There were 117 patients with chronic hepatitis and 13 patients with compensated liver cirrhosis (Child–Pugh score < 6). Patients were treated with lamivudine (GlaxoSmithKline, Brentford, UK) 100 mg daily. Lamivudine treatment was started on day 1 to day 5 on admission (median day 3). One hundred and thirty patients did not receive lamivudine in the historical control cohort selected from our database. With SAS ver. 8.2 software (SAS Institute, Cary, NC, USA), patients in the control group were matched for sex, age and

imaging finding (cirrhosis or not) with the lamivudine treatment group. The match ratio was 1:1. There were 117 patients with chronic hepatitis and 13 patients with compensated liver cirrhosis. All patients of the historical control group met the aforementioned Selleckchem Lenvatinib inclusion and exclusion criteria. The

protocol of our study conformed to the ethical guidelines of the 1975 Declaration of Helsinki and was approved by the Clinical Research Ethics Committee of the Harbin Medical University. All the patients or their relatives in the lamivudine treatment group gave written informed consent before enrolment. The level of serum creatinine, INR for prothrombin time and the level of serum total bilirubin of each ACLF patient on admission were recorded. The MELD score was calculated according to the original formula proposed by the Mayo Clinic group: 3.8 × loge (bilirubin [mg/dL]) + 11.2 × loge (INR) + 9.6 × loge (creatinine [mg/dL]) + 6.4 × (etiology:

see more 0 if cholestatic or alcoholic, 1 otherwise). Hepatitis B e-antigen and antibody to HBeAg were detected by a qualitative 上海皓元 HBeAg enzyme immunoassay (Abbott Laboratories, Chicago, IL, USA). Serum HBV DNA was measured by polymerase chain reaction (PCR) assay (Amplicor HBV Monitor Test; Roche Diagnostics, Mannheim, Germany). The detection limit was 1 × 103 copies/mL. HBV DNA levels of the patients were evaluated before and after the 4-week treatment. HBV genotyping was determined by PCR using type-specific primers. The tyrosine, methionine, aspartate, aspartate (YMDD) motif mutant was detected by PCR assay and restriction fragment length polymorphism (RFLP) assay at baseline and 3-month follow up. With the use of PCR and RFLP assay for mixed viral-genotype populations (wild-type and mutant virus), the lower limit of detection for differentiating between the two viral genotypes has been determined to be 5% of the viral population. The assay has a lower limit of detection of approximately 1 × 104 copies of viral DNA per mL of serum. The patients were questioned about adverse events. All the adverse events, regardless of their possible association with lamivudine, were recorded. The 260 patients with ACLF were followed up for at least 3 months. The outcome (recovery, bridging to liver transplantation, or death) of each patient was recorded.