21 SPSS version

15.0 (SPSS, Inc., Chicago, IL) and SAS 9.2 (SAS Institute, Inc., BEZ235 solubility dmso Cary, NC) were used to perform statistical analyses. All statistical tests were two-sided and were evaluated at the 0.05 level of significance. Twenty-four of 107 patients (22%) developed SR. The number of sustained responders was comparable between the peginterferon alfa-2a monotherapy group and the peginterferon alfa-2a and ribavirin combination therapy group [14 of 53 (26%) versus 10 of 54 patients (19%), respectively, P = 0.33]. The two treatment groups were therefore pooled for further analysis. Among the 24 sustained responders, one patient cleared of HBsAg from serum and developed antibody to HBsAg. Baseline characteristics of the 107 patients are shown in Table 1. The mean pretreatment serum HBsAg level was 3.8 log IU/mL (range

= 1.1-5.0 log IU/mL), and the mean serum HBV DNA level was 6.8 log copies/mL (range = 4.3-9.5 log copies/mL); both were stable during the screening period. There was no significant correlation between serum HBsAg and other factors at the baseline, including serum HBV DNA and ALT levels, HBV genotype, age, gender, body mass index, and liver histology. Baseline characteristics, including age, gender, HBV genotype, serum ALT, HBV DNA, and HBsAg levels, and liver necroinflammatory and fibrosis scores, were comparable for patients with and without SR (Table 1). Overall, the mean serum HBsAg concentration decreased significantly after 48 weeks of therapy (mean change versus the baseline = −0.47 log IU/mL, P < 0.001). HBsAg remained cancer metabolism signaling pathway at end-of-treatment levels during the posttreatment follow-up (mean change at week 72 versus the baseline = −0.52 log IU/mL, P < 0.001). Serum HBV DNA levels declined significantly during the treatment period as well (mean change at week 48 versus the baseline = −3.29 log copies/mL, P < 0.001). In contrast to HBsAg levels, HBV DNA levels relapsed

after treatment discontinuation second (mean change at week 72 versus the baseline = −1.55 log copies/mL, P = 0.004). A weak positive correlation was present between serum HBsAg and HBV DNA levels when all available samples were considered (r = 0.35, P < 0.001). From the baseline until week 12, serum HBsAg and HBV DNA levels were not correlated (r < 0.15, P > 0.11). However, the correlation became stronger at the end of the treatment phase (week 48; r = 0.36, P < 0.001) and further increased at the end of follow-up (week 72; r = 0.53, P < 0.001). The mean HBsAg declines from the baseline for sustained responders and nonresponders are shown in Fig. 1A. During the first 8 weeks of therapy, the mean serum HBsAg levels remained stable in both patient groups (Fig. 1A). From week 8 onward, however, HBsAg levels markedly decreased among the 24 patients who developed SR, whereas only a modest decrease in HBsAg levels was observed in patients who failed to achieve SR (P < 0.