Case Report
Copyright ©2007 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Feb 14, 2007; 13(6): 964-969
Published online Feb 14, 2007. doi: 10.3748/wjg.v13.i6.964
Fatal liver failure caused by reactivation of lamivudine-resistant hepatitis B virus: A case report
Yuka Suzuki, Hiroshi Yotsuyanagi, Chiaki Okuse, Yoshihiko Nagase, Hideaki Takahashi, Kyoji Moriya, Michihiro Suzuki, Kazuhiko Koike, Shiro Iino, Fumio Itoh
Yuka Suzuki, Chiaki Okuse, Yoshihiko Nagase, Hideaki Takahashi, Michihiro Suzuki, Fumio Itoh, Division of Gastroenterology and Hepatology, Department of Internal Medicine, St. Marianna University School of Medicine, 2-16-1 Sugao, Miyamae-ku, Kawasaki 216-8511, Japan
Hiroshi Yotsuyanagi, Kyoji Moriya, Kazuhiko Koike, Division of Infectious Diseases, Department of Internal Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan
Shiro Iino, Center for Liver Diseases, Seizankai Kiyokawa Hospital, 2-31-12 Asagayaminami, Suginami, Tokyo 166-0004, Japan
Author contributions: All authors contributed equally to the work.
Correspondence to: Hiroshi Yotsuyanagi, MD, PhD, Division of Infectious Diseases, Department of Internal Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. hyotsu-tky@umin.ac.jp
Telephone: +81-3-58008720 Fax: +81-3-58008796
Received: July 5, 2006
Revised: September 13, 2006
Accepted: December 29, 2006
Published online: February 14, 2007
Abstract

We present a case of fetal liver failure caused by the activation of lamivudine-resistant hepatitis B virus (HBV) nine months after lamivudine treatment. A 57-year old man visited our hospital for the treatment of decompensated chronic hepatitis B. Lamivudine was started in December 2001. Subsequently, serum HBV was negative for HBV DNA with seroconversion from HBeAg to anti-HBe and improvement of liver function. However, HBV DNA and HBeAg were again detected in September 2002. He was complicated by breakthrough hepatitis and admitted to our hospital in November for severely impaired liver function. Vidarabine treatment was started and serum HBV DNA and alanine aminotransferase (ALT) decreased transiently. However, after the start of α-interferon treatment, HBV DNA level increased and liver function deteriorated. He died 1 mo after admission. An analysis of amino acid sequences in the polymerase region revealed that rtM204I/V with rtL80I/V occurred at the time of viral breakthrough. After the start of antiviral treatment, rtL180M was detected in addition to rtM204I/V and rtL80I/V, and became predominant in the terminal stage of the disease. HBV clone with a high replication capacity may be produced by antiviral treatment leading to the worsening of liver function. Antiviral therapy for patients with breakthrough hepatitis in advanced liver disease should be carefully performed.

Keywords: Hepatitis B virus; Lamivudine; Polymerase; Interferon; Tyrosine-methionine-aspartate-aspartate