Hépatite chronique virale C

Abstract

The hepatitis C virus (HCV) is a common cause of cirrhosis and hepatocellular carcinoma, as well as the most common reason for liver transplantation. HCV transmission occurs through exposure to infected blood (blood transfusion before 1990), injection drug users. Publications have implied that up to 40% of HCV seropositives do not have recognized parenteral risk factors. After contamination, 50 à 80% of patients do not clear virus, but develop chronic hepatitis C. HCV is a RNA virus; the rate of viral is high (10 12 virious per day) and the turnover of virus is rapid, the half-life of 2 to 3 hours. The diagnosis of chronic hepatitis C is based on both anti-HCV detection using enzyme immunoassays (EIA) and HCV RNA detection using a polymerase chain reaction (PCR) method. The HCV genotype (numbered 1 to 6) should be determined before treatment. The chronic sequelae of hepatitis C include progressive hepatic fibrosis, cirrhosis and hepatocellular carcinoma. In the majority of patients with chronic hepatitis C, the progression of fibrosis is insidious and slow. The factors associated with rapid progression of fibrosis are excessive alcohol consumption, older age, viral co-infection, immune deficiency, overweight. Liver biopsy provides a unique source of information on fibrosis, but significant progress has been made in the non invasive assessment of hepatitis fibrosis. Treatment is recommanded for patients with on risk of developing cirrhosis, characterized by bridging fibrosis. Combinaison therapy (peg interferon and ribavirine) should be used in the treatment of hepatitis C. Choise of duration of therapy and dose of ribavirin be based on HCV genotype. Patients with genotype 1 achieve sustained virological response of 45 à 50%, compared with rates of 80% with genotypes 2 or 3.