Clinical outcome and HBsAg variability of hepatitis B virus induced acute liver failure

Introduction: Hepatitis B virus (HBV) infection remains a frequent cause of acute liver failure (ALF) worldwide. ALF can occur in 0.1 – 0.5% of infected patients and may lead to the urgent need of liver transplantation or death. The aim of this study was to scrutinize the clinical outcome of patients with HBV induced ALF and mutational patterns of HBV variants, which might contribute to ALF.

Patients and Methods: Thirty four patients with HBV-induced ALF were hospitalized at the University Hospital, University Duisburg-Essen, from 2005 to 2016. Clinical, chemical and virological data from these patients was collected and the SHB region of the HBV genome detected at the time of ALF was sequenced per NGS. As a control group 80 patients with chronic hepatitis B (CHB) were included in this study.

Results: Most HBV infections were caused by HBV genotype D (GT A: n = 6, GT B: n = 1, GT D: n = 23, GT E: n = 2 and GT F: n = 2). Antiviral therapy lead to the sustained suppression of HBV replication in all non transplanted patients and resulted in the loss of HBsAg and anti-HBs seroconversion (n = 13), the loss of HBsAg without anti-HBs seroconversion (n = 4) or chronic HBV (n = 1). Three patients died and four patients underwent liver transplantation despite antiviral treatment, while only one of them survived. Eight patients were lost to follow up. HBsAg mutations at positions and 31, 118, 127, 128 and 140 were significantly more frequent detected in HBV variants associated with ALF compared to chronic HBV (p < 0.05).

Conclusions: Antiviral therapy prevented liver transplantation or death in most patients with HBV associated ALF. HBV variants associated with ALF did not carry a specific mutational pattern but some HBsAg mutations were significantly more often detected in HBV variants of patients with ALF.