Acute Hepatitis Screen (unknown etiology)

Reporting Name


Overview

Determination of the etiological agent of acute hepatitis.

 

Useful For

Determination of an infectious cause of acute hepatitis

 

Profile Information

Acute Unknown Hepatitis Screen Available separately Always performed

HBsAg

NO YES

HBsAg Neutralization

NO NO

Anti-HBs

YES YES

Anti-HBc IgM

NO YES

Anti-HCV

YES YES

Anti-HAV IgM

YES YES

 

Reflex Tests

Reporting Name Available separately Always performed

HBsAg Confirmation (neutralization)

NO NO*

* Autoreflex of HBsAg-reactive to HBsAg Neutralization Confirmation

 

 

Testing Algorithm

Specimens submitted for Acute Unknown Hepatitis Screen will be tested for hepatitis B surface antigen with autoreflex neutralization confirmation (HBsAg); hepatitis B surface antibody (Anti-HBs); hepatitis B core IgM (Anti-HBc IgM); hepatitis C antibodies (Anti-HCV); and hepatitis A IgM (Anti-HAV IgM).

 

Hepatitis Algorithm

 

Indications for Testing

Acute onset hepatitis of unknown etiology

 

Special Instructions and Forms

Hepatitis Algorithm

Hepatitis Interpretive

 

Method Name

Chemiluminescent Microparticle Immunoassay (CMIA)

 

Reporting Name

HBsAg

Anti-HBs

Anti-HBc IgM

Anti-HCV

Anti-HAV IgM

 

Aliases

Hepatitis

Jaundice

Specimen Required

Serology: Blood in SST. Allow blood to clot at room temperature for 30 minutes and centrifuge. Do not separate serum. Maintain at 2-8°C and transport on ice packs.

 

Specimen Minimum Volume

0.6ml SERUM

 

Transport Temperature

Specimen Room temperature Refrigerated Frozen
Serum NO YES* YES**

*The samples should be stored for not more than 3 days at 2-8°C.

**For longer delay, freeze at -70°C and transport on dry ice.

 

Reject Due To

Specimens other than Serum
Anticoagulants OK
Hemolysis OK
Lipemia OK
Icteric OK

Useful For

Determination of an infectious cause of acute hepatitis

 

Clinical Information

Acute viral hepatitis can be caused by any of 5 hepatotropic viruses: hepatitis A and hepatitis E viruses are transmitted enterically and do not cause chronic hepatitis, hepatitis viruses B, C and D are transmitted parenterally and have the ability to cause chronic hepatitis. Other viruses that can cause hepatic inflammation include Epstein-Barr virus (EBV), herpes simplex virus (HSV), mumps, rubella, varicella-zoster virus, yellow fever virus, coxackie B virus, and adenovirus. Although these viruses can cause diagnostic confusion by producing liver inflammation and dysfunction, they are not primary causes of acute or chronic viral hepatitis. Clinical features of acute symptomatic viral hepatitis are common to all forms of viral hepatitis. There are no clinical features that unequivocally distinguish the individual types of hepatitis from each other; however, there are certain epidemiological patterns of transmission that may suggest a particular virus.

 

Hepatitis B virus (HBV) causes a wide spectrum of manifestations ranging from asymptomatic seroconversion, sub-acute illness with non-specific symptoms (e.g. anorexia, nausea, or malaise) or extrahepatic symptoms, and clinical hepatitis with jaundice, to fuliminant fatal hepatitis. Only 10% of children and 50% of adults will exhibit symptoms. An acute illness may last up to three months with a fatality of 1-2%. In most acute cases HBsAg serum levels are positive initially, resolve and the individual develops anti-HBs which confers immunity. HBV occurs worldwide, and is endemic in some Asian countries. In Canada the incidence of acute hepatitis B is estimated to be 2.3 per 100,000. In developed countries exposure to HBV may be common in certain high-risk groups such as injection drug users, person who have multiple sex partners, men who have sex with men, sex with HBV-infected persons and having a hepatitis B carrier in the family. The prevalence of chronic hepatitis B varies in different populations.

 

Hepatitis C virus (HCV) infected people are asymptomatic with onset of disease being insidious. Symptoms range from anorexia, fatigue, fever, myalgia, nausea and vomiting progressing to jaundice. More than 50% of those infected will develop chronic HCV infection. Of those chronically infected about half will develop cirrhosis or cancer of the liver. HCV is recognized as the cause of most cases of post-transfusion hepatitis and is a significant cause of morbidity and mortality worldwide. HCV infection has been reported in virtually every country where it has been carefully evaluated, suggesting that HCV, unlike HIV, has a long-standing global distribution. Occurrence of HCV worldwide is directly related to the prevalence of people who routinely share injection equipment. Approximately 250,000 Canadians are infected with HCV. In Newfoundland and Labrador in 2006 there were 90 cases of HCV reported with a calculated incidence rate of 17.8 per 100,000. The risk factor most commonly reported is injection drug use.

