Dominique Salmon-Ceron1,2, Pierre Nahon3,4, Richard Layese5,6,7, Valérie Bourcier3, Philippe Sogni2,8, Firouze Bani-Sadr9,10, Etienne Audureau5,6,7, Laurence Merchadou11, François Dabis11,12, Linda Wittkop11,12, Françoise Roudot-Thoraval5,6,7. 1. APHP, Hôpitaux Universitaires Paris Centre, Infectious Diseases Federation, Paris, France. 2. Paris Descartes University, Paris, France. 3. AP-HP, Hôpital Jean Verdier, Hepatology Department, Bondy, France. 4. Paris 13 University, Sorbonne Paris Cité, "Equipe Labellisée Ligue Contre le Cancer," Saint-Denis, and Inserm UMR 1162, Paris, France. 5. AP-HP, Hôpital Henri-Mondor, Public Health Department, 94000, Créteil, France. 6. AP-HP, Hôpital Henri-Mondor, Clinical Research Unit (URC-Mondor), 94000, Créteil, France. 7. Université Paris-Est, UPEC, DHU A-TVB, IMRB-EA CEpiA (Clinical Epidemiology and Ageing) Unit EA7376, 94000, Créteil, France. 8. INSERM U-1223, Institut Pasteur and APHP, Hôpitaux Universitaires Paris Centre, Hepatology Department, Paris, France. 9. Centre Hospitalier Universitaire de Reims, Internal Medicine Department, Infectious Diseases and Clinical Immunology Unit, Reims, France. 10. Reims University, Champagne-Ardenne, France. 11. Bordeaux University, ISPED, Inserm, Bordeaux Population Health Research Center, team MORPH3EUS, UMR 1219, CIC-EC 1401, F-33000, Bordeaux, France. 12. CHU de Bordeaux, Public Health and Medical Information Department, F-33000, Bordeaux, France.
Abstract
It is widely accepted that human immunodeficiency virus (HIV) infection is a risk factor for increased severity of hepatitis C virus (HCV) liver disease. However, owing to better efficacy and safety of combination antiretroviral therapy (cART), and increased access to HCV therapy, whether this condition remains true is still unknown. Overall, 1,253 HCV mono-infected patients and 175 HIV/HCV co-infected patients with cirrhosis, included in two prospective French national cohorts (ANRS CO12 CirVir and CO13 HEPAVIH), were studied. Cirrhosis was compensated (Child-Pugh A), without past history of complication, and assessed on liver biopsy. Incidences of liver decompensation (LD), hepatocellular carcinoma (HCC), and death according to HIV status were calculated by a Fine-Gray model adjusted for age. Propensity score matching was also performed to minimize confounding by baseline characteristics. At baseline, HIV/HCV patients were younger (47.5 vs. 56.0 years; P < 0.001), more frequently males (77.1% vs. 62.3%; P < 0.001), and had at baseline and at end of follow-up similar rates of HCV eradication than HCV mono-infected patients. A total of 80.4% of HIV/HCV patients had an undetectable HIV viral load. After adjustment for age, 5-year cumulative incidences of HCC and decompensation were similar in HIV/HCV and HCV patients (8.5% vs. 13.2%, P = 0.12 and 12.8% vs. 15.6%, P = 0.40, respectively). Overall mortality adjusted for age was higher in HIV/HCV co-infected patients (subhazard ratio [SHR] = 1.88; 95% confidence interval [CI], 1.15-3.06; P = 0.011). Factors associated with LD and HCC were age, absence of sustained virological response, and severity of cirrhosis, but not HIV status. Using a propensity score matching 95 patients of each group according to baseline features, similar results were observed. Conclusion: In HCV-infected patients with cirrhosis, HIV co-infection was no longer associated with higher risks of HCC and hepatic decompensation. Increased mortality, however, persisted, attributed to extrahepatic conditions.
It is widely accepted that human immunodeficiency virus (HIV) infection is a risk factor for increased severity of hepatitis C virus (HCV) liver disease. However, owing to better efficacy and safety of combination antiretroviral therapy (cART), and increased access to HCV therapy, whether this condition remains true is still unknown. Overall, 1,253 HCV mono-infectedpatients and 175 HIV/HCV co-infectedpatients with cirrhosis, included in two prospective French national cohorts (ANRS CO12 CirVir and CO13 HEPAVIH), were studied. Cirrhosis was compensated (Child-Pugh A), without past history of complication, and assessed on liver biopsy. Incidences of liver decompensation (LD), hepatocellular carcinoma (HCC), and death according to HIV status were calculated by a Fine-Gray model adjusted for age. Propensity score matching was also performed to minimize confounding by baseline characteristics. At baseline, HIV/HCVpatients were younger (47.5 vs. 56.0 years; P < 0.001), more frequently males (77.1% vs. 62.3%; P < 0.001), and had at baseline and at end of follow-up similar rates of HCV eradication than HCV mono-infectedpatients. A total of 80.4% of HIV/HCVpatients had an undetectable HIV viral load. After adjustment for age, 5-year cumulative incidences of HCC and decompensation were similar in HIV/HCV and HCVpatients (8.5% vs. 13.2%, P = 0.12 and 12.8% vs. 15.6%, P = 0.40, respectively). Overall mortality adjusted for age was higher in HIV/HCV co-infectedpatients (subhazard ratio [SHR] = 1.88; 95% confidence interval [CI], 1.15-3.06; P = 0.011). Factors associated with LD and HCC were age, absence of sustained virological response, and severity of cirrhosis, but not HIV status. Using a propensity score matching 95 patients of each group according to baseline features, similar results were observed. Conclusion: In HCV-infectedpatients with cirrhosis, HIV co-infection was no longer associated with higher risks of HCC and hepatic decompensation. Increased mortality, however, persisted, attributed to extrahepatic conditions.
Authors: James M Paik; Linda Henry; Pegah Golabi; Saleh A Alqahtani; Gregory Trimble; Zobair M Younossi Journal: Open Forum Infect Dis Date: 2020-01-07 Impact factor: 3.835
Authors: Sara Cuesta-Sancho; Mercedes Márquez-Coello; Francisco Illanes-Álvarez; Denisse Márquez-Ruiz; Ana Arizcorreta; Fátima Galán-Sánchez; Natalia Montiel; Manuel Rodriguez-Iglesias; José-Antonio Girón-González Journal: World J Hepatol Date: 2022-01-27