Interpretive Handbook

Test 9022 :
Acute Hepatitis Profile

Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test

Hepatitis A:

Hepatitis A virus (HAV) is an RNA virus (enterovirus) that accounts for 20% to 25% of the 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. 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:

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 chronic liver disease, including cirrhosis and hepatocellular carcinoma.


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.


See Advances in the Laboratory Diagnosis of Hepatitis C (2002) in Publications, and HBV Infection-Diagnostic Approach and Management Algorithm and Testing Algorithm for the Diagnosis of Hepatitis C in Special Instructions.

Useful For Suggests clinical disorders or settings where the test may be helpful

The differential diagnosis of recent acute hepatitis

Interpretation Provides information to assist in interpretation of the test results

Hepatitis A:

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 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.


See HBV Infection-Diagnostic Approach and Management Algorithm in Special Instructions.


Hepatitis C:

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.


See Advances in the Laboratory Diagnosis of Hepatitis C (2002) in Publications and Testing Algorithm for the Diagnosis of Hepatitis C in Special Instructions.

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 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.


Positive hepatitis B surface antigen (HBsAg) and/or positive hepatitis A virus antibody (anti-HAV) IgM test results should be reported by the attending physician to the State Department of Health, as required by law in some states.


Performance characteristics have not been established for the following specimen characteristics:

-Grossly icteric (total bilirubin level of >15 mg/dL)

-Grossly lipemic (triolein level of >3,000 mg/dL)

-Grossly hemolyzed (hemoglobin level of >500 mg/dL)

-Containing particulate matter

-Cadaveric specimens

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.













Interpretation depends on clinical setting. See Viral Hepatitis Serologic Profile in Special Instructions.

Clinical References Provides recommendations for further in-depth reading of a clinical nature

1. Lemon SM: Type A viral hepatitis: epidemiology, diagnosis, and prevention. Clin Chem 1997;43:1494-1499

2. Marcus EL, Tur-Kaspa R: Viral hepatitis in older adults. J Am Geriatr Soc 1997;45:755-763

3. Mahoney FJ: Update on diagnosis, management, and prevention of hepatitis B virus infection. Clin Microbiol Rev 1999;12:351-366