2001 Fiscal Year Final Research Report Summary
The mechanism which causes fulminant hepatic failure after immune suppression therapy on HBV carrier patients
| Project/Area Number |
11670480
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
MARUYAMA Toshiyuki The University of Tokyo, Graduate School of Medicine, Lecturer, 大学院・医学系研究科, 講師 (30219571)
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| Co-Investigator(Kenkyū-buntansha) |
MAEKAWA Hisato The University of Tokyo, Graduate School of Medicine, Assistant Professor, 大学院・医学系研究科, 助手 (10301102)
MITSUI Hiroshi The University of Tokyo, Graduate School of Medicine, Assistant Professor, 大学院・医学系研究科, 助手 (30239280)
KOIKE Kazuhiko The University of Tokyo, Graduate School of Medicine, Associate Professor, 大学院・医学系研究科, 助教授 (80240703)
TOMA Shigeto The University of Tokyo, Graduate School of Medicine, Assistant Professor, 大学院・医学系研究科, 助手 (50207528)
AOKI Katsunori The University of Tokyo, Graduate School of Medicine, Assistant Professor, 大学院・医学系研究科, 助手 (40291322)
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| Project Period (FY) |
1999 – 2000
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| Keywords | HBV-DNA / fulminant hepatitis / immune suppression therapy / mutation / cytokine |
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| Research Abstract |
13 HBV carrier patients (group A) who developed fulminant hepatic failure after immune suppression therapy and 11 HBV carrier patients (group B) who did not develop hepatitis after immune suppression therapy were analyzed for liver function test, and cytokine production and virological profile.
We analyzed the nucleotide sequence in the whole genome of HBV-DNA from patients to investigate the virological factor. A precore stop codon mutation at nucleotide position 1896 or an A-to-T mutation at nucieotide position 1762 and a G-to-A mutation at nucleotide position 1764 in the core promoter region were frequently present in patients from group A as well as group B.
Fulminant HBV infection does not appear to be caused by a specific genomic mutation or an amino acid mutation. To the contrary, the average interleukin 1 levels were higher in group A than that in group B. Similarly, and tumor necrosis factor alfa levels were higher in group A than that in group B.
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