We therefore conducted this study, which also aimed to validate the APASL stopping rule in our HBeAg-negative patients with CHB treated with ETV. This study used a retrospective-prospective cohort, approved by the Institutional Review Board of the Chang Gung Memorial Hospital, Taiwan. Excluding patients with coexisting HCV or HDV infection, alcoholism, autoimmune hepatitis, and malignancy, all HBeAg-negative, anti-HBe-positive patients with CHB who had been treated with ETV and were followed for a minimum of 12 months (48 weeks) after cessation

of ETV therapy by the stopping rule of APASL (undetectable LDK378 molecular weight HBV-DNA by PCR had been demonstrated on three occasions at least 6 months apart[7]) were included. After cessation of ETV therapy, serum ALT was monitored every 1-1.5 months in the first 3 months and then at least every 3 months along with serum HBV DNA assay every 3 months during off-therapy follow-up. Alfa-fetoprotein and ultrasonography were performed every 3-6 selleck chemicals llc months. If serum HBV DNA increases over 2,000 IU/mL or ALT level increases over ULN during off-therapy follow-up, HBV DNA and/or ALT were retested for confirmation and further evaluation. The “consolidation duration” was calculated from the first demonstration of undetectable HBV DNA to the end of treatment. According to the APASL guidelines, “clinical relapse” was defined as an event with an increase of serum HBV-DNA level over

2,000 IU/mL and serum ALT levels >2 × ULN, which is the AASLD and

APASL indication of anti-HBV therapy for CHB.[1, 2] Age, gender, presence of cirrhosis, prior treatment, baseline biochemical data and viral features, serum HBV DNA and ALT at the end of 3 and 6 months on therapy, serum HBsAg, HBV-DNA and ALT levels at baseline and at end of therapy, as well as treatment duration and consolidation duration were compared between patients with clinical relapse (relapsers) and those with sustained response (nonrelapsers). Since there was no APASL stopping rule for HBeAg-negative patients before 2008[7] and most of our patients have been treated with ETV after 2008, only 22 LAM-treated and 30 telbivudine (LdT)-treated HBeAg-negative patients had stopped drug therapy after a consolidation therapy >1 year and were followed for 1 year off-therapy, as the ETV cohort in the present selleck chemicals study did. The occurrences of clinical relapse in these 52 patients were searched by chart review retrospectively for comparison. The biochemical tests were performed using routine automated techniques at our clinical pathology laboratories. The serum ALT ULN was set by the laboratory at 36 U/L for both male and female. Serum hepatitis markers including HBsAg, anti-HBs, HBeAg, anti-HBe, anti-HDV, and anti-HCV were assayed using the EIA kit (Abbott Diagnostics, North Chicago, IL). HBV genotype was determined using PCR-restriction fragment length polymorphism of the surface gene of HBV.