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Conversion to mycophenolate mofetil for modulating recurrent hepatitis C in liver transplant recipients
Author(s) -
Kornberg A.,
Küpper B.,
Wilberg J.,
Tannapfel A.,
Thrum K.,
Bärthel E.,
Hommann M.,
Settmacher U.
Publication year - 2007
Publication title -
transplant infectious disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.69
H-Index - 67
eISSN - 1399-3062
pISSN - 1398-2273
DOI - 10.1111/j.1399-3062.2007.00228.x
Subject(s) - medicine , immunosuppression , creatinine , gastroenterology , mycophenolate , renal function , urology , liver function , liver function tests , hepatitis c virus , hepatitis c , mycophenolic acid , transplantation , surgery , immunology , virus
Background. The aim of this study was to analyze the influence of cyclosporine A (CsA) taper in conjunction with mycophenolate mofetil (MMF) therapy on recurrent hepatitis C virus (HCV) in liver transplant patients. Patients and methods. Nineteen liver recipients with serologically and morphologically confirmed recurrent HCV were included in this study. After MMF introduction up to a maximum dose of 2000 mg/day, CsA dose was significantly tapered. In the control group immunosuppression remained unchanged. Allograft function and morphology, viral loads, and renal function were analyzed continuously. Results. MMF treatment was well tolerated without risk of rejection. Allograft fibrosis progressed in 6 patients of the MMF group (66.6%) and none (0%) of the controls at 12‐month biopsy ( P =0.005). Moreover, aminotransferases and viral loads increased slightly in the MMF‐treated patients. Renal function improved significantly (serum creatinine: 239.3±90.2 μmol/L vs. 175.8±46.0 μmol/L; P= 0.008) in the treatment group, while deteriorating (serum creatinine: 156.8±44.6 μmol/L vs. 214.8±120.1 μmol/L; P= 0.06) in the controls. Conclusion. MMF introduction allows a safe CsA taper in HCV‐positive liver transplant patients and results in significant improvement of renal function. However, there seems to be a risk of marked progression of HCV‐induced allograft injury.