Hepatitis B Surface Antibody, Quantitative

Hepatitis B surface antibody quantitation is used to determine hepatitis B immune status, ie, to determine if the patient has developed immunity against the hepatitis B virus. Such immunity may develop following exposure to the hepatitis B virus or its vaccine.

Patients at higher risk of exposure to the virus include:

• Infants born to infected mothers
• Sex partners of infected persons
• People with more than 1 sex partner in the last 6 months
• People with a history of sexually transmitted infection
• Men who have sex with men
• Injection drug users
• Household contacts of an infected person
• Healthcare and safety workers who have contact with blood and body fluids
• People who have lived or traveled in an area in which hepatitis B is common
• People who live or work in a prison

Testing is not recommended routinely following vaccination. It is advised only for people whose subsequent clinical management depends on knowledge of their immune status. These people include:

• Chronic hemodialysis patients
• Immunocompromised people, including those with HIV infection, hematopoietic stem-cell transplant recipients, and people receiving chemotherapy
• Infants born to women who test positive for the hepatitis B surface antigen
• Sex partners of people who test positive for the hepatitis B surface antigen
• Healthcare and public safety workers who have contact with blood or body fluids

The hepatitis B surface antibody (anti-HBs) is the antibody that is produced in response to hepatitis B surface antigen (HbsAg), a protein present on the surface of the hepatitis B virus. Anti-HBs appears after convalescence from acute infection and lasts for many years. It can also be produced in response to hepatitis B vaccination.

Other hepatitis B antibodies (eg, antibodies against the hepatitis B core and B e antigens) are not produced in response to vaccination. This is because these antigens are not in the vaccine.

An immunometric technique is used. The anti-HBs binds to HBsAg ad and ay subtypes, which are coated on the test wells. Binding of a horseradish peroxidase-labeled HBsAg conjugate to the anti-HBs completes the “sandwich” formation. Unbound materials are then washed away. In the next step, the horseradish peroxidase catalyzes oxidation of a luminogenic substrate, producing light. Light signals are detected and quantified. Intensity of the light is proportional to the amount of anti-HBs present in the patient sample. The result is standardized to an international unit system and reported as milliinternational units per milliliter (mIU/mL).

Results are interpreted as shown in the table.

HBsAg can be detected in the blood 4 to 10 weeks after exposure. This corresponds to onset of symptoms and viremia detectable by nucleic acid amplification methods. Most hepatitis B infections are self-limited and are associated with disappearance of HBsAg within 4 weeks of onset of symptoms. The anti-HBs then appears and increases to a plateau level that persists indefinitely.²

No. Some acute infections in healthy adults (generally <5%) do not resolve but become persistent. In these patients, antibody response is vigorous and sustained; however, anti-HBs is not detectable in these carriers, because excess circulating HBsAg binds to the antibodies.²

No. After 3 intramuscular doses of vaccine, >90% of healthy adults and >95% of those <19 years of age develop immunity (ie, anti-HBs ≥10 mIU/mL).¹ However, there is an age-specific decline in development of immunity. After age 40 years, about 90% of people become immune, but by age 60 years, only 75% of people become immune.¹ Larger vaccine doses (2 to 4 times the normal adult dose) or an increased number of doses are required to induce immunity in many hemodialysis patients and in other immunocompromised people.¹