https://scholars.lib.ntu.edu.tw/handle/123456789/537019
Title: | Clinical course of de novo hepatitis B infection after pediatric liver transplantation | Authors: | Su W.-J. MING-CHIH HO YEN-HSUAN NI JIA-FENG WU YUNG-MING JENG HUEY-LING CHEN YAO-MING WU REY-HENG HU MEI-HWEI CHANG PO-HUANG LEE |
Issue Date: | 2010 | Journal Volume: | 16 | Journal Issue: | 2 | Start page/Pages: | 215-221 | Source: | Liver Transplantation | Abstract: | The characteristics of hepatitis B virus (HBV) in vaccinated children who acquire de novo HBV infections after orthotopic liver transplantation (OLT) remain largely unknown. The aim of this study was to explore HBV mutants in pediatric OLT recipients with de novo HBV infections. In all, 50 recipients underwent OLT between December 1997 and October 2005, and they were regularly checked for HBV serum markers from November 2005 to April 2009. Before OLT, all were hepatitis B surface antigen (HBsAg)-negative and under the coverage of the universal infant HBV vaccination program. Those who became HBsAg-positive after OLT were diagnosed with de novo HBV infection. HBV viral loads and full-length genome sequencing were determined when the diagnosis of de novo HBV infection was established. Nine patients (9/50, 18%) acquired de novo HBV infections after OLT. None had graft loss or fulminant hepatitis. Five cleared HBsAg, and 4 of the 5 even recovered with antibody to hepatitis B surface antigen (anti-HBs) formation. The other 4 were persistently HBsAg-positive. Mutations in the major S gene (681 base pairs) were discovered in 8 (88.9%) of the de novo HBV-infected children. Six of them harbored mutations within the "a" determinant region (codons 124-147), whereas the other 2 had mutations outside this region. These 2 cleared HBsAg and recovered with anti-HBs formation. HBV DNA levels were not different between those who cleared HBsAg and those who did not. In conclusion, surface mutants are frequent among pediatric liver transplant recipients with de novo HBV infections, but their clinical relevance requires further study. ? 2010 AASLD. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-75449103939&doi=10.1002%2flt.21980&partnerID=40&md5=3a87bed1d83f0e327f7bdd24c7817db4 https://scholars.lib.ntu.edu.tw/handle/123456789/537019 |
ISSN: | 1527-6465 | DOI: | 10.1002/lt.21980 | SDG/Keyword: | adefovir dipivoxil; biological marker; cyclosporin; hepatitis B antibody; hepatitis B surface antibody; hepatitis B surface antigen; hepatitis B vaccine; lamivudine; tacrolimus; virus DNA; Alagille syndrome; amino acid sequence; article; base pairing; bile duct atresia; Caroli disease; child; clinical article; codon; disease course; drug withdrawal; female; gene mutation; gene sequence; graft failure; graft recipient; health program; hepatitis B; hepatoblastoma; human; immunoprophylaxis; immunosuppressive treatment; infant; intrahepatic cholestasis; liver biopsy; liver disease; liver graft rejection; liver transplantation; male; methylmalonic acidemia; neontal fulminant hepatitis; nucleotide sequence; pediatric surgery; preschool child; primary sclerosing cholangitis; priority journal; promoter region; reinfection; school child; urea cycle disorder; vaccination; virus diagnosis; virus examination; virus genome; virus load; virus mutant; virus strain; Adolescent; Antiviral Agents; Child; Child, Preschool; Female; Hepatitis B; Hepatitis B Surface Antigens; Hepatitis B Vaccines; Hepatitis B virus; Humans; Incidence; Infant; Liver Failure; Liver Transplantation; Male; Mutation; Postoperative Complications; Taiwan; Tissue Donors; Treatment Outcome |
Appears in Collections: | 醫學系 |
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