TY - JOUR T1 - Reactivation of hepatitis B virus with mutated hepatitis B surface antigen in a liver transplant recipient receiving a graft from an antibody to hepatitis B surface antigen- and antibody to hepatitis B core antigen-positive donor. JF - Transfusion// // Transfusion Y1 - 2012 A1 - Blaich, Annette A1 - Manz, Michael A1 - Dumoulin, Alexis A1 - Schuttler, Christian G A1 - Hirsch, Hans H A1 - Gerlich, Wolfram H A1 - Frei, Reno KW - *Hepatitis B Antibodies/bl [Blood] KW - *Hepatitis B Surface Antigens/ge [Genetics] KW - *Hepatitis B virus/ph [Physiology] KW - *Hepatitis B/tm [Transmission] KW - *Liver Transplantation/ae [Adverse Effects] KW - *Virus Activation/ph [Physiology] KW - Hepatitis B Core Antigens/im [Immunology] KW - Hepatitis B Surface Antigens/im [Immunology] KW - Hepatitis B virus/ge [Genetics] KW - Hepatitis B virus/im [Immunology] KW - Hepatitis B/bl [Blood] KW - Hepatitis B/et [Etiology] KW - Hepatitis B/vi [Virology] KW - Humans KW - Male KW - Middle Aged KW - Mutation/ph [Physiology] KW - Tissue Donors AB - BACKGROUND: Fresh-frozen plasma (FFP) may contain antibodies to hepatitis B surface antigen (HBsAg, anti-HBs). These anti-HBs may lead to a misinterpretation of the actual hepatitis B immune status. Furthermore, they may not only confer protection against hepatitis B virus (HBV), but may also favor the selection of HBsAg mutants., CASE REPORT: We report a case of de novo HBV infection in a HBV-naive recipient with alcoholic liver disease, who received a liver from a donor with antibodies to hepatitis B core antigen (HBcAg, anti-HBc) and anti-HBs., RESULTS: A lookback investigation revealed the following: 1) Due to anti-HBs passively acquired through FFP, the recipient was considered immune to HBV and did not receive anti-HBV prophylaxis. 2) Within 1 year after transplantation he developed hepatitis B in absence of any elevated liver enzymes after the anti-HBs by FFP declined. 3) Despite an infection with HBV-containing wild-type HBcAg, the patient did not seroconvert to anti-HBc positivity. 4) The replicating HBV encoded two HBsAg mutations, first sQ129R and 4 months later sP127S. They map to the highly conserved "alpha" determinant of the HBsAg loop., CONCLUSION: 1) Passive transfer of anti-HBs from FFP led to an erroneous pretransplant diagnosis of HBV immunity when the patient was in fact HBV-naive. 2) HBsAg mutations might have been selected in escape from donor's actively produced anti-HBs and the recipient's anti-HBs by FFP might have favored this selection. 3) It is doubtful whether hepatitis B immunoglobulin could have prevented the reactivation. 4) Antiviral prophylaxis would have been crucial.Copyright © 2012 American Association of Blood Banks. M1 - wdn, 0417360 CY - United States VL - 52 SN - 1537-2995 CP - 9 L2 - http://ovidsp.ovid.com/ovidweb.cgi?T=JS&PAGE=reference&D=medl&NEWS=N&AN=22313146 ID - 4510 ER -