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  1. Carol A Seymour, professor of clinical biochemistry and metabolisma
  1. aSt George's Hospital Medical School, London SW17 ORE
  • Accepted 13 February 1996

The case for

In some respects hepatitis C is hepatitis B revisited. Years after the discovery of hepatitis B virus and 11 years after development of a safe, efficacious vaccine, consensus has emerged in the international health community that decisive global action against hepatitis B is a necessity.1 Those who doubt that a similar approach will be needed towards hepatitis C point to a relative lack of knowledge of the clinical course of hepatitis C and the efficacy of treatment.

In 1989 hepatitis C virus was cloned and characterised as a positive sense, single stranded RNA genome containing 9400 nucleotides. It is a major cause of post-transfusion hepatitis2; up to 50% of patients commonly progress to chronic hepatitis and 20% to cirrhosis with secondary complications such as hepatocellular carcinoma.3 A problem arises because hepatitis C may have a progressive course to chronic disease occurring over decades, during which time the individual may be symptom free and the disease remain undiagnosed until the patient presents with liver disease or its complications.2 3

Likely size of the problem

In the United States 3.5 million people are estimated to have chronic hepatitis C; of these, 8000-10000 die of liver related complications and 1000 undergo liver transplantation.4 Around 23% of patients given a transplant had hepatitis C virus, and 19% of those given transplants for seronegative cryptogenic cirrhosis developed hepatitis C after transplantation.4 5 Prevalence is similar in Europe and higher in Japan and other eastern countries.

The hepatitis C virus is transmitted parenterally through blood, blood products, injecting drug misuse, and tattooing, as well as by sexual6 and household transmission. Serological identification of hepatitis C virus by second and …

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