論文

査読有り
2014年10月

Plasma cell hepatitis induced by the termination of antiviral therapy for recurrent hepatitis C after living donor liver transplantation

HEPATOLOGY RESEARCH
  • Yoshihide Ueda
  • ,
  • Atsushi Yoshizawa
  • ,
  • Yasuhiro Ogura
  • ,
  • Aya Miyagawa-Hayashino
  • ,
  • Hironori Haga
  • ,
  • Tsutomu Chiba
  • ,
  • Shinji Uemoto

44
10
開始ページ
E279
終了ページ
E283
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1111/hepr.12243
出版者・発行元
WILEY-BLACKWELL

Plasma cell hepatitis (PCH) is an idiopathic disorder characterized by plasma cell infiltration in the allografts of patients who have undergone liver transplantation. Although an increasing number of cases of PCH have been reported in liver transplant recipients with hepatitis C recurrence treated with interferon, it is unclear whether PCH is induced by interferon itself. Here, we describe the cases of two patients who developed PCH just after the termination of antiviral therapy for recurrent hepatitis C after living donor liver transplantation. Liver dysfunction appeared at 1 month in one patient and 2 months in the other patient after pegylated interferon plus ribavirin therapy, and liver histology showed interface hepatitis with plasma cell-rich lymphoid aggregates. Both patients recovered after steroid therapy and achieved sustained virological response. These cases suggest that PCH could be induced by the alteration of the immune condition resulting from the termination of antiviral therapy. PCH should be considered when the transaminase levels increase after antiviral therapy, and it should be carefully distinguished from hepatitis C relapse.

リンク情報
DOI
https://doi.org/10.1111/hepr.12243
J-GLOBAL
https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201402255768315027
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/24112365
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000343806700034&DestApp=WOS_CPL
ID情報
  • DOI : 10.1111/hepr.12243
  • ISSN : 1386-6346
  • eISSN : 1872-034X
  • J-Global ID : 201402255768315027
  • PubMed ID : 24112365
  • Web of Science ID : WOS:000343806700034

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