Hepatitis B Surface Antigen
CPT Test code: 87340
|Test Includes:||Confirmation of a positive result by a neutralization assay at no additional charge|
|Specimen:||Serum or plasma|
|Minimum Volume:||1.5 mL (Note: This volume does not allow for repeat testing.)|
|Container:||Red-top tube, gel-barrier tube, or lavender-top (EDTA) tube|
|Collection:||If tube other than a gel-barrier tube is used, transfer separated serum or plasma to a plastic transport tube.|
|Causes for Rejection:||Non-EDTA plasma specimen; PST gel-barrier tube|
|Use:||Test blood donors (HBsAg positive individuals are rejected). Hepatitis B surface antigen is the earliest indicator of the presence of acute infection. Also indicative of chronic infection. Test is useful in the differential diagnosis of hepatitis.|
|Limitations:||Patients who are negative for HBsAg may still have acute type B viral hepatitis. There is sometimes a “core window” stage when HBsAg has become negative and the patient has not yet developed the antibody (anti-HBs). On such occasions, both tests for anti-HBc are usually positive and anti-HBc, IgM is the only specific marker for the diagnosis of acute infection with hepatitis B. In cases with strong clinical suspicion of viral hepatitis, serologic testing should not be limited to detecting HBsAg, but should include a battery of tests to evaluate different stages of acute and convalescent hepatitis.|
|Additional Information:||Hepatitis B virus (HBV) is a DNA virus with a protein coat, the surface antigen (HBsAg) and a nucleic acid core, the core antigen (HBcAg). There are eight different serotypes. Early in infection, HBsAg, HBV DNA, and DNA polymerase can all be detected in serum.
HBsAg can be detected one to seven weeks before liver enzyme elevation or the appearance of clinical symptoms. Three weeks after the onset of acute hepatitis, about 50% of patients will still be positive for HBsAg, while at 17 weeks only 10% are positive. The best available markers for infectivity are HBsAg and HBeAg. The presence of anti-HBs is frequently associated with noninfectivity. The chronic carrier state is indicated by the persistence of HBsAg and/or HBeAg over long periods (six months to years) without seroconversion to the corresponding antibodies. Such a condition has the potential to lead to serious liver damage, but may be an isolated asymptomatic serologic phenomenon.
Persistence of HBsAg, without anti-HBs, with combinations of positivity of anti-HBc, HBeAg, or anti-HBe indicates infectivity and need for investigation for chronic persistent or chronic aggressive hepatitis. See figure in Hepatitis B Core Antibody, IgM .
|References:||Edwards MS. Hepatitis B serology-Help in interpretation.Pediatr Clin North Am. 1988; 35(3):503-515 (review). PubMed 3287312
Favero MS, Maynard JE, Leger RT, et al. Guidelines for the care of patients hospitalized with viral hepatitis. Ann Intern Med. 1979; 91(6):872-876. PubMed 517890
Lee HS, Vyas GN. Diagnosis of viral hepatitis. Clin Lab Med. 1987; 7(4):741-757 (review). PubMed 3319367
Mushahwar IK, Dienstag JL, Polesky HF, et al. Interpretation of various serological profiles of hepatitis B virus infection. Am J Clin Pathol. 1981; 76(6):773-777.PubMed 7315794