Nicolás Merchante1, Antonio Rivero-Juárez2, Francisco Téllez3, Dolores Merino4, María J Ríos-Villegas5, Marina Villalobos6, Mohamed Omar7, Pilar Rincón1, Antonio Rivero2, Montserrat Pérez-Pérez8, Miguel Raffo4, Inmaculada López-Montesinos5, Rosario Palacios6, María A Gómez-Vidal7, Juan Macías1, Juan A Pineda1. 1. Unidad Clínica de Enfermedades Infecciosas y Microbiología, Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario de Valme, Sevilla, Spain. 2. Unidad de Enfermedades Infecciosas, Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Hospital Universitario Reina Sofía, Universidad de Córdoba (UCO), Córdoba, Spain. 3. Unidad de Enfermedades Infecciosas, Hospital Universitario de Puerto Real, Cádiz, Spain. 4. Unidad de Gestión Clínica de Enfermedades Infecciosas, Hospitales Juan Ramón Jiménez e Infanta Elena, Huelva, Spain. 5. Unidad de Enfermedades Infecciosas, Hospital Universitario Virgen Macarena, Sevilla, Spain. 6. Unidad de Gestión Clínica de Enfermedades Infecciosas, Microbiología y Medicina Preventiva, Instituto de Biomedicina de Málaga (IBIMA), Hospital Virgen de la Victoria, Málaga, Spain. 7. Unidad de Enfermedades Infecciosas, Complejo Hospitalario de Jaén, Jaén, Spain. 8. Unidad de Gestión Clínica de Enfermedades Infecciosas y Microbiología, Hospital de La Línea de la Concepción, AGS Campo de Gibraltar, Cádiz, Spain.
Abstract
Objectives: To assess the impact of all-oral direct-acting antiviral agent (DAA) regimens on the risk of hepatocellular carcinoma (HCC) in HIV/HCV-coinfected patients with cirrhosis. Methods: This was a multicentre prospective cohort study recruiting HIV/HCV-coinfected patients with a new diagnosis of compensated cirrhosis. Patients were followed up until HCC, death or the censoring date (March 2017). The primary endpoint was the emergence of HCC. The incidence rate (IR) (95% CI) of HCC in different groups was computed. Time-to-event analyses were performed to identify predictors of HCC emergence. Results: The study included 495 HIV/HCV-coinfected patients with cirrhosis. After a median (IQR) follow-up of 59 (27-84) months, 22 (4.4%; 95% CI 2.6-6.3) patients developed an HCC. The IR (95% CI) of HCC was 0.93 (0.06-1.42) per 100 person-years (PY). Three hundred and three (61%) patients achieved sustained virological response (SVR) during follow-up, 79 after interferon (IFN)-based regimens and 224 after an all-oral DAA regimen. The IR (95% CI) of HCC after all-oral DAA was 0.35 (0.14-0.85) per 100 PY whereas it was 1.79 (1.11-2.88) per 100 PY in the remaining cohort (P = 0.0005). When only patients with SVR were considered, the IR (95% CI) of HCC after all-oral DAA was 0.32 (0.12-0.86) whereas it was 0 per 100 PY among those with SVR after IFN-based therapies (P = 0.27). Achieving SVR with an all-oral DAA regimen during follow-up was independently associated with a lower risk of HCC emergence (subhazard ratio 0.264; 95% CI 0.070-0.991; P = 0.049). Conclusions: SVR with all-oral DAA regimens reduces the risk of HCC in HIV/HCV-coinfected patients with compensated cirrhosis.
Objectives: To assess the impact of all-oral direct-acting antiviral agent (DAA) regimens on the risk of hepatocellular carcinoma (HCC) in HIV/HCV-coinfectedpatients with cirrhosis. Methods: This was a multicentre prospective cohort study recruiting HIV/HCV-coinfectedpatients with a new diagnosis of compensated cirrhosis. Patients were followed up until HCC, death or the censoring date (March 2017). The primary endpoint was the emergence of HCC. The incidence rate (IR) (95% CI) of HCC in different groups was computed. Time-to-event analyses were performed to identify predictors of HCC emergence. Results: The study included 495 HIV/HCV-coinfectedpatients with cirrhosis. After a median (IQR) follow-up of 59 (27-84) months, 22 (4.4%; 95% CI 2.6-6.3) patients developed an HCC. The IR (95% CI) of HCC was 0.93 (0.06-1.42) per 100 person-years (PY). Three hundred and three (61%) patients achieved sustained virological response (SVR) during follow-up, 79 after interferon (IFN)-based regimens and 224 after an all-oral DAA regimen. The IR (95% CI) of HCC after all-oral DAA was 0.35 (0.14-0.85) per 100 PY whereas it was 1.79 (1.11-2.88) per 100 PY in the remaining cohort (P = 0.0005). When only patients with SVR were considered, the IR (95% CI) of HCC after all-oral DAA was 0.32 (0.12-0.86) whereas it was 0 per 100 PY among those with SVR after IFN-based therapies (P = 0.27). Achieving SVR with an all-oral DAA regimen during follow-up was independently associated with a lower risk of HCC emergence (subhazard ratio 0.264; 95% CI 0.070-0.991; P = 0.049). Conclusions: SVR with all-oral DAA regimens reduces the risk of HCC in HIV/HCV-coinfectedpatients with compensated cirrhosis.
Authors: Omar A Saldarriaga; Bradley Dye; Judy Pham; Timothy G Wanninger; Daniel Millian; Michael Kueht; Benjamin Freiberg; Netanya Utay; Heather L Stevenson Journal: Sci Rep Date: 2021-07-15 Impact factor: 4.379