Page 85 - The Flying Publisher Guide to Hepatitis C Treatment

Management of recurrent HCV infection following liver transplantation | 85

Histological benefits in virologic nonresponders have been
demonstrated in a study where only 22% in a group receiving
preemptive therapy progressed vs. 49% of patients not receiving
preemptive therapy (Kuo 2008). However, this prophylactic
approach cannot be used in a considerable proportion of
patients due to initially intense immunosuppression,
pancytopenia, postoperative infections and insufficient recovery
after the surgery.

Therapy of recurrent hepatitis C after LT
Posttransplant antiviral therapy in recipients with evidence of
biochemical and histological recurrent disease, usually 6 months
after LT, is the mainstay of management. Although a high
number of transplant centers use antiviral therapy, the
treatment is not standardized and is still associated with low
rates of SVR, less than those reported in the non-transplant
setting. The main reasons include high VL post-LT, a higher
frequency of genotype 1 patients, poor tolerability of treatment
after LT, and need for frequent dose reductions.
The combination of PegIFN/RBV is the treatment of choice also
in transplant recipients. The SVR associated with PegIFN/RBV
therapy in predominantly genotype 1 infected populations has
been reported to range from 12% to as high as 50% (Gonzalez
2010). A recent extensive review of 19 prospective and
retrospective clinical studies describing antiviral therapy with
PegIFN/RBV in this population reported a mean SVR of 30.2%
(Berenguer 2008). End of treatment virologic response (EoTR)
was 42.2% (range 17-68%), indicating that relapse was a major
factor in the low SVR rates. Biochemical responses were
registered in 54.8% and histological endpoints were judged to be
too heterogeneous in definition and assessment to provide a
summary estimate. However, it was noted that histological
improvements were generally confined to treated patients who
achieve SVR. Fibrosis has been shown to progress significantly
more in nonresponders to antiviral therapy. Even in the absence
of virological response, the rate of progression of fibrosis was