Case Report
Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Clin Cases. Mar 16, 2016; 4(3): 71-75
Published online Mar 16, 2016. doi: 10.12998/wjcc.v4.i3.71
Hepatitis B surface antigen escape mutations: Indications for initiation of antiviral therapy revisited
Jennifer Leong, Derek Lin, Mindie H Nguyen
Jennifer Leong, Division of Liver Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 10029, United States
Derek Lin, Department of Medicine, Stanford University Medical Center, Palo Alto, CA 94304, United States
Mindie H Nguyen, Division of Gastroenterology and Hepatology, Stanford University Medical Center, Palo Alto, CA 94304, United States
Author contributions: Leong J and Lin D contributed to data acquisition and writing the manuscript; Leong J and Nguyen MH provided the study concept and critical revision of the manuscript.
Institutional review board statement: This chart review was approved by the Institutional Review Board at Stanford University, Stanford, CA and at Icahn School of Medicine at Mount Sinai, New York, NY.
Informed consent statement: Informed consent was waived by approval of the Instituional Review Board from both institutions due to the retrospective nature of the study.
Conflict-of-interest statement: Jennifer Leong has received honoraria for serving as an advisory board member for Gilead Sciences. Derek Lin has no conflicts of interest to declare. Mindie H Nguyen has received honoraria and research support from Roche Pharmaceuticals, Bristol-Myers Squibb and Gilead Sciences.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See:
Correspondence to: Jennifer Leong, MD, Assistant Professor, Division of Liver Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1104, New York, NY 10029, United States.
Telephone: +1-212-2418035 Fax: +1-212-7317340
Received: August 26, 2015
Peer-review started: August 27, 2015
First decision: October 14, 2015
Revised: November 16, 2015
Accepted: December 13, 2015
Article in press: December 14, 2015
Published online: March 16, 2016

Approximately 240 million people are chronically infected with hepatitis B. The implementation of rigorous vaccination programs has led to an overall decrease in the prevalence of this disease worldwide but this may also have led to emergence of viral mutations that can escape the protection of hepatitis B surface antibody. As this phenomenon is increasingly recognized, concern for transmission to vaccinated individuals has also been raised. Herein, we describe two cases where the suspected presence of a hepatitis B surface antigen escape mutation impacted the decision to initiate early antiviral therapy, as well as provide a brief review of these mutations. Our findings described here suggest that a lower threshold for initiating therapy in these individuals should be considered in order to reduce the risk of transmission, as vaccination does not provide protection.

Keywords: Hepatitis B virus, Hepatitis B surface antigen, Escape mutant, Hepatitis B immunoglobulin, Vaccination

Core tip: Hepatitis B surface antigen escape mutations are being increasingly recognized, along with concern for the risk of transmission to vaccinated individuals. The management of these patients and the natural history of the disease remain controversial due to insufficient data. However, transmission of this mutated virus to vaccinated individuals has been reported in the literature. Herein, we discuss two different clinical scenarios that led to the initiation of early antiviral therapy in order to decrease the risk of transmission to others due to the suspected presence of this mutation.