[Hepatitis B: clinical application of HBsAg quantification]

Since its discovery by Blumberg in 1965, hepatitis B virus antigen (HBsAg) is used as the fingerprint of hepatitis B infection. HBsAg level reflects the transcriptional activity of the cccDNA. It is an important marker that might not only indicate active hepatitis B infection, but may also predict clinical and treatment outcomes. Assays for HBsAg quantification are fully automated with a high output capacity. HBsAg titer is higher in HBe antigen (HBeAg) positive chronic hepatitis B than in HBeAg negative patients and is negatively correlated with liver fibrosis in HBeAg positive patients. In HBeAg negative chronic hepatitis B, an HBsAg level < 1,000 IU/mL and an HBV DNA titer < 2,000 IU/mL allow the accurate identification of inactive carriers. On pegylated-interferon (PEG-IFN) treatment, HBsAg quantification allows identifying, as early as week 12 PEG-IFN therapy, patients that will not benefit from therapy and thus stop or switch treatment "week 12 stopping rule". Genotype A and D: stop at week 12 if no HBsAg decrease; Genotype B and C: stop at week 12 if titer > 20,000 UI/mL. With regards to nucleos[t]ides analogues therapy the role of HBsAg quantification remains to be clarified. Several studies indicate that baseline and on-treatment HBsAg levels might allow identifying patients that can end up with treatment with no subsequent risk of reactivation. In clinical practice, HBsAg quantification is a simple and reproducible worthwhile tool that can be used in association with HBV DNA to classify patients during HBV infection and to monitor therapy.