Hepatitis flare was defined as ALT >5 times

Hepatitis flare was defined as ALT >5 times Ceritinib FDA of the upper normal limit (2000 IU/mL, [18] at least 6 months after inclusion. Cirrhosis was defined by histological or ultrasonographic findings (two consecutive examinations 6 months apart for confirmation) along with clinical features of splenomegaly, esophageal varices, or ascites. [19] HCC was diagnosed either by histology/cytology or by typical dynamic imaging study (CT, MRI or angiography) plus a serum alpha-fetoprotein level >200 ng/mL. [20]. Statistics Continuous variables were expressed as median (25�C75th percentile) and categorical variables were expressed as number (percentage) as appropriate. The HBsAg, HBV-DNA and HBV-DNA/HBsAg levels were logarithmically transformed for analysis.

For those with HBsAg or HBV-DNA level below the detection limit (0.05 IU/mL for HBsAg and 20 IU/mL for HBV-DNA), an arbitrary value of 0.025 IU/mL for HBsAg and 10 IU/mL for HBV-DNA were assigned for analysis. Differences between subgroups were analyzed using one-way ANOVA tests or Student��s t test as appropriate. Categorical variables were compared by the Chi-square test as appropriate. The decline of HBsAg and HBV-DNA were calculated by the value at baseline �C value at EOF. Paired t test was used to compare the decline of HBsAg and HBV-DNA levels between the baseline and EOF. The annualized rate of HBsAg decline was computed by dividing the HBsAg decline by individual duration of follow-up. Nonparametric trend test was used for trend across ordered groups.

Receiver Operating Characteristic (ROC) analysis was used for a cut-off HBsAg level to predict HBsAg loss in the LVL group. The statistical analysis was performed by STATA (version 11.0; Stata Corp, College Station, TX, USA). All tests were 2-sided and a p value <0.05 was considered significant. Results Baseline and End-of-follow-up HBsAg and HBV-DNA Levels Differed Significantly between Active and Inactive Carriers The baseline and EOF data of our patients are shown in Table 1. The distribution of HBV genotypes was mostly B (126/166, 76%), followed by C (38/166, 23%), B+C (2/166, 1%) and was undetermined in 21 patients because of low viral-load. The median follow-up duration was 8 years. Two patients developed HCC during the longitudinal follow-up in the HVL and FVL groups, respectively.

Table 1 Characteristics of HBeAg-negative HBsAg carriers according to their hepatitis activities. The baseline characteristics were comparable in terms of gender, genotype, and percentage of liver cirrhosis among three groups [Table 1]. The baseline HBsAg and HBV-DNA levels were significantly lower in the LVL group compared with the GSK-3 FVL and HVL groups (HBsAg: 2.84, 3.43 and 3.37 log10 IU/mL, P<.001; HBV-DNA: 1.77, 3.43 and 4.78 log10 IU/mL, P<.001). Among them, HBsAg was quantified in 165 patients (LVL/FVL/HVL: 39/101/25) with available first-year sera. The median first-year HBsAg were 2.59, 3.29 and 3.

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