Should Surveillance for Liver Cancer be Modified in Hepatitis C Patients After Treatment-related Cirrhosis Regression?

Roberta D'Ambrosio; Massimo Colombo


Liver International. 2016;36(6):783-790. 

In This Article

Risk Stratification of HCC in SVR Patients

In viraemic patients, many efforts have been made to identify HCC predictors a part from portal hypertension which is the single, stronger predictor in patients with chronic liver disease.[35] A prognostic score (King score), comprehensive of 186-gene signature and such laboratory parameters as bilirubin and platelets, allowed stratification of early cirrhotics with viraemia into three different risk classes for hepatic decompensation, HCC and death.[36] Though risk scores of HCC and decompensation in SVR patients incorporate the same markers of liver disease severity as those in viraemic patients, it is unknown whether such a prognostic score developed by King and colleagues retains its predictive power for end-stage HCV complications in SVR patients too. Single or combined serum biomarkers utilized in the diagnosis of HCC like serum AFP, DCP, AFP-L3, PIVKA-II, GP73 and SCCA failed to predict the clinical outcome of SVR patients.[37] To the best of our knowledge, no predictors of cirrhosis regression have been identified so far.

As viraemic patients with METAVIR F3 stage of liver fibrosis because of HCV are recommended by EASL to undergo surveillance with US owing to their increased risk of developing HCC,[32] regression from METAVIR F4 to F3 following antiviral therapy still leaves SVR patients at a substantial risk of HCC, even though it is not clear whether SVR patients have the same risk of HCC as viraemic patients. Attenuating the need of a distinction between F3 and F4 in SVR patients, however, is that often fibrosis staging is misclassified by percutaneous liver biopsy or by non-invasive methods in these two populations of patients.[38–41] In the HALT-C trial, enrolling non responders to interferon regimens only, the 6.4% incidence of HCC among Ishak S4 patients, corresponding to METAVIR F3, compared to 15.5% in patients with more advanced liver fibrosis or cirrhosis, i.e. Ishak 5 or 6.[42] Owing to the relationships between portal hypertension and HCC, cancer risk in patients with decompensated or marginally compensated cirrhosis is greater than in compensated patients, yet the clinical benefits of SVR in patients with this clinical profile are sparse owing to the fact that this patient population was almost invariably unfit to receive or tolerate interferon therapy. Eradication of HCV in marginally compensated or decompensated patients using oral DAA has been pursued worldwide, thus providing an opportunity to assess the clinical benefits of SVR in this population in terms of increased survival and, ultimately, prevention of HCC.[43–45]