الفهرس 
Introduction and Aim of the WorkOnly 14 pages are availabe for public view
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Abstract
** In the present study we aimed to assess the association between chronic HCV infection and HCC. Modes of transmission of HCV, duration of infection, and cofactors in the development of HCC were considered. Also, we evaluated changes in the prevalence of Hepatocellular Carcinoma over the last two decades in various geographical areas and compared this with rates of HBV, HCV infection and alcohol consumption as major risk factors for development of HCC.
** We investigated the relation of serum retinol and retinoic acid levels in chronic liver disease and HCC in low incidence area, with emphasis on the potential impacts of serum retinol on risk factors for HCC.
** We aimed to test the hypothesis that nitric oxide has a role in the pathogenesis of HCC in patients with chronic liver disease and HCV infection. We also, evaluated the relationship between plasma NO levels, biochemistry (parameters of liver function and AFP) and severity of liver disease.
From this study we conclude the following:
1- It appears that HCV infection is an independent and major risk factor for development of cirrhosis and Hepatocellular Carcinoma. Furthermore, HCV is responsible for increasing prevalence of HCC in many parts of the world. Screening of blood donors for HCV and education of general population for methods of transmission will decrease incidence of HCV infection and possibly prevalence of Hepatocellular Carcinoma.
2- Serum retinol level was found decreased in patients with chronic hepatitis and continue to decrease through progression to liver cirrhosis and Hepatocellular Carcinoma. It may be suggested that lower serum retinol levels may increase risk of Hepatocellular Carcinoma development. However, the mechanism of decreased serum retinol levels in chronic hepatitis C patients and whether it has a role in development of Hepatocellular Carcinoma is unclear. Vitamin A supplements may possibly prevent development of this tumor.
3- the results of this study demonstrated that non cirrhotic patients with chronic hepatitis C have similar plasma nitric oxide levels as healthy control subjects and Alpha-IFN therapy had no effect on NO production in these patients. However, patients with HCC have elevated plasma NO levels compared with patients with liver cirrhosis. These data support the concept that NO is elevated in cirrhosis and HCC, but hepatitis C infection does not appear to be responsible for the increase level of NO in these patients. The severity of liver disease may be an important factor.
4- The molecular mechanism of hepatocarcinogenesis in hepatitis C virus infection remains uncertain and needs further investigations.