Hepatitis: Clinical Features and Treatment

Abstract There are five hepatitis viruses, A–E. Hepatitis A and E are enterically transmitted, cause an acute hepatitis, often asymptomatic, rarely fulminant and never resulting in chronic infection. The vaccine for prevention of hepatitis A infection is well established and the vaccine against hepatitis E is currently completing clinical evaluation in field trials. Hepatitis B causes acute and chronic hepatitis, the latter resulting in cirrhosis and hepatocellular carcinoma. Infection in adult life is usually the result of sexual activity or IV drug use, results in a symptomatic self‐limiting illness and causes chronic infection in 5–10% of cases. Infection at birth or in utero invariably results in chronic infection. The chronic infection requires treatment with either pegylated interferon or nucleoside analogues, if there is evidence of continuing hepatitis B virus (HBV) replication (HBV DNA >10 5 genomes mL −1 ) and evidence on liver biopsy of significant liver disease. Hepatitis D co‐infection or super‐infection is seen in some cases of HBV infection and generally results in more rapidly progressive disease. Hepatitis C causes acute self‐limiting hepatitis in 30–40% of cases, usually after parenteral transmission as a result of inadequate sterilization of medical equipment, IV drug use or rarely after blood transfusion in countries where adequate testing of donations is not undertaken. Sexual and neonatal transmission are rare. Most cases of chronic infection develop some degree of hepatitis and fibrosis over several decades and those with cirrhosis are at risk of developing hepatocellular carcinoma. Treatment with pegylated interferon and ribavirin produces a sustained viral response with resolution of the liver disease (cure) in 50–60% of cases with 6–12 months treatment. Response rates vary from 40% in genotypes 1 and 4 to 80% in genotypes 2 and 3.