Hepatitis Serology

Hepatitis A virus (HAV), hepatitis B virus (HBV), and less often hepatitis C virus (HCV) are the usual causes of acute viral hepatitis. A person with symptoms of acute hepatitis should have these four hepatitis serologies performed: immunoglobulin M (IgM) anti-HAV, hepatitis B surface antigen (HBsAg), IgM anti-HBc, and anti-HCV. At present, stool and blood assays for HAV antigen are not available. The diagnosis of hepatitis A is made by the detection of IgM anti-HAV during acute illness. A positive anti-HAV with only IgG anti-HAV indicates previous infection.

In hepatitis B, HBsAg is the earliest serologic marker of infection and is present before elevation of the aminotrans-ferases. If HBsAg is present for more than 6 months, the patient should be considered chronically infected (carrier). Antibodies to HBsAg (anti-HBs) indicate immunity to hepatitis B and appear several weeks to months after HBsAg disappears. The gap between the presence of HBsAg and anti-HBs is a window period; during this time antibody to hepatitis core antigen (anti-HBc) can be detected in the blood. Anti-HBc can be differentiated into an IgM anti-HBc, which indicates recent infection, and an IgG anti-HBc, which indicates previous infection. HBeAg, a subparticle of core antigen, is present only when HBsAg is present and is a marker for infectiousness. Anti-HBe appears after HBeAg disappears, indicates decreasing infectivity, a good prognosis, and remains detectable for years. HBV DNA testing can be used to follow titers in patients receiving antiviral therapy for chronic hepatitis B infection. Hepatitis delta virus (HDV) infection coexists with hepatitis B in about 4% of hepatitis B infections and carries an increased mortality rate. HDV depends on the presence of HBV for expression and replication and can cause acute or chronic infection. Previous vaccination for hepatitis B should produce a positive titer only for anti-HBs.

Hepatitis C occasionally presents as acute hepatitis, but more frequently is detected in the evaluation of patients with elevated aminotransferases or chronic liver disease. With chronic hepatitis, aminotransferases are often only mildly elevated and occasionally, normal. The diagnosis is made by detecting antibody to hepatitis C (anti-HCV). Anti-HCV does not differentiate acute from chronic infection and does not indicate immunity. In acute hepatitis C the antibody may not be detected initially, and the test may need to be repeated later to confirm infection. In a patient with abnormal liver enzymes and a risk factor for hepatitis C (e.g., injection drug use, hemophilia, history of blood transfusions before 1985), a positive anti-HCV is sufficient to make the diagnosis.

A quantitative HCV-RNA assay can be used for diagnosis of acute infection as early as 1 to 2 weeks after exposure, and before anti-HCV appears. Quantification of viral ribonucleic acid (RNA) by the reverse-transcriptase polymerase chain reaction (RT-PCR) also can confirm hepatitis C infection, as well as measure viral load. These tests are particularly useful in the absence of risk factors or abnormal liver enzymes, when antibody testing is indeterminate, or with immunodeficiency. In addition, quantification of viral RNA can assess response to treatment.

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