Hepatitis B (HBV) is a blood-borne virus and one of the most common infectious diseases in the world.
Epidemiology
Incidence – about 50,000/year
Transmission
Parenteral
Sexual
Perinatal vertical
Horizontal – from chronically infected person in a household
Organism
Eight HBV subgroups (A-H) based on genetic differences
Genotype may be associated with disease progression
Not directly cytotoxic to hepatocytes
Severity of injury is modulated by host immune responses
Risk Factors
Intravenous drug abusers
Multiple sex partners (more than 1 partner during the preceding 6 months)
Men who have sex with men
Infants of infected mothers
Persons infected with human immunodeficiency virus (HIV)
High rates of HBV infection continue to occur among Alaska Native and Pacific Islander children and among children residing in households of first-generation immigrants from countries where HBV infection is endemic
Clinical Presentation
Acute HBV
Approximately 50% of the people who are infected will have symptoms which usually appear within 25 to 180 days following exposure
The mildest attacks are asymptomatic and detectable only by an increase in serum transaminase levels
Influenza-like symptoms – fatigue, malaise, fever
Jaundice and gastrointestinal symptoms
A few develop acute fulminant hepatic failure requiring transplantation
Chronic HBV
Phases of infection
Immune tolerance
Immune clearance
Inactive carriers
Reactivation
Infants and young children are at the greatest risk for becoming chronically infected if exposed to the hepatitis B virus
90% of exposed infants will develop chronic hepatitis
30% of exposed children ages 1-5 will develop chronic hepatitis
Only 5% of exposed adults will develop chronic hepatitis
Most common findings are fatigue and modestly elevated transaminases
Patients may have systemic symptoms that are associated with the deposition of circulating hepatitis B antigen-antibody immune complexes such as arthritis, leukocytoclastic vasculitis, glomerulonephritis, cryoglobulinemia and generalized vasculitis
Long-term consequences include cirrhosis and hepatocellular carcinoma
Diagnose chronic hepatitis B infection; order along with HBV surface antigen and HBV surface antibody
This assay tests for IgG and IgM antibodies but does not differentiate between them
Approximately 1% of blood donors will have a positive anti-HBc and negative HBsAg These donors should be further evaluated by measuring anti-HBs; however, most of these donors will have a negative anti-HBs
Monitor hepatitis B therapy; order along with HBV DNA, HBV surface antigen, HBV surface antibody and HBe antibody
Hepatitis B Virus DNA Ultrasensitive Quantitative Real-Time PCR 0056025
Method: Real-Time Polymerase Chain Reaction
Monitor hepatitis B therapy; order along with HBV surface antigen, HBV surface antibody, HBe antigen and HBe antibody
Monitor patients who were infected with hepatitis B virus prior to liver transplantation
A result of less than 40 HBV IU/mL does not rule out the presence of PCR inhibitors in the patient specimen or HBV DNA concentrations below the limit of detection by the assay
Acute HBV infection, follow to determine resolution
positive
negative
HBV infection (could be chronic), consider possibility of contamination
negative
positive
HBV infection, probably resolving
negative
negative
Not HBV infection, consider other forms of hepatitis (A, C, E), CMV, EBV and others
Guidelines
(1) Chronic hepatitis B. (2) Corrections to AASLD guidelines on chronic hepatitis B. American Association for the Study of Liver Diseases - Private Nonprofit Research Organization. 2001 Dec (revised 2007 Feb; addendum released 2007 Jun). Original guideline: 25 pages; Addendum: 1 page. NGC:005652
(Link to NGC)
Hepatitis B virus. New York State Department of Health - State/Local Government Agency [U.S.]. 2003 Mar (revised 2004 Sep). 12 pages. NGC:004534
(Link to NGC)
Screening for hepatitis B virus infection: recommendation statement. United States Preventive Services Task Force - Independent Expert Panel. 1996 (revised 2004 Feb 24). 4 pages. NGC:003453
(Link to NGC)
General References
Bowden S.Serological and molecular diagnosis.Semin Liver Dis. 2006;26(2):97-103. (Link to PubMed)
Chu CJ, Lok AS.Clinical utility in quantifying serum HBV DNA levels using PCR assays.J Hepatol. 2002;36(4):549-551. (Link to PubMed)
Ganem D, Prince AM.Hepatitis B virus infection--natural history and clinical consequences.N Engl J Med. 2004;350(11):1118-1129. (Link to PubMed)
Gish RG, Locarnini SA.Chronic hepatitis B: current testing strategies.Clin Gastroenterol Hepatol. 2006;4(6):666-676. (Link to PubMed)
References from the ARUP Institute for Clinical and Experimental Pathology®
Konnick EQ, Erali M, Ashwood ER, Hillyard DR.Evaluation of the COBAS amplicor HBV monitor assay and comparison with the ultrasensitive HBV hybrid capture 2 assay for quantification of hepatitis B virus DNA.J Clin Microbiol. 2005;43(2):596-603. (Link to PubMed)
La'ulu SL, Roberts WL.The analytic sensitivity and mutant detection capability of six hepatitis B surface antigen assays.Am J Clin Pathol. 2006;125(5):748-751. (Link to PubMed)
Reviewed by
Ashwood, Edward R., M.D. Senior Vice President, Director of Laboratories and Chief Medical Officer at ARUP Laboratories; Professor of Pathology, University of Utah
Hillyard, David R., M.D. Medical Director, Molecular Infectious Diseases at ARUP Laboratories; Associate Professor, Pathology, University of Utah
Comprehensive Review: September 2007
Last Update: November 2007