection (CHB), 48 patients with resolved HBV infection, and 100 healthy volunteers. Associations of the selected polymorphisms with susceptibility to chronic HBV infection, liver injury progression, and outcomes were investigated.

Host genetic background affects the course of infection and treatment response in patients with chronic hepatitis B.

Background: Hepatitis B virus (HBV) utilizes proteins encoded by the host to infect hepatocytes and replicate. Recently, several novel host factors have been identified and described as important to the HBV lifecycle. The influence of host genetic background on chronic hepatitis B (CHB) pathogenesis is still poorly understood.

TNF-α polymorphisms affect persistence and progression of HBV infection.

Background: Hepatitis B virus (HBV) infections are a major threat worldwide. Disease progression and outcome is diverse and depends on host genetic background. Recently, a high rate of HBV reactivation in individuals receiving tumor necrosis factor-α (TNF-α) antagonists showed the importance of this cytokine in HBV infection control.

Hepatitis D, B and C virus (HDV/HBV/HCV) coinfection as a diagnostic problem and therapeutic challenge.

Coinfection with hepatitis D virus (HDV) in chronic hepatitis B is associated with more rapid progression to liver cirrhosis. We present two cases of infection with hepatitis D, B and C viruses. Both male patients were primarily diagnosed as infected with hepatitis B virus (HBV) and hepatitis C virus (HCV), HBsAg-positive and anti-HCV-positive.

Differences in sequences between HBV-relaxed circular DNA and covalently closed circular DNA.

The hepatitis B virus (HBV) genome exists in two forms: circular covalently closed DNA (cccDNA) and relaxed circular DNA (RCDNA). Here, we investigated the presence of differences in the sequences of both forms in paired samples of serum and liver tissue. The serum and liver biopsy samples were collected at the same time from 67 chronically infected patients.

Current molecular methods for the detection of hepatitis B virus quasispecies.

Chronic HBV infection affects more than 240 million people worldwide and is associated with a broad range of clinical manifestations including liver cirrhosis, liver failure and hepatocellular carcinoma. Because of the lack of an efficient cure for chronic hepatitis B, the main goal of antiviral therapy is the prevention of liver disease progression coupled with prolonged survival of patients. Because HBV viral load has been shown to be a crucial determinant of the progression of liver damage, these goals can be achieved as long as HBV replication can be suppressed.

The prevalence and co-occurrence of hematological complications at the time of diagnosis of chronic hepatitis C in Poland: a cross-sectional study.

Objectives: To evaluate the frequency, co-occurrence, and risk factors for hematological complications at the time of diagnosis of chronic hepatitis C (CHC).

Methods: This study included 1237 patients with CHC aged 18-88 years diagnosed in the years 1998-2010 in the Pomeranian region of Poland. Clinical data, cell blood count, liver biopsy, and biochemistry results were obtained retrospectively.

Dynamics of hepatitis B virus quasispecies heterogeneity in association with nucleos(t)ide analogue treatment determined by MALDI-TOF MS.

Minor drug-resistant variants may preexist in every subject infected with hepatitis B virus (HBV). However, understanding the dynamic of genotypic evolution within the HBV population requires accurately following allele frequencies through time. We used MALDI-TOF MS (matrix-assisted laser desorption-ionization time-of-flight mass spectrometry) for localization and quantitative allele frequency detection to investigate preexisting HBV quasispecies and the genotypic evolution of drug-resistant variants during nucleos(t)ide analogue therapy.

Association of hepcidin mRNA expression with hepatocyte iron accumulation and effects of antiviral therapy in chronic hepatitis C infection.

Background: Iron overload is frequently observed in patients with chronic hepatitis C (CHC) and is associated with the increased risk of liver fibrosis and carcinogenesis. Hepcidin is a regulator of iron homeostasis and a component of innate immunity. Based on experimental studies, iron overload might be a result of low hepcidin synthesis in CHC.

An initial assessment of correlations between host- and virus-related factors affecting analogues antiviral therapy in HBV chronically infected patients.

Background: Success in treating hepatitis B virus (HBV) infection with nucleoside analogues drugs is limited by the emergence of drug-resistant viral strains upon prolonged therapy. In addition to mutation patterns in the viral polymerase gene, host factors are assumed to contribute to failure of treatment in chronic HBV infections. The aim of this study was to analyze the correlation between efficacy of antiviral therapy and the prevalence of HBV pretreatment drug-resistant variants.

High-throughput matrix-assisted laser desorption ionization-time of flight mass spectrometry as an alternative approach to monitoring drug resistance of hepatitis B virus.

Long-term antiviral therapy of chronic hepatitis B virus (HBV) infection can lead to the selection of drug-resistant HBV variants and treatment failure. Moreover, these HBV strains are possibly present in treatment-naive patients. Currently available assays for the detection of HBV drug resistance can identify mutants that constitute ≥5% of the viral population.

Liver steatosis correlates with iron overload but not with HFE gene mutations in chronic hepatitis C.

