13, 14 In contrast, the clinical usefulness of qHBsAg in patients receiving oral nucleos(t)ide analogues remains largely unknown; previous studies have investigated the relevance of qHBsAg in patients treated with LAM or adefovir, which are known to be less potent agents.4, 6, 9 Furthermore, for the most part, the available data were not derived from independent studies but were incorporated into studies in which either a combination was used or a comparison with PEG-IFN was made.7, 10-12, 14, 29 Therefore, the data in this study are valuable because the clinical significance of serial qHBsAg was systematically analyzed in patients treated with
ETV as a first-line therapy for CHB. We report a significant Smoothened Agonist clinical trial decrease in qHBsAg with ETV therapy. However, the overall decline was modest, with a mean drop of −0.24 log selleck products IU/mL in HBeAg(+) patients and a mean drop of −0.21 log IU/mL in HBeAg(−) patients after 2 years of therapy. Although this was greater than the drop achieved with 1 year of LAM (−0.02 log IU/mL), it was less than that reported with PEG-IFN (−0.71 log IU/mL).14
There are several potential explanations for this modest decline of qHBsAg. First, the mechanism of action of oral nucleos(t)ide analogues is the suppression of viral replication through inhibition of HBV polymerase; because HBsAg production proceeds by a pathway distinct from that of HBV DNA, the effect of ETV on qHBsAg is possibly less prominent.24 Second, the HBV genotype seems to play a major role in qHBsAg. In a large series of retrospective data by Gish et al.,16 less HBsAg loss was seen in patients with genotype C (0.5%, 1/201) versus 上海皓元 patients with genotype A (7.7%, 15/194) or D (8.1%, 7/79). Our entire cohort was infected with genotype C HBV, and this may also explain the modest decline in qHBsAg. We have shown that the baseline qHBsAg level has a high predictive value for VR in HBeAg(+) patients (AUC = 0.823, P < 0.001) with a sensitivity of 86.8%, a specificity of 78.9%, a PPV of 89.2%, and an NPV of 75.0%. These values compare favorably
to those reported for the prediction of SVR in patients treated with PEG-IFN (86%, 56%, 43%, and 92%, respectively).7 We were unable to further enhance the on-treatment predictive value of changes in qHBsAg; this might be due to the modest decline in the titers. Taken together, these results demonstrate that qHBsAg has clinical utility in the prediction of VR in HBeAg(+) patients and that a single titer at the baseline provides the best predictive value. Meanwhile, because almost all HBeAg(−) patients achieved VR (36/38, 94.7%), VR prediction in this group was neither statistically appropriate nor clinically valuable. Even though there is less activity in comparison with qHBsAg, studies on qHBeAg have continued to be reported since Perrillo et al.