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Unit Code 9022:
Acute Hepatitis Profile

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Useful For

The differential diagnosis of recent acute hepatitis

Clinical Information

Hepatitis A

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 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

over-crowded 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, e.g., 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 "Recommended Approach to the Diagnosis

and Monitoring of Patients with Hepatitis C Virus" in Special Instructions.

Reference Values

HEPATITIS B SURFACE ANTIGEN

      Negative

HEPATITIS A IGM ANTIBODY

      Negative

HEPATITIS B CORE ANTIBODY, IgM, (ANTI-HBc, IgM)

      Negative

HEPATITIS C  VIRUS ANTIBODY (ANTI-HCV)

      Negative

Interpretation depends on clinical setting. See "Viral Hepatitis

Serologic Profile" in Special Instructions.

Interpretation

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. 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 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,

i.e., window period.

 

Hepatitis C

Hepatitis C antibody is usually not detectable during the early

months following infection and is almost always detectable by the

late convalescent stage of infection. Hepatitis C antibody 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 "HBV Infection-Diagnostic Approach and

Management Algorithm" and "Recommended Approach to the Diagnosis

and Monitoring of Patients with Hepatitis C Virus" in Special Instructions.

Cautions

Consider administration of immune globulin to individuals

exposed to patients with hepatitis A.

  

Consider administration of hepatitis B immune globulin (HBIG)

and/or hepatitis B vaccine to individuals exposed to hepatitis B

patient's blood and/or body fluids.

 

Positive HBsAg and/or positive 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 >20 mg/dL)

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

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

-  Containing particulate matter

-  Cadaveric specimens

Special Instructions and Forms

• Viral Hepatitis Serologic Profile 
• HBV Infection-Diagnostic Approach and Management Algorithm 
• Recommended Approach to the Diagnosis and Monitoring of Patients with Hepatitis C 

Clinical Reference

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

Key