Page 80 - The Flying Publisher Guide to Hepatitis C Treatment

80 | Hepatitis C Treatment

post-transplant. The progression of fibrosis occurs at a rate 1.4
times faster when compared to progression of fibrosis in the
non-transplant population (Mohsen 2003).
The estimated rate of allograft cirrhosis reaches 30% at 5 years
of follow-up, leading to increasing incidence of
retransplantation in HCV recipients. After the diagnosis of
cirrhosis, the decompensation risk appears to be accelerated
(17% and 42% at 6 and 12 months, respectively). Patient survival
is also significantly decreased: 66% and 30% at 1 and 5 years,
respectively (Berenguer 2000). HCV infection-associated
allograft injury is incriminated as the most common cause of
both death (28-39%) and graft failure (~40%) among transplant
recipients (Charlton 2004). Retransplantation represents the last
option for these patients in the context of increasing demands
for LT.
Many factors such as donor and host characteristics, virologic
features and immunosuppression have been shown to influence
the progression of post-transplant liver disease.
Viral factors. As early as the first week postoperatively, the
HCV RNA level increases 10- to 20-fold and plateaus at 1 month,
with higher levels noted in those with more severe recurrent
hepatitis (Berenguer 2001). However, the role of HCV RNA levels
in determining severity of HCV recurrence remains
controversial. The single exception is the well-proven
relationship between very high VL and occurrence of cholestatic
hepatitis (~2-5% of patients). Other viral factors that may
influence the severity of the recurrence are difficult-to-treat
viral genotype (1 and 4) and the quasi-species.
Recipient factors. Increasing age of the recipient (>50 years)
and female sex, as well as non-Caucasian (Afro-American, Asian)
have a more aggressive recurrence (Belli 2007). Thus, a
combination of a liver from an old donor with an old recipient
should be avoided. Presence of a necroinflammatory score ≥2 in
the explants was shown to be a predictor of progressive fibrosis.
Also, the HLA donor-recipient matching was associated with a