Mathieu Chalouni1, Stanislas Pol2, Philippe Sogni2, Hélène Fontaine2, Karine Lacombe3, Jean Marc-Lacombe4, Laure Esterle1, Celine Dorival5, Marc Bourlière6, Firouzé Bani-Sadr7, Victor de Ledinghen8, David Zucman9, Dominique Larrey10, Dominique Salmon11, Fabrice Carrat12, Linda Wittkop13. 1. ISPED, INSERM, Bordeaux Population Health Research Center, Team MORPH3EUS, UMR 1219, CIC-EC 1401, University of Bordeaux, Bordeaux, France. 2. Assistance Publique - Hôpitaux de Paris, Hôpital Cochin, Département d'Hépatologie, Université de Paris, INSERM U-1223 et ICD, Institut Pasteur, Paris, France. 3. INSERM, Institut Pierre Louis d'Epidémiologie et de Santé Publique, IPLESP, Sorbonne Université, Paris, France; APHP, Hôpital Saint-Antoine, Service de Maladies Infectieuses et Tropicales, Paris, France. 4. INSERM Transfert, Paris, France. 5. INSERM, Institut Pierre Louis d'Epidémiologie et de Santé Publique, IPLESP, Sorbonne Université, Paris, France. 6. Department of Hepatology and Gastroenterology, Hôpital Saint Joseph, Marseille, France. 7. Department of Internal Medicine, Clinical Immunology and Infectious Diseases, Robert Debré Hospital, University Hospital, Reims, France. 8. Service d'Hépatologie, Centre Hospitalier Universitaire de Bordeaux, Hôpital Haut-Lévêque, Bordeaux, France; INSERM U1053, Université de Bordeaux, Bordeaux, France. 9. Service de Médecine Interne, Hôpital Foch, Suresnes, France. 10. Service des Maladies de l'Appareil Digestif, Hôpital Saint Eloi, IBR - INSERM, Montpellier, France. 11. Université de Paris, Paris, France; Service Maladies Infectieuses et Tropicales, AP-HP, Hôpital Cochin Hôtel Dieu, Paris, France. 12. INSERM, Institut Pierre Louis d'Epidémiologie et de Santé Publique, IPLESP, Sorbonne Université, Paris, France; AP-HP, Hôpital Saint-Antoine, Unité de Santé Publique, Paris, France. 13. ISPED, INSERM, Bordeaux Population Health Research Center, Team MORPH3EUS, UMR 1219, CIC-EC 1401, University of Bordeaux, Bordeaux, France; CHU de Bordeaux, Pôle de Santé Publique, Bordeaux, France. Electronic address: linda.wittkop@u-bordeaux.fr.
Abstract
BACKGROUND & AIMS: Direct-acting antivirals (DAA) lead to high sustained virological response (SVR) rates and decrease the risk of disease progression. We compared SVR rates and all-cause, liver- and non-liver-related deaths, liver-related events, and non-liver-related cancers in HIV/HCV-coinfected and HCV-monoinfected participants from 2 French cohort studies after initiation of DAA treatment. METHODS: Up to 4 HCV-monoinfected participants from the ANRS CO22 HEPATHER cohort were matched by age and sex to each HIV/HCV-coinfected patient from the ANRS CO13 HEPAVIH cohort; both are nationwide, prospective, multicentre, and observational. Participants were initiated on DAAs between March 2014 and December 2017. Cox proportional hazards models adjusted by age, sex, duration since HCV diagnosis, HCV transmission routes, HCV genotypes, cirrhosis, tobacco, alcohol consumption, and SVR (time dependent) were used. RESULTS: A total of 592 HIV/HCV-coinfected and 2,049 HCV-monoinfected participants were included; median age was 53.3 years (inter-quartile range: 49.6-56.9) and 52.9 years (49.6; 56.7), 1,498 (73.1%) and 436 (73.6%) were men, and 159 (28.8%) and 793 (41.2%) had cirrhosis, respectively. SVR was observed in 92.9% and 94.6%, respectively. HIV coinfection was associated with higher risk of all-cause death (hazard ratio [HR] 1.93; 95% CI 1.01-3.69), non-liver-related death (HR 2.84; 95% CI 1.27-6.36), and non-liver-related cancer (HR 3.26; 95% CI 1.50-7.08), but not with liver-related-death (HR 1.04; 95% CI 0.34-3.15) or liver-related events (HR 0.66; 95% CI 0.31-1.44). CONCLUSIONS: After DAA treatment, HIV-coinfected individuals had similar SVR rates and risk of liver-related deaths and events compared with HCV-monoinfected individuals, but had a higher risk of all-cause and non-liver-related deaths and non-liver-related cancers. LAY SUMMARY: We compared the risk of several clinical events in participants infected by human immunodeficiency virus and hepatitis C virus with those infected with hepatitis C virus alone, matched on age and sex, after treatment with contemporary direct-acting antivirals. We found a higher risk of all-cause deaths, non-liver-related deaths, and non-liver-related cancers in participants coinfected with the human immunodeficiency virus and hepatitis C virus, and no differences for the risk of liver-related deaths or events.
BACKGROUND & AIMS: Direct-acting antivirals (DAA) lead to high sustained virological response (SVR) rates and decrease the risk of disease progression. We compared SVR rates and all-cause, liver- and non-liver-related deaths, liver-related events, and non-liver-related cancers in HIV/HCV-coinfected and HCV-monoinfected participants from 2 French cohort studies after initiation of DAA treatment. METHODS: Up to 4 HCV-monoinfected participants from the ANRS CO22 HEPATHER cohort were matched by age and sex to each HIV/HCV-coinfected patient from the ANRS CO13 HEPAVIH cohort; both are nationwide, prospective, multicentre, and observational. Participants were initiated on DAAs between March 2014 and December 2017. Cox proportional hazards models adjusted by age, sex, duration since HCV diagnosis, HCV transmission routes, HCV genotypes, cirrhosis, tobacco, alcohol consumption, and SVR (time dependent) were used. RESULTS: A total of 592 HIV/HCV-coinfected and 2,049 HCV-monoinfected participants were included; median age was 53.3 years (inter-quartile range: 49.6-56.9) and 52.9 years (49.6; 56.7), 1,498 (73.1%) and 436 (73.6%) were men, and 159 (28.8%) and 793 (41.2%) had cirrhosis, respectively. SVR was observed in 92.9% and 94.6%, respectively. HIV coinfection was associated with higher risk of all-cause death (hazard ratio [HR] 1.93; 95% CI 1.01-3.69), non-liver-related death (HR 2.84; 95% CI 1.27-6.36), and non-liver-related cancer (HR 3.26; 95% CI 1.50-7.08), but not with liver-related-death (HR 1.04; 95% CI 0.34-3.15) or liver-related events (HR 0.66; 95% CI 0.31-1.44). CONCLUSIONS: After DAA treatment, HIV-coinfected individuals had similar SVR rates and risk of liver-related deaths and events compared with HCV-monoinfected individuals, but had a higher risk of all-cause and non-liver-related deaths and non-liver-related cancers. LAY SUMMARY: We compared the risk of several clinical events in participants infected by human immunodeficiency virus and hepatitis C virus with those infected with hepatitis C virus alone, matched on age and sex, after treatment with contemporary direct-acting antivirals. We found a higher risk of all-cause deaths, non-liver-related deaths, and non-liver-related cancers in participants coinfected with the human immunodeficiency virus and hepatitis C virus, and no differences for the risk of liver-related deaths or events.