Hepatitis B Surface Antigen, Quantitative, Monitor

CPT: 87467
Updated on 07/3/2024


  • Quantitative HBsAg
  • Quantitative HBV surface antigen
  • Quantitative Hepatitis B Virus Surface Antigen

Expected Turnaround Time

5 - 8 days

3 - 6 days

5 - 8 days

Related Documents

Specimen Requirements


Serum (preferred) or plasma, frozen


2 mL

Minimum Volume

1 mL (Note: This volume does not allow for repeat testing.)


Gel-barrier tube, PPT™ tube or lavender-top (EDTA) tube

Gel-barrier tube, PPT™ tube or lavender-top (EDTA) tube

Gel-barrier tube, PPT™ tube or lavender-top (EDTA) tube

Gel-barrier tube, PPT™ tube or lavender-top (EDTA) tube

Gel-barrier tube, PPT™ tube or lavender-top (EDTA) tube


Draw blood in either a serum gel tube, a PPT™ or a lavender-top (EDTA) tube and centrifuge. If tube other than a gel-barrier tube is used, transfer separated serum or plasma to a plastic transport tube (not a "pop-top" or "snapcap"). Specimen must be refrigerated immediately and frozen within 3 hours of collection.

Storage Instructions

Freeze at -20°C and ship frozen.

Freeze at -20°C and ship frozen.

Freeze at -20°C and ship frozen.

Stability Requirements



Room temperature



< 3 hours


14 days

Freeze/thaw cycles

Stable x5

Causes for Rejection

Incorrect anticoagulant; PPT™ or gel-barrier tube not centrifuged

Test Details


Quantitative HBV surface antigen (HBsAg) testing is intended for use in individuals with a confirmed diagnosis of Hepatitis B Virus infection based on positive HBsAg, Anti-HBs antibody and/or Anti-core antigen (anti-HBc) antibody test results. Quantitative HBsAg testing has utility in assessing HBV replication in the absence and presence of antiviral therapy, which may inform monitoring treatment response and relapse in the setting of initial and prolonged antiviral therapy, respectively. Recent studies indicate that rapid decay and loss of HBsAg expression are strong predictors of sustained HBV clearance.


Quantitative HBsAg testing is not intended for the diagnosis of HBV infection. The relationship between HBsAg levels and ongoing HBV replication and/or persistent infection has not been fully defined. HBV DNA viral load measurements reflect the extent of ongoing HBV replication. HBsAg levels reflect the transcription and trranslational expression of HBV DNA. The clinical ramifications of detectable levels of HBsAg in the absence of detectable levels of HBV DNA are the subject of ongoing investigation.


Immunochemiluminometric assay (ICMA)

Additional Information

Hepatitis B is an infectious disease caused by Hepatitis B Virus (HBV). Worldwide, more than 350 million persons are chronically infected with HBV. Chronic HBV infection often leads to premature death as a result of liver cirrhosis and cancer. An estimated 3,000 to 4,000 persons die of hepatitis B-related cirrosis each year in the United States. The risk of hepatocellular carcinoma is significantly higher in persons with chronic HBV infection, which results in 1,000 to 1,500 deaths each year in the United States.

HBV virions consist of a DNA genome that is packaged within an icosahedral nucleocapsid, comprised of core antigen (HBcAg), surrounded by a lipid envelope containing surface antigens (HBsAg). There are four distinct HBV serotypes (adr, adw, ayr, ayw) and at least eight different genotypes (A-H).

HBV infection is characterized by the transient detection of HBsAg and HBV DNA in serum. The most reliable markers for infectivity are HBsAg and HBV "e" antigen (HBeAg). HBsAg is the first serolgic marker to appear following acute infection, with detection averaging one month after HBV exposure. HBeAg indicates active infection and the ability to spread the virus to others. Spontaneous recovery is characterized by undetectable HBsAg and HBV DNA apprximately 15 weeks after the appearance of symptoms. The presence of anti-HBs antibody is strongly associated with reduced infectivity and clearance. In contrast, the chronic carrier state is indicated by the persistence of HBsAg and/or HBeAg in the absence of seroconversion characterized by anti-HBs and/or anti-HBe antibody, respectively. This clinical condition has the potential to lead to serious liver damage, but may be an isolated asymptomatic serologic phenomenon. Persitence of HBsAg expression in the absence of anti-HBs antibody, in combination with anti-HBc, HBeAg, or anti-HBe reactivity is an indication of ongoing HBV replication and the need to investigate chronic persistent or chronic aggressive hepatitis.


Schillie S, Vellozzi C, Reingold A, et al. Prevention of Hepatitis B Virus Infection in the United States: Recommendations of the Advisory Committee on Immunization Practices. MMWR Recomm Rep. 2018 Jan 12;67(1):1-31.29939980
Seto WK, Lo YR, Pawlotski JM, Yuen MF. Chronic hepatitis B virus infection. Lancet. 2018 Nov 24;392(10161):2313-2324.30496122
World Health Organization. Global Hepatitis Report, 2017. Geneva, Switzerland: World Health Organiztion; 2017.

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