Hepatitis C is one of the hepatotrophic viruses, which predominantly causes a chronic hepatitis.
Common worldwide. Carrier rate of 0.2% in northern Europe.
Five per cent carrier rate in Far East; 1–2% in Mediter-ranean.
ssRNA virus of the flavivirus group. It was discovered in 1988 as being the most common cause of non-A, non-B hepatitis, particularly in blood transfusion recipients. The main route of HCV transmission is parenteral, most patients will give a history of either intravenous drug abuse or a blood/blood product transfusion prior to testing. There is some evidence of sexual transmission, which may be facilitated by coinfection with HIV. Vertical transmission may occur especially if the mother is HIV positive or has a high viral load.
Less than 10% of patients have an acute flulike illness with jaundice, the remainder are asymptomatic at the time of infection. Very rarely hepatitis C can cause fulminant hepatic failure. Following infection most patients develop chronic hepatitis C, which predisposes to cirrhosis and hepatocellular carcinoma. Chronic hepatitis C is often asymptomatic but may cause fatigue, myalgia, nausea, anorexia and right upper quadrant pain. Symptoms and signs of chronic liver disease occur years after initial infection.
Lymphocytic infiltration within the vascular sinusoids. Fatty change is seen in the hepatocytes, with little active hepatocellular necrosis.
Chronic active hepatitis may be associated with autoimmune hepatitis, Sjogren’s syndrome, lichen planus, thyroiditis, membranous glomerulonephritis, polyarteritis nodosa and mixed essential cryoglobulinemia.
Seroconversion occurs several months after infection, but anti-HCV is found in chronic sufferers of hepatitis, carriers (using ELISA) and those who have recovered from infection.
Acute infection is diagnosed by the presence of HCV RNA in the serum, using PCR. A positive PCR indicates current viraemia whereas a negative test with positive anti-HCV antibodies suggests non-viraemic infection, transient absence of viraemia or recovered infection. Quantification of the viral load may be of use in tailoring treatment.
Liver biopsy is used for assessing liver inflammation, potential progression of fibrosis and the presence or absence of cirrhosis.
Counselling regarding transmission is essential. In acute infection supportive treatment may be necessary. Combination therapy with pegylated interferon α and ribavirin is recommended for the treatment of people aged 18 years and over with moderate to severe chronic hepatitis C (histological evidence of significant scarring and/or significant necrotic inflammation). If ribavirin is contraindicated or not tolerated, pegylated interferon αmonotherapy should be used. Patients with severe cirrhosis may require liver transplantation. There is no available vaccine.