Among them, 10 patients had HBsAg reduction by greater than 1 log IU/mL

at the second visit (Fig. 2). The baseline HBV DNA, HBsAg, ratio of HBsAg/HBV DNA, and ALT levels had no relationship with chance of greater HBsAg reduction at subsequent follow-up (Table 4). In general, an HBsAg reduction of greater than 1 log IU/mL could reflect a better viral control. The reduction in HBV DNA among patients with greater HBsAg reduction (median 2.30, range 0.04-6.59, log IU/mL) was more dramatic than that among patients with HBsAg reduction <1 log IU/mL (median 0.58, range −3.50 to 5.53, log IU/mL; P < 0.001). Patients with greater HBsAg reduction also tend to have lower HBsAg/HBV DNA from the second to the last visit. Three patients (two in Tamoxifen mw Group 2 and one in Group 4) developed hepatocellular carcinoma; all of them had HBsAg reduction <1 log IU/mL. A good immune control was most obvious among patients who were negative for HBeAg while having an HBsAg NVP-BKM120 nmr reduction of >1 log IU/mL (Table 5). There was a trend, though not statistically significant, of higher proportion of low HBV DNA and HBsAg loss among patients who underwent HBeAg seroconversion (Group 3) if they had HBsAg reduction by >1 log IU/mL. Among HbeAg-negative patients (Group 4 and Group 5), HBsAg reduction >1 log IU/mL was associated with higher chance of HBsAg loss and better viral suppression.

Among nine patients who experienced HBsAg loss, eight had HBsAg reduction by >1 log IU/mL at the last visit. The remaining patient had HBsAg level lower than 0.5 IU/mL at the first visit and had undetectable HBsAg (<0.05 IU/mL) starting the second visit. Twenty patients had a total of 27 hepatitis flares (12 HBeAg-positive, 14 HBeAg-negative, and one with absent HBeAg result) during the follow-up period. The ALT levels at the visits before flare, during flare, and after flare were 53 (24-185) IU/L, 330 (214-1066) IU/L, and 46

(24-128) IU/L, respectively. There was a significant increase in HBV DNA level at hepatitis flare (from 5.27 ± 1.89 log IU/mL to 6.79 ± 1.09 log IU/mL; P < 0.001) but the HBsAg level remained relatively static (from 3.32 ± 1.17 log IU/mL to 3.28 ± 0.98 log IU/mL; P = 0.72) (Fig. 1C). The HBsAg/HBV DNA ratio decreased from 0.68 ± 0.34 before flare to 0.48 ± 0.14 at ALT flare (P < 0.001) and increased back to 0.74 Carnitine palmitoyltransferase II ± 0.33 after flare (P < 0.001). Overall, with the 585 samples from 49 HBeAg-positive and 68 HBeAg-negative patients at five time points of assessment, the HBsAg levels had moderate correlation with HBV DNA (r = 0.61, P < 0.001). The correlation of HBsAg with HBV DNA was higher in the 176 HBeAg-positive samples (r = 0.66, P < 0.001) than that in the 409 HBeAg-negative samples (r = 0.41, P < 0.001; Fig. 3). Based on an 8-year follow-up of patients at different stages of chronic HBV infection, we found that serum HBsAg quantification was closely related to the HBeAg status and HBV DNA levels.