The goal of treatment of CHB is to suppress replication of HBV. Because the duration of treatment is long, prediction of the response to treatment during the course of treatment is necessary. Theoretically, cccDNA is the best indicator of transcriptional activity of HBV in hepatocytes, and the level of cccDNA at the end of the treatment is associated with a sustained virological response following treatment cessation [13
]. According to previous studies, the level of HBsAg correlates with the level of cccDNA [3
]. Until the development of automated quantification of HBsAg, measurement of HBsAg levels was laborious and needed serial dilution, lacked standardization, and was difficult to use in clinical practice [11
]. Recently, an automated method for quantification of HBsAg has been developed, and the clinical use of HBsAg has now been highlighted [11
]. There are 2 automated quantification assays for HBsAg. Milan et al. [6
] and Karsten et al. [7
] reported that the correlation between the assays was excellent (r=0.96 and 0.97, respectively; P
In clinical use, quantification of HBV DNA by PCR can monitor the response to treatment. Several studies have shown the presence of a good correlation between HBsAg and HBV DNA levels [15
], but others have shown the absence of a correlation [17
]. Rather than a simple correlation between HBsAg and HBV DNA levels, the correlation between mean changes in HBsAg and HBV DNA level is important [16
]. However, serial changes in HBsAg and HBV DNA of each patient during treatment do not always correlate well [16
]. The pattern of changes in HBsAg and HBV DNA may differ owing to differences in disease status, in particular the presence of HBeAg and anti-HBe-antibodies, and the mechanism of action of the drug used [17
]. Therapy with interferon (IFN) gamma clears HBV-infected hepatocytes noncytolytically and leads to a greater reduction in HBsAg. Adefovir or entecavir are nucleoside analogues that target the HBV reverse transcriptase and selectively inhibit virion production. The efficacy of these drugs for lowering HBsAg and cccDNA levels is poorer than that of IFN therapy [13
]. The patients involved in our study were treated with adefovir or entecavir. None were treated with IFN. Additionally, the disease status of the patients differed; some achieved seroconversion of HBeAg, whereas others did not. These differences led to the discordance between changes in HBsAg and HBV DNA levels during the 96 weeks of follow-up for each patient.
Quantification of HBsAg and HBV DNA levels enabled prediction of response to treatment. Even though the cut off value for the HBsAg level at baseline or the reduced levels from baseline differed between studies, the initial HBsAg level and reduced HBsAg levels could predict the response according to type of treatment. A lower HBsAg level at baseline or a greater reduction in HBsAg level from the baseline at 12 or 24 weeks after the start of the treatment was correlated with achievement of a sustained virological response [13
]. In our study, the level of HBsAg at pretreatment, 12 weeks, and 24 weeks after the start of the treatment was useful for the prediction of response to treatment. Thus, serial follow-up for HBsAg is useful for defining the level at baseline and analyzing the level of decline at a given time point, but not for determining a simple correlation with HBV DNA level.
According to our study, the Elecsys HBsAg II quant assay shows good performance in precision, linearity, carryover rate, and specificity. The level of HBsAg at baseline, 12 weeks, and 24 weeks after the start of the treatment is useful for predicting virologic response in patients with CHB virus infection. Therefore, the Elecsys HBsAg II quant assay can be applied for HBsAg quantification in clinical practice.