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Severe clinical course of de novo hepatitis B infection after liver transplantation

Authors

  • Dr. Javier Crespo,

    Corresponding author
    1. Gastroenterology and Hepatology Unit, University Hospital Marqués de Valdecilla, Faculty of Medicine, Santander, Spain
    • Servicio Aparato Digestivo, Hospital Universitario Marqués de Valdecilla, Av Valdecilla s/n, Santander, E-39008, Cantabria, Spain
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  • Emilio Fábrega,

    1. Gastroenterology and Hepatology Unit, University Hospital Marqués de Valdecilla, Faculty of Medicine, Santander, Spain
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  • Fernando Casafont,

    1. Gastroenterology and Hepatology Unit, University Hospital Marqués de Valdecilla, Faculty of Medicine, Santander, Spain
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  • Monserrat Rivero,

    1. Gastroenterology and Hepatology Unit, University Hospital Marqués de Valdecilla, Faculty of Medicine, Santander, Spain
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  • Gonzalo de las Heras,

    1. Gastroenterology and Hepatology Unit, University Hospital Marqués de Valdecilla, Faculty of Medicine, Santander, Spain
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  • Joaquín de la Peña,

    1. Gastroenterology and Hepatology Unit, University Hospital Marqués de Valdecilla, Faculty of Medicine, Santander, Spain
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  • Fernando de la Cruz,

    1. Department of Molecular Biology, Faculty of Medicine, Santander, Spain
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  • Fernando Pons-Romero

    1. Gastroenterology and Hepatology Unit, University Hospital Marqués de Valdecilla, Faculty of Medicine, Santander, Spain
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Abstract

The aim of this study is to determine the origin, clinical outcome, allograft histological characteristics, and virological outcome of de novo hepatitis B virus (HBV) infection after orthotopic liver transplantation (OLT). We studied 136 hepatitis B surface antigen (HBsAg)-negative liver transplant recipients. HBV DNA was detected by dot-blot hybridization and polymerase chain reaction (PCR). The S gene was sequenced. Hepatitis C virus (HCV) RNA was assessed by PCR. The long-term clinical and histological outcome was determined. Six of 136 HBsAg-negative patients (4.4%) became HBsAg positive after transplantation. The source of HBV infection was reactivation of latent HBV infection in 2 patients and was not identified in 4 patients. Two donors had isolated core antibody. Two of these 6 patients developed acute liver failure related to hepatitis B. The 4 other patients had severe chronic hepatitis related to hepatitis B. All patients had high-level HBV replication. No significant mutations in the S gene were found. These data suggest that de novo hepatitis B infection is not a mild disease and might represent a significant cause of graft dysfunction. This is the first report of fulminant hepatitis caused by de novo hepatitis B infection after OLT.

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