François Bailly1, Victor Virlogeux2, Cécilie Dufour3, Pierre Pradat1, Christophe Hézode4, Dominique Larrey5, Laurent Alric6, Didier Samuel7, Marc Bourlière8, Sophie Métivier9, Jean-Pierre Zarski10, Hélène Fontaine11, Véronique Loustaud-Ratti12, Lawrence Serfaty13, Jean-Pierre Bronowicki14, Fabrice Carrat3, Fabien Zoulim15. 1. Department of Hepatology, Hôpital de la Croix-Rousse, Hospices Civils de Lyon, 69004 Lyon, France; Inserm U1052, 69003 Lyon, France; Université Lyon I, 69622 Villeurbanne, France. 2. Department of Hepatology, Hôpital de la Croix-Rousse, Hospices Civils de Lyon, 69004 Lyon, France; École Normale Supérieure, 69007 Lyon, France. 3. Inserm UMR-S 707, Université Pierre-et-Marie-Curie Paris 6, 75012 Paris, France. 4. Hépato-gastro-entérologie, CHU Henri-Mondor, 94010 Créteil, France. 5. Hépato-gastroentérologie, CHU de Montpellier, Hôpital Saint-Éloi, 34090 Montpellier, France. 6. Pôle Digestif, CHU Purpan, UMR 152, Université Toulouse 3, 31059 Toulouse, France. 7. Centre Hépato-Biliaire, AP-HP Hôpital Paul-Brousse, 94870 Villejuif, France; Unité 785, Inserm, 94870 Villejuif, France; Université Paris-Sud, 94270 Le Kremlin-Bicêtre, France. 8. Department of Hepatology and Gastroenterology, Hôpital Saint-Joseph, 13285 Marseille, France. 9. Pôle Digestif-Gastro-entérologie-Hépatologie, CHU Purpan, 31059 Toulouse, France. 10. Clinique universitaire d'Hépato-Gastroentérologie, CHRU Michallon, 38043 Grenoble, France. 11. Hôpital Cochin, AP-HP, Université Paris-René Descartes, Inserm U1016, 75014 Paris, France. 12. Fédération Hépatologie, CHU Dupuytren, 87042 Limoges, France. 13. Hépato-gastro-entérologie orienté en hépatologie, CHU Saint-Antoine, 75012 Paris, France. 14. Department of Hepatology and Gastroenterology, CHU de Nancy, Université de Lorraine, Inserm U954, 54500 Vandœuvre-lès-Nancy, France. 15. Department of Hepatology, Hôpital de la Croix-Rousse, Hospices Civils de Lyon, 69004 Lyon, France; Inserm U1052, 69003 Lyon, France; Université Lyon I, 69622 Villeurbanne, France. Electronic address: fabien.zoulim@inserm.fr.
Abstract
BACKGROUND AND OBJECTIVE: To assess within the ANRS CO20-CUPIC cohort whether the viral load (VL) at week 2/week 6 for telaprevir/boceprevir-based triple therapy, respectively, was predictive of sustained virological response (SVR) in patients with hepatitis C virus (HCV) infection and to study the relevance of this measurement to early diagnose drug resistance. METHODS: Observational study of HCV genotype 1 patients with compensated cirrhosis (Child-Pugh A), non-responders to a prior course of interferon (IFN)-based therapy and who started triple therapy. Patients received either 12 weeks of telaprevir in combination with PEG-IFN/ribavirin (RBV), then 36 weeks of PEG-IFN/RBV, or 4 weeks of PEG-IFN/RBV, then 44 weeks of PEG-IFN/RBV and boceprevir. RESULTS: A total of 262 patients were analyzed. For telaprevir-treated patients, 28% had undetectable VL at W2 of whom 81% achieved SVR12 whereas 67% had undetectable VL at W4 of whom 67% achieved SVR12. For boceprevir-treated patients 20% had undetectable VL at W6 and 86% of them achieved SVR12 whereas 36% had undetectable VL at W8 among whom 73% achieved SVR12. Five telaprevir-treated patients had a VL increase between W2 and W4 after a decrease between D0 and W2. Four of them did not achieve SVR12. Similarly, six boceprevir-treated patients had a VL increase between W6 and W8 after a decrease between D0 and W6. Five did not reach SVR12. CONCLUSIONS: The assessment of HCV RNA level after two weeks of triple therapy in cirrhotic non-responder patients is a good predictor of SVR. This assessment was useful to do an early diagnosis of viral breakthrough.
BACKGROUND AND OBJECTIVE: To assess within the ANRS CO20-CUPIC cohort whether the viral load (VL) at week 2/week 6 for telaprevir/boceprevir-based triple therapy, respectively, was predictive of sustained virological response (SVR) in patients with hepatitis C virus (HCV) infection and to study the relevance of this measurement to early diagnose drug resistance. METHODS: Observational study of HCV genotype 1 patients with compensated cirrhosis (Child-Pugh A), non-responders to a prior course of interferon (IFN)-based therapy and who started triple therapy. Patients received either 12 weeks of telaprevir in combination with PEG-IFN/ribavirin (RBV), then 36 weeks of PEG-IFN/RBV, or 4 weeks of PEG-IFN/RBV, then 44 weeks of PEG-IFN/RBV and boceprevir. RESULTS: A total of 262 patients were analyzed. For telaprevir-treated patients, 28% had undetectable VL at W2 of whom 81% achieved SVR12 whereas 67% had undetectable VL at W4 of whom 67% achieved SVR12. For boceprevir-treated patients 20% had undetectable VL at W6 and 86% of them achieved SVR12 whereas 36% had undetectable VL at W8 among whom 73% achieved SVR12. Five telaprevir-treated patients had a VL increase between W2 and W4 after a decrease between D0 and W2. Four of them did not achieve SVR12. Similarly, six boceprevir-treated patients had a VL increase between W6 and W8 after a decrease between D0 and W6. Five did not reach SVR12. CONCLUSIONS: The assessment of HCV RNA level after two weeks of triple therapy in cirrhotic non-responder patients is a good predictor of SVR. This assessment was useful to do an early diagnosis of viral breakthrough.
Authors: Helena Hl Borba; Astrid Wiens; Laiza M Steimbach; Fernanda S Tonin; Maria LA Pedroso; Cláudia Ap Ivantes; Fernando Fernandez-Llimos; Roberto Pontarolo Journal: Ther Clin Risk Manag Date: 2017-01-10 Impact factor: 2.423