Roberta D'Ambrosio1, Alessio Aghemo2,3, Maria Grazia Rumi4, Elisabetta Degasperi1, Angelo Sangiovanni1, Marco Maggioni5, Mirella Fraquelli6, Riccardo Perbellini1, William Rosenberg7, Pierre Bedossa8, Massimo Colombo3, Pietro Lampertico1. 1. A. M. and A. Migliavacca Center for Liver Disease, Division of Gastroenterology and Hepatology, Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico, Università degli Studi di Milano, Milan, Italy. 2. Department of Biomedical Sciences, Humanitas University, Rozzano-Milan, Italy. 3. Humanitas Clinical and Research Center, Rozzano-Milan, Italy. 4. Division of Hepatology, Ospedale San Giuseppe, Università degli Studi di Milano, Milan, Italy. 5. Division of Pathology, Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico, Università degli Studi di Milano, Milan, Italy. 6. Division of Gastroenterology and Endoscopy, Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico, Università degli Studi di Milano, Milan, Italy. 7. Center for Hepatology, Division of Medicine, University College of London, London, UK. 8. Department of Pathology and INSERM U773, Hopital Beaujon, Universitée Paris-Diderot, Clichy, France.
Abstract
BACKGROUND AND AIM: In patients with HCV-related cirrhosis, a sustained virological response may lead to cirrhosis regression. Whether histological changes translate into prevention of long-term complications, particularly hepatocellular carcinoma is still unknown. This was investigated in a cohort of histological cirrhotics who had been prospectively followed-up for 10 years after the achievement of a sustained virological response to IFN. METHODS: In all, 38 sustained virological response cirrhotics who underwent a liver biopsy 5 years post-SVR were prospectively followed to assess the impact of cirrhosis regression on clinical endpoints. RESULTS: During a follow-up of 86 (30-96) months from liver biopsy, no patients developed clinical decompensation, whilst 5 (13%) developed hepatocellular carcinoma after 79 (7-88) months. The 8-year cumulative probability of hepatocellular carcinoma was 17%, without differences between patients with or without cirrhosis regression (19% [95% CI 6%-50%] vs 14% [95% CI 4%-44%], P = .88). Patients who developed or did not an hepatocellular carcinoma had similar rates of residual cirrhosis (P = 1.0), collagen content (P = .48), METAVIR activity (P = .34), portal inflammation (P = .06) and steatosis (P = .17). At baseline, patients who developed an hepatocellular carcinoma had higher γGT (HR 1.03, 95% CI 1.00-1.06; P = .014) and glucose (HR 1.02, 95% CI 1.00-1.02; P = .012) values; moreover, they had increased Forns Score (HR 12.8, 95% CI 1.14-143.9; P = .039), Lok Index (HR 6.24, 95% CI 1.03-37.6; P = .046) and PLF (HR 19.3, 95% CI 1.72-217.6; P = .016) values. One regressor died of lung cancer. The 8-year cumulative survival probability was 97%, independently on cirrhosis regression (96% vs 100%, P = 1.0) or hepatocellular carcinoma (100% vs 97%, P = 1.0). CONCLUSIONS: Post-SVR cirrhosis regression does not prevent hepatocellular carcinoma occurrence.
BACKGROUND AND AIM: In patients with HCV-related cirrhosis, a sustained virological response may lead to cirrhosis regression. Whether histological changes translate into prevention of long-term complications, particularly hepatocellular carcinoma is still unknown. This was investigated in a cohort of histological cirrhotics who had been prospectively followed-up for 10 years after the achievement of a sustained virological response to IFN. METHODS: In all, 38 sustained virological response cirrhotics who underwent a liver biopsy 5 years post-SVR were prospectively followed to assess the impact of cirrhosis regression on clinical endpoints. RESULTS: During a follow-up of 86 (30-96) months from liver biopsy, no patients developed clinical decompensation, whilst 5 (13%) developed hepatocellular carcinoma after 79 (7-88) months. The 8-year cumulative probability of hepatocellular carcinoma was 17%, without differences between patients with or without cirrhosis regression (19% [95% CI 6%-50%] vs 14% [95% CI 4%-44%], P = .88). Patients who developed or did not an hepatocellular carcinoma had similar rates of residual cirrhosis (P = 1.0), collagen content (P = .48), METAVIR activity (P = .34), portal inflammation (P = .06) and steatosis (P = .17). At baseline, patients who developed an hepatocellular carcinoma had higher γGT (HR 1.03, 95% CI 1.00-1.06; P = .014) and glucose (HR 1.02, 95% CI 1.00-1.02; P = .012) values; moreover, they had increased Forns Score (HR 12.8, 95% CI 1.14-143.9; P = .039), Lok Index (HR 6.24, 95% CI 1.03-37.6; P = .046) and PLF (HR 19.3, 95% CI 1.72-217.6; P = .016) values. One regressor died of lung cancer. The 8-year cumulative survival probability was 97%, independently on cirrhosis regression (96% vs 100%, P = 1.0) or hepatocellular carcinoma (100% vs 97%, P = 1.0). CONCLUSIONS: Post-SVR cirrhosis regression does not prevent hepatocellular carcinoma occurrence.
Authors: Ameer Abutaleb; Jose Antonio Almario; Saleh Alghsoon; Ji Ae Yoon; Kate Gheysens; Shyam Kottilil; Eleanor Wilson Journal: J Clin Exp Hepatol Date: 2020-08-09
Authors: Lucia Cerrito; Maria Elena Ainora; Alberto Nicoletti; Matteo Garcovich; Laura Riccardi; Maurizio Pompili; Antonio Gasbarrini; Maria Assunta Zocco Journal: World J Hepatol Date: 2021-11-27