Hepatitis frequently recurs after liver transplantation for early recurrence is associated with a higher risk of disease progression. (HEPATOLOGY 1997;26:1646-1652.) hepatitis C. However, the histological progression of disease, predictors of recurrence and disease severity, and patient survival remain uncertain. Fifty-five patients with cirrhosis Hepatitis C virus (HCV) infection has become the leadcaused by chronic hepatitis C underwent liver transplantation ing indication for orthotopic liver transplantation (OLT) between January 1990 and December 1993. Hepatitis C genoin the United States. Approximately 50% to 60% of patients type was determined, and liver biopsies were performed at develop recurrent liver disease in the first few years after frequent intervals posttransplantation. The median follow-up transplantation, whereas the remaining patients remain distime was 40.4 months. The cumulative rate of survival was ease-free despite persistent viremia. Although recurrent no different in liver transplant recipients for hepatitis C than disease is often clinically mild, early graft failure and morin liver transplant recipients for other chronic liver diseases tality have been reported. The reasons for the variation (P Γ
.62). Histological recurrent hepatitis C developed in 33 in disease expression remain uncertain. Studies of the relaof 50 patients assessable for disease recurrence; the median tionship between circulating viral levels and recurrent herecurrence-free survival time was 13.4 months. Histological patocellular injury have yielded conflicting results. [12] Paactivity and stage were mild in most cases. Only 2 patients tients infected with genotype 1b have been reported to have developed cirrhosis, and no patient required a second transa greater incidence of recurrent hepatitis and more severe plantation for recurrent disease. Patients with acute cellular liver disease. It also has been suggested that immunorejection had a shorter recurrence-free survival (P Γ
.0141). In suppression for cellular rejection may play a role in disease patients with recurrent hepatitis, rejection also was correlated recurrence. 14 Finally, a correlation between donor-recipiwith increased histological grade 2 years after transplantation ent matching and recurrent hepatitis has been shown in (P Γ
.0061). Recurrence-free survival was decreased in pasome, but not all, studies (Unpublished data, September tients infected with genotype 1 (1a and 1b combined) com-1996). Reports on rates of patient survival have also been pared with genotypes 2 and 3 combined (P Γ
.02), whereas conflicting. Although short-term survival appears to be there was no difference between genotypes 1a and 1b (P ΓΊ good, 2,5 preliminary data from one U.S. center suggest de-.80). Only patients infected with genotype 1a or 1b developed creased survival rates among patients undergoing liver bridging fibrosis or cirrhosis. In addition, patients who had an transplantation for HCV. 15 To date, only two centers have early recurrence had a greater risk of progressing to bridging reported long-term survival results. 16 In both studies, fibrosis or cirrhosis (hazard ratio, 5.1; P Γ
.0473). In our survival did not differ between liver transplant recipients experience, recurrent hepatitis C after liver transplantation for hepatitis C and those with other nonmalignant liver in most cases is mild and survival is unaffected. Both acute diseases. cellular rejection and infection with genotype 1 are indepen-
The purpose of this study was to review the natural history dent risk factors for reduced recurrence-free survival, and in our patients undergoing liver transplantation for hepatitis C and to specifically address the following: 1) the incidence and timing of recurrent hepatitis; 2) the histological activity and progression of hepatitis; 3) whether patient and graft Abbreviations: HCV, hepatitis C virus; OLT, orthotopic liver transplantation; HBV, survival are adversely affected; and 4) whether cellular rejechepatitis B virus; HBsAg, hepatitis B surface antigen; anti-HBc, antibody to hepatitis B core antigen; EIA, enzyme immunoassay; anti-HCV, antibody to hepatitis C virus;
tion or viral genotype influence the incidence of histological RIBA, recombinant immunoblot assay; HIV, human immunodeficiency virus; PCR, recurrence or disease severity.