الفهرس 
Hepatitis C virus infectionOnly 14 pages are availabe for public view
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Abstract
Hepatitis B virus (HBV) and hepatitis C virus (HCV) infections are responsible for the majority of chronic hepatitis, liver cirrhosis and hepatocellular carcinoma (HCC) cases world wide. Dual infection by hepatitis B and hepatitis C viruses constitutes 4% of cases with chronic liver disease among Egyptians (Waked et al., 1995). However, the natural course of the liver disease induced by the coinfection has not been well documented and the mechanisms of interaction between the two viruses and humans have not been fully clarified. The rationale aim for treatment of chronic hepatitis is to prevent progression to cirrhosis and hepatocellular carcinoma through the eradication of the virus, although, until now, this goal has not been very realistic. However, the main aim is that the control disease activity and viral replication could lead to improvement in the prognosis of patients with chronic liver damage. This study was aimed at characterizing the biochemical, virological and histological profiles among Egyptian patients co infected by both HBV and HCV and to study the biochemical and viralogical responses to antiviral treatment among HBV infected patients and among HCV infected patients. This study was done on 212 patients with viral chronic hepatitis 72 patients were positive for HBsAg and anti HCV (group BC), 70 patients were positive for HBsAg and negative for antiHCV (group B) and 70 patients were positive for antiHCV and negative for HBsAg (group C). Patients were investigated for HBV and HCV serological markers, liver function, detection of HBVDNA using PCR. Liver biopsies were studied for scores of HAI. The results showed that patients with HBV infection were significantly younger than those with HCV infection with or without HBV infection. Concurrent HBV and HCV infection cause more severe liver damage where ALT and AST levels were significantly higher in patients with dual infection and in patients with HCV than in patients with HBV infection alone. Also, thrombocytopenia has been found in patients with dual infection by HBV/HCV and in patients with HCV infection alone. The serological results showed that prevalence of HBeAg was higher in patients with concurrent HBV and HCV infection than in those with HBV infection alone although this difference was statistically insignificant. Also, the high prevalence of eminus strain in the patients with dual infection by HBV/HCV may be due to early mutation of the HBV genotype D which is the dominant genotype among Egyptians. This study has confirmed an inhibitory effect of HCV on HBV replication where HBVDNA was found more frequently in group B than in group BC. On the other hand, it was found that HBV had no influence over HCV replication where HCVRNA was detected by PCR in all patients coinfected by both viruses and patients with HCV infection alone. The histological data showed that the scores of HAI and fibrosis were significantly higher in coinfected patients than in those patients with HBV alone, but similar to those in patients with HCV alone. The treatment of HBV with lamivudine showed that 41.4% of patients became negative for HBVDNA after 12 months of treatment. Also, the results of treatment of HCV with ribavirin suggested that ribavirin has a beneficial effect on patients with chronic hepatitis C although all patients relapsed after stopping the treatment, while the combination therapy with interferon and ribavirin results in higher rates of sustained virolgical and biochemical response. Our study considers that the suitable treatment for our patients with dual HBV and HCV infection is the combination therapy with gas2b interferon and ribavirin for 6 months which is the same treatment for patients with HCV infection alone. In addition, future studies are needed to follow up and assess the effectiveness of the combination therapy for dual HBV and HCV infection.