By Liz Highleyman

Over the course of years or decades, chronic hepatitis C virus (HCV) infection can lead to severe liver disease including cirrhosis and hepatocellular carcinoma, which in advanced cases may necessitate a liver transplant.

Unfortunately, HCV typically infects the new donor liver soon after transplantation. Recurrent HCV after transplantation can lead cirrhosis in the graft in up to 30% of patients within 5 years.

As reported at the 43rd annual meeting of the European Association for the Study of the Liver (EASL 2008) last month in Milan, researchers undertook a study to describe the natural history of recurrent HCV-related cirrhosis after liver transplantation in a U.S. population.

The investigators reviewed all adult patients at a Florida center undergoing liver transplantation secondary to hepatitis C. Of the total 1085 adult liver transplants performed between 1991 and 2007, 505 were due to HCV-related cirrhosis.

Transplant recipients were prospectively monitored with liver biopsies at month 4 and then annually after transplantation. Cirrhosis was defined as a fibrosis score of F5 or F6 using a modified Ishak scale. Antiviral therapy for HCV was started when the fibrosis score was greater than F2.

The investigators collected demographic, clinical, and histological data. Kaplan-Meier curves were calculated to estimate the probability of liver decompensation and patient survival. Cox regression analysis was used to determine risk factors associated with decompensation and survival.

Results

• 69 patients (14%) had biopsy-proven cirrhosis after a median follow-up period of 36 months.

• 53 of these (77%) had clinically compensated cirrhosis at diagnosis.

• 26 patients (49%) had at least 1 episode of liver decompensation.

• The median time to the first decompensation event was 15 months.

• The cumulative probability of clinical decompensation was 22% at 1 year and 54% at 3 years after cirrhosis developed.

• A MELD score of 17 was predictive of decompensation (RR 8.7).

• Sustained virologic response (SVR) to interferon-based therapy reduced the risk of decompensation (RR 0.1).

• The cumulative survival rate was 92% at 1 year and 78% at 5 years in patients with compensated cirrhosis.

• This was significantly greater than the rates of 64% and 17%, respectively, in patients with decompensated liver disease (P = 0.001).

• Poor survival was predicted by MELD score of 17 (RR 15.3), hepatocellular carcinoma (RR 7.8), and progression to cirrhosis in less than 2 years (RR 3.9).

Conclusion

Based on what they said was "the largest natural history series of recurrent HCV cirrhosis in the U.S.," the investigators concluded that, "The rate of decompensation is 4 times faster than a non-transplant population, but slower than previous reports."

"Successful antiviral therapy may protect against decompensation," they added, "however, once decompensation occurs, survival is negatively effected."

Department of Medicine, Division of Gastroenterology, Section of Hepatobiliary Diseases and Liver Transplantation, University of Florida, Gainesville, FL.

5/09/08

Reference
VC Clark, RJ Firpi, C Soldevila-Pico, and others. The natural history of HCV-related cirrhosis after liver transplantation. 43rd annual meeting of the European Association for the Study of the Liver (EASL 2008). Milan, Italy. April 23-27, 2008.