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Fatal liver failure with the emergence of hepatitis B surface antigen variants with multiple stop mutations after discontinuation of lamivudine therapy
Author(s) -
Zhang JiMing,
Wang XinYu,
Huang YuXian,
Yin YouKuan,
Guan Shihe,
Xu Yang,
Roggendorf Michael,
Lu Mengji
Publication year - 2006
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.20543
Subject(s) - lamivudine , discontinuation , hbsag , medicine , virology , hepatitis b virus , exacerbation , hepatitis b , immunology , gastroenterology , virus
Treatment of chronic hepatitis B virus (HBV) infection with lamivudine is effective and well‐tolerated. However, discontinuation of the treatment is associated frequently with acute exacerbation of liver diseases. A patient suffering from acute liver failure after discontinuation of lamivudine treatment is described. The patient was treated with lamivudine for 4 months and ceased the treatment without consulting. After receiving lamivudine, the patient developed anti‐HBs and became negative for hepatitis B surface antigens (HBsAg). However, HBV DNA reappeared to a level of 6.47 × 10 5 copies/ml. The patient died due to acute liver failure. Sequencing of HBV isolates revealed that mutations including G145R and stop codons occurred within the HBsAg coding region. In conclusion, HBV replication resumed after the uncontrolled cessation of lamivudine treatment in this patient and may have triggered the process leading to liver failure. Anti‐HBs antibody appeared and may be the selective force for the emergence of HBV mutants. J. Med. Virol. 78:324–328, 2006. © 2006 Wiley‐Liss, Inc.