Incidence of de-novo hepatocellular carcinoma after treatment with direct antiviral agents for hepatitis C: A multicenter prospective cohort study from Latin America

PIÑERO, FEDERICO; RIDRUEJO, EZEQUIEL; MENDIZABAL, MANUEL; ALONSO, CRISTINA; VARON, A; SOZA, A; PALAZZO, M; SIXTO, MARCELA; HERNANDEZ, NELIA; SCHINONI, MI; CEBALLOS, SUSANA; GADEA, CLAUDIA; PEREZ, D; REGGIARDO, MV; MORENO, V; MENGARELLI, SILVIA; BRUNO, A; MENDOZA, G; VILAR, JOSE; BARREYRO, FERNANDO; ZUAIN, MGV; PARANA, RAYMUNDO; SILVA, MARCELO

Paris

Congreso; The International Liver Congress 2018; 2018

European Association for the Study of the Liver

Background and Aims: Information about the development of denovohepatocellular carcinoma (HCC) after achieving sustainedvirologic response (SVR) with all-oral direct antiviral agents (DAA)in Latin America is scarce. The aim of this study was to evaluate theincidence of HCC after therapy with DAA in patients with advancedfibrosis. Methods: A prospective cohort from the Latin-American LiverResearch, Educational and Awareness Network (LALREAN) wasanalyzed. Patients from Argentina, Brazil, Chile, Uruguay and Colombia who received DAAs since their approval in 2015?2016were included. Advanced fibrosis was defined as liver fibrosis grade 3or 4 (METAVIR F3-4/LSM > 9.5 kPa). De-novo HCC was defined as thenewly development of HCC after DAA regimens. All patients underwent routine ultrasound screening every 6 months before, during and after DAAs therapy. Results: Of the 378 patients who received DAA therapy, a total of 229patients with F3 (n = 45) and F4 (n = 184) were included for theanalysis. Baseline patient characteristics were: age 55 ± 11, male sex48.5%, HIV co-infection 3.5%, HBV co-infection 0.4%. Proportion of genotypes was as follows: 1a 19%, 1b 57%, 2 10%, 3 4% and 4 1%(genotype 1 without subgenotype in 8%). Median elastography assessment before treatment was 33 kPa (IQR 15?55 kPa), with apre-treatment MELD score of 9 ± 3, Child Pugh A 84%, B 15% and C 1%(32 patients were listed for liver transplantation). Overall, 88.3% ofthe initial cohort completed DAAs treatment, with an SVR12 of 96.9%.During post-SVR12 follow-up 3 patients developed ascites, 2 encephalopathy and 2 variceal hemorrhage. Seven (22%) patientswere delisted. Cumulative incidence of HCC in the overall cohort was3% (n = 7) during a median follow-up since end of treatment of 14.5weeks (IQR 8.6?31.3 weeks) with an incidence rate of 0.003 perperson/weeks (HCC per Child Pugh A 2.7% and Child Pugh B 7.4%; p =NS). All patients who developed de-novo HCC achieved SVR12; onlyonewas F3. At HCC diagnosis, 2 patients presented with extrahepaticHCC with a median major tumor size of 40 mm. Conclusions: Our study demonstrates that there still exists a high risk of newly HCC development in patients with advanced fibrosis treated with DAA. Routine screening of HCC in this population should be strict during the first months after treatment with DAAs.