PMID- 19804502
OWN - NLM
STAT- MEDLINE
DCOM- 20101019
LR  - 20100720
IS  - 1365-2893 (Electronic)
IS  - 1352-0504 (Linking)
VI  - 17
IP  - 7
DP  - 2010 Jul
TI  - Clinical features of biochemical cholestasis in patients with recurrent hepatitis 
      C after living-donor liver transplantation.
PG  - 481-7
LID - 10.1111/j.1365-2893.2009.01207.x [doi]
AB  - Recurrent hepatitis C after liver transplantation (HepC-LT) progresses faster 
      than hepatitis C in non-transplant settings. Cholestasis has been suggested to be 
      one characteristic of HepC-LT related to the rapid progression. We investigated 
      the clinical features of biochemical cholestasis, which we defined as high serum 
      concentrations of alkaline phosphatase and gamma-glutamyl transpeptidase, in 
      patients with recurrent hepatitis C after living-donor liver transplantation. 
      Eighty patients were diagnosed with post-transplant recurrent hepatitis C after 
      exclusion of other aetiologies of cholestasis by liver biopsy and imaging. The 
      clinical features of biochemical cholestasis in the patients with HepC-LT, 
      including histological changes, the efficacy of interferon therapy and helper 
      T-cell (Th) subsets in the peripheral blood, were analysed. Fifty-five of the 80 
      patients with HepC-LT (69%) had evidence of biochemical cholestasis. Progression 
      of liver fibrosis to stage F3 or F4 was significantly accelerated in patients 
      with biochemical cholestasis compared with patients without cholestasis. The 
      biochemical cholestasis in patients with HepC-LT improved after interferon 
      therapy in 22 of 39 patients (56%) who showed a virological response to the 
      therapy, suggesting that hepatitis C virus (HCV) caused the biochemical 
      cholestasis in these patients. Patients with biochemical cholestasis who had a 
      biochemical response to interferon therapy showed an increased Th1 responses in 
      peripheral blood. In conclusion, biochemical cholestasis is the characteristic 
      feature of HepC-LT and is related to progression of liver fibrosis. An increased 
      Th1 response is associated with cholestasis caused by HCV after liver 
      transplantation.
FAU - Ueda, Y
AU  - Ueda Y
AD  - Department of Gastroenterology and Hepatology, Graduate School of Medicine, Kyoto 
      University, Kyoto, Japan. yueda@kuhp.kyoto-u.ac.jp
FAU - Takada, Y
AU  - Takada Y
FAU - Marusawa, H
AU  - Marusawa H
FAU - Haga, H
AU  - Haga H
FAU - Sato, T
AU  - Sato T
FAU - Tanaka, Y
AU  - Tanaka Y
FAU - Egawa, H
AU  - Egawa H
FAU - Uemoto, S
AU  - Uemoto S
FAU - Chiba, T
AU  - Chiba T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Viral Hepat
JT  - Journal of viral hepatitis
JID - 9435672
RN  - 9008-11-1 (Interferons)
RN  - EC 2.3.2.2 (gamma-Glutamyltransferase)
RN  - EC 3.1.3.1 (Alkaline Phosphatase)
SB  - IM
MH  - Alkaline Phosphatase/blood
MH  - Cholestasis/*pathology
MH  - Hepatitis C/*complications
MH  - Histocytochemistry
MH  - Humans
MH  - Interferons/therapeutic use
MH  - Liver/pathology
MH  - Liver Cirrhosis/pathology
MH  - Liver Transplantation
MH  - Living Donors
MH  - Recurrence
MH  - T-Lymphocyte Subsets/immunology
MH  - Treatment Outcome
MH  - gamma-Glutamyltransferase/blood
EDAT- 2009/10/07 06:00
MHDA- 2010/10/20 06:00
CRDT- 2009/10/07 06:00
PHST- 2009/10/07 06:00 [entrez]
PHST- 2009/10/07 06:00 [pubmed]
PHST- 2010/10/20 06:00 [medline]
AID - JVH1207 [pii]
AID - 10.1111/j.1365-2893.2009.01207.x [doi]
PST - ppublish
SO  - J Viral Hepat. 2010 Jul;17(7):481-7. doi: 10.1111/j.1365-2893.2009.01207.x.