Résumé
Egypt has a high prevalence of hepatitis C virus [HCV] infection, resulting in a high morbidity and mortality from chronic hepatitis, cirrhosia, and hepathocellular carcinoma. It is unclear why some patients with HCV infection do better than others with the same physical and epidemiological characteristics, Recently, environmental pollution was accused in many chronic diseases including liver disease. We designed this study to clarify the impact of heavy metals and oxidative stress in cigarette smoke on liver disease in HCV patients. Fifty male Egyptian patients with positive HCV-RNA were studied. Twenty-five of them were smokers with an average smoking index of 183.16 and the other 53 were non-smokers. Both groups were matched as regards age and have no home or occupational exposure to heavy metals. The antioxidant defense system of erythrocytes, liver function tests, serum trace elements, and serum heavy metals were measured for all patients. A significant increase in serum cadmium and lead was found in smoker patients. Also, the liver enzymes [alanine aminotranserferase; ALT, aspartate aminotranseferase; AST, and alkaline phosphatase; ALP], were significantly elevated in the serum of smoker patients. The histologic activity index [HAI] was higher in smokers than non-smoker patients, but the difference was statistically non-significant. On the other hand, a significant decrease in serum albumin and serum selenium was found in smoker patients. Also, the activities of the antioxidant enzymes in the erythrocytes [glutathione reductase; GR, superoxide dismutase; SOD, catalase; CAT, and reduced glutathione; GSH] were significantly lower in smoker than non-smoker patients. The results of this study concluded that patients with hepatitis C should be informed about the possible hepatotoxsicity of heavy metals and oxidants in cigarette smoke and advised to quit smoking as a part of their life style modification. Further studies are encouraged to discover other aspects of tobacco toxicities on the human liver and the pathogenesis of this potential harmful effect