Previous Hepatitis Exposure Profile
Determining if an individual has been infected following exposure to an unknown type of hepatitis
Obtaining baseline serologic markers of an individual exposed to a source with an unknown type of hepatitis
Determining immunity to hepatitis A and B viral infections
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
Hepatitis A virus (HAV) is an RNA virus (enterovirus) that accounts for 20% to 25% of the viral hepatitis in United States adults. HAV infection is spread by the oral/fecal route and produces acute hepatitis that follows a benign, self-limited course. 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.
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.
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 post-transfusion 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.
-Advances in the Laboratory Diagnosis of Hepatitis C (2002)
The following algorithms are available in Special Instructions:
-HBV Infection-Diagnostic Approach and Management Algorithm
-Testing Algorithm for the Diagnosis of Hepatitis C
Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.
HEPATITIS B SURFACE ANTIGEN
HEPATITIS B SURFACE ANTIBODY, QUALITATIVE/QUANTITATIVE
Hepatitis B Surface Antibody
Hepatitis B Surface Antibody, Quantitative
Unvaccinated: <5.0 mIU/mL
Vaccinated: > or =12.0 mIU/mL
HEPATITIS B CORE TOTAL ANTIBODIES
HEPATITIS A TOTAL ANTIBODIES
HEPATITIS C ANTIBODY SCREEN
Interpretation depends on clinical setting. See Viral Hepatitis Serologic Profiles in Special Instructions.
Antibody against hepatitis A antigen (anti-HAV) is almost always detectable by the onset of symptoms (usually 15-45 days after exposure). The initial antibody consists almost entirely of the IgM subclass of antibody. Anti-HAV IgM usually falls to undetectable levels 3 to 6 months after infection. Anti-HAV, IgG levels rise quickly once the virus is cleared and persist for many years.
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.
Hepatitis B core antibody (anti-HBc) appears shortly after the onset of symptoms of HBV infection and may be the only serologic marker remaining years after exposure to hepatitis B.
Hepatitis C virus antibody (anti-HCV) is usually not detectable during the early months following infection, but is almost always detectable by the late convalescent stage of infection. Anti-HCV is not neutralizing and does not provide immunity.
Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances
Consider administration of immune globulin to the individual exposed to hepatitis A.
Consider administration of hepatitis B immune globulin and/or hepatitis B vaccine to the individual exposed to hepatitis B.
Positive hepatitis B surface antigen test results should be reported by the attending physician to the State Department of Health, as required by law in some states.
Type-specific tests should be used to evaluate individuals who have been exposed to a source with a known type of hepatitis (eg, hepatitis A, hepatitis B, hepatitis C).
Performance characteristics have not been established for the following specimen characteristics:
-Grossly icteric (total bilirubin level of >20 mg/dL)
-Grossly lipemic (triolein level of >3,000 mg/dL)
-Grossly hemolyzed (hemoglobin level of >125 mg/dL)
-Containing particulate matter
-Immunocompromised or immunosuppressed specimens
Clinical Reference Provides recommendations for further in-depth reading of a clinical nature
Hochman JA, Balistereri WF: Viral hepatitis: expanding the alphabet. Adv Pediatr 1999;46:207-243