 

Hepatitis A virus (HAV) infection characteristically is an acute, self-limited illness associated with fever, malaise, jaundice, anorexia, and nausea. Among older children and adults, infection usually is symptomatic and typically lasts several weeks, with jaundice occurring in 70% or more. Symptomatic infection occurs in approximately 30% of infected children younger than 6 years of age; few of these children will have jaundice. Fulminate hepatitis is rare but is more common in people with underlying liver disease. Chronic infection does not occur. Hepatitis A virus (HAV) is endemic throughout the world, occurring most commonly in areas of poor hygiene and low socioeconomic conditions. The virus is transmitted by the fecal-oral route, and
it is spread by close person-to-person contact and by contaminated food and water. Thorough cooking is necessary to inactivate HAV in contaminated foods. Outbreaks frequently occur in overcrowded situations and in high-density institutions and centers, such as prisons and health care or day care centers. Viral spread by parenteral routes (eg, exposure to blood) is possible but rare, because infected individuals are viremic for a short period of time (usually <3 weeks). There is little or no evidence of transplacental transmission from mother to fetus or transmission to newborn during delivery.

 

Reference Values

NONREACTIVE

 

Interpretation

Special instructions, Hepatitis Interpretive

 

Special instructions,  Pediatric HCV Interpretation

 

Clinical Reference

Anderson, D. A. 2007. Hepatitis A and E Viruses, p. 1424-1436. In Murray, P. R., Baron, E. J., Jorgensen, J. H., Landry, M. L., and Pfaller, M. A. Manual of Clinical Microbiology, 9th ed., vol. 2. ASM Press, American Society for Microbiology, Washington, DC.

 

Curry, M. P., and Chopra, S. 2010. Acute Viral Hepatitis, p. 1577-1592. In Mandell, D., Bennett, J. E., and Dolin, R. Principles and practice of infectious diseases, 7th ed., vol. 2. Churchill Livingstone, Elsevier, Philadelphia, PA.

Curry, M. P., and Chopra, S. 2010. Acute Viral Hepatitis, p. 1577-1592. In Mandell, D., Bennett, J. E., and Dolin, R. Principles and practice of infectious diseases, 7th ed., vol. 2. Churchill Livingstone, Elsevier, Philadelphia, PA.

 

Horvat, R. T., and Tegtmeier, G. E. 2007. Hepatitis B and D Viruses, p. 1641-1659. In Murray, P. R., Baron, E. J., Jorgensen, J. H., Landry, M. L., and Pfaller, M. A. Manual of Clinical Microbiology, 9th ed., vol. 2. ASM Press, American Society for Microbiology, Washington, DC.

James Koziel, M., and Thio, C. L. 2010. Hepatitis B Virus and Hepatitis Delta Virus, p. 2059-2086. In Mandell, D., Bennett, J. E., and Dolin, R. Principles and practice of infectious diseases, 7th ed., vol. 2. Churchill Livingstone, Elsevier, Philadelphia, PA.

 

Ray, S. C., and D. L. Thomas. 2010. Hepatitis C, p. 2157-2185. In Mandell, D., Bennett, J. E., and Dolin, R. Principles and practice of infectious diseases, 7th ed., vol. 2. Churchill Livingstone, Elsevier, Philadelphia, PA.

 

Scott, J. D., and Gretch, D. R. 2007. Hepatitis C and G Viruses, p. 1437-1452. In Murray, P. R., Baron, E. J., Jorgensen, J. H., Landry, M. L., and Pfaller, M. A. Manual of Clinical Microbiology, 9th ed., vol. 2. ASM Press, American Society for Microbiology, Washington, DC.

 

Sherman, M., S. Shafran, K. Burak, et al. 2007. Management of chronic hepatitis C: Consensus guidelines. Can J Gastroenterol 21:25C-34C.

 

Wasley, A., Feinstone, S. M, and Bell, B. P. 2010. Hepatitis A Virus, p. 2367-2387. In Mandell, D., Bennett, J. E., and Dolin, R. Principles and practice of infectious diseases, 7th ed., vol. 2. Churchill Livingstone, Elsevier, Philadelphia, PA.

 

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