Alcoholic and virus C hepatitis currently represent the main causes of chronic liver disease
worldwide. Every year many people die and are subjected to complex hospitalization and medical
assistance due to these pathologies. Alcoholic liver disease and hepatitis C virus chronic infection are
often present in the same patient. These two pathologies sinergically act in determining the onset and
progression of liver damage that, from the chronic hepatitis staging, may rapidly progress to fibrosis,
cirrhosis and hepatocellular carcinoma. In this review we analysed physiopathological aspects and biomolecular
interactions that relate ethanol and hepatitis C virus in determining liver damage; moreover we took into account the effect
on the natural history of liver disease deriving from the co-presence of these pathologies. Therefore we paid particular
attention to the ability of ethanol and hepatitis C virus to in inducing oxidative stress or lipid accumulation, and analyzed
the basic mechanisms of fibrogenesis that both diseases have got, amplified by their co-presence in the same patient.
Finally we paid attention to the oncogenetic mechanisms inducing hepatocellular carcinoma and variability of response to
antiviral therapy that derives from alcohol abuse in a subject affected by C hepatitis.
Keywords: Antiviral therapy, ethanol, hepatitis C virus, hepatocellular carcinoma, liver chirrosis, oxidative stress.
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