Background: Liver steatosis and iron overload, which are frequently observed in chronic hepatitis C (CHC), may contribute to the progression of liver injury. This study aimed to evaluate the correlation between liver steatosis and iron overload in Polish patients with CHC compared to non-alcoholic fatty liver disease (NAFLD) and HFE-hereditary hemochromatosis (HH) patients.

Methods: A total of 191 CHC patients were compared with 67 NAFLD and 21 HH patients.

Distribution of HCV genotypes in Poland.

Unlabelled: Available data on prevalence of HCV genotypes in Poland are insufficient. The aim of the study was the analysis of distribution of HCV genotypes in Poland over the period of recent 10 years regarding the age of patients and the regions of the country.

Material And Methods: Analysis of HCV genotypes in Poland was carried out between 2003 and 2012, and included 14 651 patients from 22 centers where patients with chronic viral hepatitis C are diagnosed and treated.

Host response to the presence of Helicobacter spp. DNA in the liver of patients with chronic liver diseases.

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.

[The influence of hepatitis B virus polymorphism on the progression of chronic liver disease].

Hepatitis B virus (HBV) infection is one of the major human health problems worldwide. It is estimated that chronic HBV infection affects more than 350 million people globally. It is one of the leading causes of liver cirrhosis and hepatocellular carcinoma.

Iron overload and HFE gene mutations in Polish patients with liver cirrhosis.

Background: Increased liver iron stores may contribute to the progression of liver injury and fibrosis, and are associated with a higher risk of hepatocellular carcinoma development. Pre-transplant symptoms of iron overload in patients with liver cirrhosis are associated with higher risk of infectious and malignant complications in liver transplant recipients. HFE gene mutations may be involved in the pathogenesis of liver iron overload and influence the progression of chronic liver diseases of different origins.

[Helicobacter spp. infections in chronic liver damage].

Liver is a key organ responsible for organism’s homeostasis. A proper function of this organ is crucial for detoxification of metabolic products and regulation of metabolic processes of macromolecules (proteins, lipids, carbohydrates). The most important infectious factors, leading to liver damage, are primary hepatotropic viruses, particularly those causing chronic inflammation of the organ (HBV, HCV, HDV), which may subsequently cause cirrhosis and/or primary hepatocellular carcinoma.

Detection of Helicobacter rodentium-like DNA in the liver tissue of patients with chronic liver diseases by polymerase chain reaction-denaturing gradient gel electrophoresis and DNA sequence analysis.

Many Helicobacter spp. were isolated from the stomach, intestinal tract, and liver of different animals and humans. The association between Helicobacter spp.

Coexistence of HFE and rare UGT1A1 genes mutations in patients with iron overload related liver injury.

This report describes two patients hospitalised in Hepatology Unit, Infectious Diseases Department Medical University of Gdansk because of liver damage discovered in family doctor's practice. Hereditary hemochromatosis was diagnosed in both cases. Diagnosis was established basing on medical records review, and biochemical, molecular and liver specimen tests.

The role of iron overload and HFE gene mutations in the era of pegylated interferon and ribavirin treatment of chronic hepatitis C.

Background: Iron overload observed in chronic hepatitis C (CHC) has been suggested to be one of the negative prognostic factors influencing liver disease progression and failure of treatment with recombinant interferon in monotherapy or in combination with ribavirin. The aim of this study was to assess occurrence of iron overload in relation to polymorphism of the HFE and the influence of both these factors on efficacy of antiviral treatment with pegylated interferon and ribavirin in patients with CHC.

Material/methods: Liver function tests, serum indices of iron metabolism, and HFE mutations were assayed in 152 patients with CHC from Poland.

Duplex scan in patients with clinical suspicion of deep venous thrombosis.

Background: The incidence of deep venous thrombosis is 0.6/1000 habitants and when symptomatic its diagnosis by duplex scan has 100% sensitivity and 98% specificity.

Objectives: The aim of this study was to evaluate the findings of the duplex scan in patients with clinical suspicion of deep venous thrombosis.

Could iron deposits in hepatocytes serve as a prognostic marker of HFE gene mutations?

Background/aims: The diagnosis of hereditary hemochromatosis (HH) is based on qualitative measurement of tissue iron concentration and genetic tests. The aim of this study was to evaluate the correlation between the presence of iron deposits in the liver and the HFE gene mutations in patients with chronic liver diseases (CLD).

Methodology: The 182 patients, age range 18-71 years, were hospitalized in Gdansk because of CLD.

Determination of lamivudine-resistant variants of hepatitis B virus by denaturing gradient gel electrophoresis: a novel approach to monitoring drug resistance.

Background: A DGGE-based assay for hepatitis B virus (HBV) drug-resistance monitoring was designed and checked for feasibility. It detects mutations within the YMDD motif related to lamivudine resistance.

Material/methods: The YMDD motif of HBV polymerase was amplified by the set of primers designed in this study.