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Impact of cytomegalovirus infection, year of transplantation, and donor age on outcomes after liver transplantation for hepatitis C
Author(s) -
Burak Kelly W.,
Kremers Walter K.,
Batts Kenneth P.,
Wiesner Russell H.,
Rosen Charles B.,
Razonable Raymund R.,
Paya Carlos V.,
Charlton Michael R.
Publication year - 2002
Publication title -
liver transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.814
H-Index - 150
eISSN - 1527-6473
pISSN - 1527-6465
DOI - 10.1053/jlts.2002.32282
Subject(s) - medicine , liver transplantation , transplantation , cytomegalovirus , cytomegalovirus infection , cytomegalovirus infections , virology , immunology , human cytomegalovirus , viral disease , virus , herpesviridae
Recurrence of hepatitis C virus (HCV) infection after liver transplantation (LT) is almost universal. However, variables that hasten the progression of allograft injury have not been fully defined. Cytomegalovirus (CMV) is a common infection post‐LT, and its impact on the course of post‐LT HCV infection remains unclear. We investigated the impact of CMV infection on patient and graft outcomes in 93 consecutive HCV‐infected liver transplant recipients. Data were collected prospectively, with surveillance cultures for CMV and protocol liver biopsies. CMV infection (defined as isolation of CMV from blood and treatment with ganciclovir) occurred in 25 patients (26.9%). Graft failure (defined as cirrhosis, relisting for LT, re‐LT, or death) was significantly more common in CMV‐positive compared with CMV‐negative patients (52% v 19.1%; P = .002). Fibrosis stage 2 or greater on the 4‐month liver biopsy specimen was more common in CMV‐infected patients (45% v 16.4%; P = .01). Patients who underwent LT in more recent years had an increased risk for graft failure. Donor and recipient age, CMV infection, and mycophenolate mofetil use were significantly associated with graft failure in a stepwise multivariate analysis. CMV infection occurs in approximately one quarter of HCV‐infected liver transplant recipients and is an independent risk factor for graft failure in these patients. Whether CMV mediates this by inducing increased immunosuppression or directly enhancing HCV replication requires further study.