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Viral hepatitis—clinical aspects 

Viral hepatitis—clinical aspects

Viral hepatitis—clinical aspects

H.J.F. Hodgson



Treatment of hepatitis C—discussion of new and effective treatment regimens, with links to the website giving most up-to-date recommendations.

Updated on 28 Aug 2014. The previous version of this content can be found here.
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date: 28 April 2017

There are five major hepatitis viruses—A, B, C, D, and E—with the clinical picture depending on the severity of the inflammation induced in the liver, and on whether the virus is cleared from the liver or persists long-term.

Acute icteric hepatitis, characterized by jaundice and right upper quadrant abdominal tenderness, is the commonest clinically recognized consequence of infection. This is generally a self-limited condition with low mortality and complete recovery: only hepatitis B and C have the propensity to cause chronic viral hepatitis. Typically, hepatocellular enzyme levels in blood are prominently raised at the time of the onset of symptoms, whilst the serum alkaline phosphatase level is only slightly increased. Specific diagnosis is made by serological testing for particular viruses. Uncomplicated cases recover spontaneously; there is no proven therapy to enhance recovery, but alcohol and potentially hepatotoxic drugs should be withdrawn. Fulminant hepatic failure caused by viral hepatitis has 80% mortality and should be treated (if possible) by orthotopic liver transplantation.

Protection against hepatitis A and B is available, both passive (gammaglobulin preparations) and active (vaccinations). Vaccines are not yet available for hepatitis C, but are in clinical trial for E. Vaccination against hepatitis B also protects against hepatitis D.

Features of particular hepatitis viruses

Hepatitis A virus (HAV)—faecal–oral transmission; incubation 2–6 weeks; acute self-limited hepatitis; no specific treatment.

Hepatitis B virus (HBV)—parenteral transmission; incubation 4–24 weeks; may present with acute hepatitis, with prodrome sometimes including prominent arthritis, fever, and urticarial rash, but anicteric attacks are common; most (>90%) patients clear HBV after acute infection, but failure to clear HBsAg (hepatitis B surface antigen) within 6 months defines ‘chronic carriage’, which is associated with a spectrum of histological damage and clinical manifestations ranging from being clinically silent to producing cirrhosis and hepatocellular cancer. Some patients with chronic infection will benefit from treatment with α‎-interferons and/or inhibitors of viral replication (nucleotide and nucleoside analogues).

Hepatitis C virus (HCV)—parenteral transmission; incubation 2 to 26 weeks; acute episode most often subclinical; 70% of patients fail to clear the virus and become chronic carriers, which often leads to cirrhosis after 15 to 25 years and then predisposes to hepatocellular cancer; treatment is with the combination of IFN-α‎2a or IFN-α‎2b plus ribavirin, and more recently direct anti-viral drugs.

Hepatitis D virus (HDV)—an RNA virus ‘parasitic’ on HBV, with dual infection tending to produce more severe liver disease; treatment is as for hepatitis B.

Hepatitis E virus (HEV)—faecal–oral transmission; incubation about 6 weeks; high risk of fulminant hepatitis if acquired during mid-trimester pregnancy; no specific treatment.

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