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Interpretive Handbook

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Test 86137 :
Acute Hepatitis Profile with Hepatitis C Virus Reflex

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 (an 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 results in acute hepatitis with usually 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, and sharing of needles by drug addicts. The virus is also found in all types 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, but it is not commonly transmitted transplacentally. After a course of acute illness, HBV persists in approximately 10% of patients. While 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.

 

Publications

-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

-Viral Hepatitis Serologic Profiles

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

Differential diagnosis of acute viral 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 to 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 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 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.

 

Publications

-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

 

If screening test results for hepatitis A virus, hepatitis B virus, and hepatitis C virus infection are negative in a patient with signs and symptoms consistent with acute hepatitis, consider testing for Epstein-Barr virus or cytomegalovirus as possible etiologic agents.

Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances

Positive results for hepatitis A virus IgM antibody, hepatitis B core IgM antibody, and hepatitis B surface antigen confirmation tests are required by law in many states to be reported by the patient care providers to the respective State Department of Health.

 

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

-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)

-Presence of particulate matter

-Cadaveric specimen

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

Negative

 

HEPATITIS A IgM ANTIBODY

Negative

 

HEPATITIS B CORE ANTIBODY, IgM

Negative

 

HEPATITIS C ANTIBODY SCREEN

Negative

 

Interpretation depends on clinical setting.

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

1. Nainan OV, Xia G, Vaughan G, Margolis HS: Diagnosis of hepatitis A infection: a molecular approach. Clin Microbiol Rev 2006;19:63-79

2. Servoss JC, Friedman LS: Serologic and molecular diagnosis of hepatitis B virus. Clin Liver Dis 2004;8:267-281

3. Carithers RL, Marquardt A, Gretch DR: Diagnostic testing for hepatitis C. Semin Liver Dis 2000;20(2):159-171 


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