Cryptogenic liver cirrhosis and hepatitis E virus (HEV): Are they related?

INTRODUCTION AND OBJECTIVES: Hepatitis E virus (HEV) is one of the most common causes of acute hepatitis. In recent years, its role in the development of chronic hepatitis and cirrhosis especially in immunosuppressed patients and its wide range of extrahepatic involvement have increased the amount of research on HEV. In this study we aimed to investigate the presence of HEV infection in individuals with cryptogenic cirrhosis. MATERIALS AND METHODS: HEV antibodies were analysed using the Anti HEV enzyme-linked immunosorbent assay (ELISA) kit (anti-HEV ELISA; Diapro Prodiagnostic Bioprobes, Milan, Italy). HEV RNA was isolated with using QIAMP Viral RNA mini kit (QIAGEN, Hilden, Germany). The HEV RNA titre was detected with the Rotor Gene 3000 real time polymerase chain reaction (PCR) system using GenoSen's HEV (Rotor Gene) Quantitative Real Time PCR Kit (Genome Diagnostics Private Limited, the Netherlands). RESULTS: Our study included 21 healthy volunteers (12 males) and 35 cryptogenic cirrhosis patients (19 males). The ages of the patients and the controls were similar (46±12.1 vs. 37.5±9.7years). The mean Child-Pugh score was 8±2.5. The anti HEV immunoglobulin G(IgG) positivity rate was 9.5% and 25.7% in the control and patient groups respectively (p>0.05). HEV RNA positivity was not detected in the control group, but 3 cases (8.6%) in the patient group were positive (p>0.05). The HEV RNA, aspartate aminotransferase (AST) and alanine aminotransferase(ALT) levels for these 3 cases were 326.461copies/mL, 91IU/L and 67IU/L; 480copies/mL, 68IU/L and 36IU/L and 72copies/mL, 42IU/L and 24IU/L respectively. There were positive correlations between HEV RNA levels and AST and ALT levels (p<0.05). CONCLUSIONS: Anti HEVIgG and HEV RNA positivity rates are high in cryptogenic cirrhosis although it is not statistically significant and there is a positive correlation between HEV RNA and aminotransferases.

Mutations in influenza A virus (H5N1) and possible limited spread, Turkey, 2006.

We report mutations in influenza A virus (H5N1) strains associated with 2 outbreaks in Turkey. Four novel amino acid changes (Q447L, N556K, and R46K in RNA polymerase and S133A in hemagglutinin) were detected in virus isolates from 2 siblings who died.

Prevalence and clinical significance of SEN-H virus in chronic hepatitis B, C and delta infections in Turkey.

BACKGROUND/AIMS: SEN viruses are transmitted parenterally and can cause post-transfusion hepatitis. The prevalence and clinical significance of SEN viruses have been investigated in patients with chronic hepatitis C and B but not in D. We aimed to determine the prevalence and clinical significance of SEN viruses- H in patients with chronic hepatitis C, B and delta in Turkey. METHODS: SEN viruses-H was analyzed in 85 patients with chronic viral hepatitis (30 HCV, 30 HBV and 25 HDV) and 43 non-professional blood donors. HBV DNA, HCV RNA and HDV RNA were positive in patients with hepatitis B, C and D, respectively. SEN viruses-H DNA was detected by semi-nested polymerase chain reaction method (L2AS, C5S primer in first step, L2AS, D11 in second step) after extraction of DNA from sera (NucleoSpin blood; Macherey-Nagel GmbH & Co KG, Germany). RESULTS: SEN viruses-H DNA was found to be positive in 7/30 (23.3%), 10/30 (33.3%), 6/25 (24%), and 7/43 (16.2%) of patients with chronic C, B, and D hepatitis and healthy blood donors, respectively. There was no significant difference in clinical features and treatment response between SEN viruses- H-positive and -negative patients with chronic viral hepatitis. CONCLUSIONS: SEN viruses is more frequent in chronic hepatitis patients than in healthy blood donors. These results indicate that SEN viruses has no effect on the clinical course and treatment response of chronic viral hepatitis.

Alpha interferon and ribavirin combination therapy of chronic hepatitis D.

The success of alpha interferon (IFN-alpha) monotherapy for the treatment of chronic hepatitis D is very limited. In this study, the efficacy of IFN-alpha and ribavirin combination therapy for chronic hepatitis D was investigated. Nineteen patients (15 males; mean age +/- standard deviation, 36.8 +/- 12.8 years) with chronic hepatitis D who were treated with IFN-alpha2b (10 million U, three times/week, subcutaneously) and ribavirin (1,000 to 1,200 mg/day, orally) for 24 months were studied. All patients had compensated liver disease (15 were precirrhotic), elevated transaminase levels, and hepatitis D virus RNA positivity at baseline. Genotypic analyses revealed hepatitis D virus genotype I and hepatitis B virus genotype D. All patients completed the 24 months of treatment and at least 6 months (7 to 19 months) of a follow-up period. Biochemical responses were observed in eight patients (42.1%) at the end of treatment and in seven patients (36.8%) at the end of follow-up. Eight patients (42.1%) at the end of treatment and four patients (21%) at the end of follow-up had virological responses. In conclusion, combination treatment of IFN-alpha and ribavirin for chronic hepatitis D is not able to induce virological responses at a sufficient rate, despite its partial effectiveness in improving biochemical responses, and is not superior to IFN-alpha monotherapy.