Clinical and Interpretive

This test panel aids in the differential diagnosis of recent acute hepatitis.

Hepatitis A:
Hepatitis A virus (HAV) is an RNA virus (enterovirus) that accounts for 20% to 25% of viral hepatitis in US adults. HAV infection is spread by the oral/fecal route and produces acute hepatitis, which follows a benign, self-limited course. The spread of the disease is usually associated with contaminated food or water caused by poor sanitary conditions. Outbreaks frequently occur in overcrowded situations and in institutions or high-density centers such as prisons and health care centers. Epidemics may occur following floods or other disaster situations. Chronic carriers of HAV have never been observed. Antibody against hepatitis A antigen is usually detectable by the onset of symptoms (usually 15-45 days after exposure). The initial antibody consists almost entirely of IgM subclass antibody. Antibody to hepatitis A virus (anti-HAV) IgM usually falls to undetectable levels 3 to 6 months after infection.

Hepatitis B:
Hepatitis B virus (HBV) is a DNA virus that is endemic throughout the world. The infection is spread primarily through percutaneous contact with infected blood products (eg, blood transfusion, sharing of needles by drug addicts). The virus is also found in virtually every type of human body fluid and is known to be spread through oral and genital contact. HBV can be transmitted from mother to child during delivery through contact with blood and vaginal secretions; it is not commonly transmitted transplacentally. After a course of acute illness, HBV persists in approximately 10% of patients. Some of these chronic carriers are asymptomatic; others develop a chronic liver disease, including cirrhosis and hepatocellular carcinoma. Hepatitis B surface antigen (HBsAg) is the first serologic marker appearing in the serum 6 to 16 weeks following hepatitis B virus (HBV) infection. In acute cases, HBsAg usually disappears 1 to 2 months after the onset of symptoms. Hepatitis B surface antibody (anti-HBs) appears with the resolution of HBV infection after the disappearance of HBsAg. Anti-HBs also appears as the immune response following a course of inoculation with the hepatitis B vaccine. Initially, hepatitis B core antibody (anti-HBc) consists almost entirely of the IgM subclass. Anti-HBc, IgM can be detected shortly after the onset of symptoms and is usually present for 6 months. Anti-HBc may be the only marker of a recent HBV infection detectable following the disappearance of HBsAg, and prior to the appearance of anti-HBs, ie, window period.

Hepatitis C:
Hepatitis C virus (HCV) is an RNA virus that is a significant cause of morbidity and mortality worldwide. HCV is transmitted through contaminated blood or blood products or through other close, personal contacts. It is recognized as the cause of most cases of posttransfusion hepatitis. HCV shows a high rate of progression (>50%) to chronic disease. In the United States, HCV infection is quite common, with an estimated 3.5 to 4 million chronic HCV carriers. Cirrhosis and hepatocellular carcinoma are sequelae of chronic HCV. Hepatitis C virus antibody (anti-HCV) is usually not detectable during the early months following infection and is almost always detectable by the late convalescent stage of infection. Anti-HCV is not neutralizing and does not provide immunity.

If HBsAg, anti-HAV (IgM), and anti-HCV are negative and patient’s condition warrants, consider testing for Epstein-Barr virus or cytomegalovirus.

Consider administration of immune globulin to individuals exposed to patients with hepatitis A.

Consider administration of hepatitis B immune globulin and/or hepatitis B vaccine to individuals exposed to hepatitis B patient’s blood or body fluids.