Sonia Alonso López1,2, María Luisa Manzano3, Francisco Gea4, María Luisa Gutiérrez5, Adriana Maria Ahumada1, María José Devesa6, Antonio Olveira7, Benjamin Arturo Polo8, Laura Márquez1, Inmaculada Fernández3, Juan Carlos Ruiz Cobo4, Laura Rayón1, Daniel Riado5, Sonia Izquierdo6, Clara Usón1, Yolanda Real9, Diego Rincón1,2,10,11, Conrado M Fernández-Rodríguez5,12, Rafael Bañares1,2,10,11. 1. Liver Unit, Hospital General Universitario Gregorio Marañón, Madrid, Spain. 2. Instituto De Investigación Sanitaria Gregorio Marañón (IiSGM), Madrid, Spain. 3. Liver Unit, Hospital Universitario 12 De Octubre, Madrid, Spain. 4. Liver Unit, Hospital Universitario Ramón y Cajal, Madrid, Spain. 5. Gastroenterology Unit, Hospital Universitario Fundación Alcorcón, Madrid, Spain. 6. Gastroenterology Unit, Hospital Universitario Clínico San Carlos, Madrid, Spain. 7. Hepatology Unit, Hospital Universitario La Paz, Madrid, Spain. 8. Gastroenterology Unit, Hospital Universitario Fundación Jiménez Díaz, Madrid, Spain. 9. Gastroenterology Unit, Hospital Universitario La Princesa Madrid, Madrid, Spain. 10. Universidad Complutense de Madrid, Madrid, Spain. 11. Centro de Investigación Biomédica En Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Madrid, Spain. 12. Universidad Rey Juan Carlos Madrid, Madrid, Spain.
Abstract
BACKGROUND AND AIMS: Patients with hepatitis C virus (HCV) and advanced fibrosis remain at risk of hepatocellular carcinoma (HCC) after sustained viral response (SVR) and need lifelong surveillance. Because HCC risk is not homogenous and may decrease with fibrosis regression, we aimed to identify patients with low HCC risk based on the prediction of noninvasive markers and its changes after SVR. APPROACH AND RESULTS: This is a multicenter cohort study, including patients with HCV and compensated advanced fibrosis that achieved SVR after direct antivirals. Clinical and transient elastography (TE) data were registered at baseline, 1 year, and 3 years after the end of treatment (EOT). All patients underwent liver ultrasound scan every 6 months. Patients with clinical evaluation 1 year after EOT were eligible. Univariate and multivariate Cox regression analysis were performed, and predictive models were constructed. HCC occurrence rates were evaluated by Kaplan-Meier. Nine hundred and ninety-three patients were eligible (56% male; 44% female; median age 62 years), 35 developed HCC (3.9%), and the median follow-up was 45 months (range 13-53). Baseline liver stiffness measurement (LSM) (HR 1.040; 95% CI 1.017-1.064), serum albumin (HR 0.400; 95% CI 0.174-0.923), 1-year DeltaLSM (HR 0.993; 95% CI 0.987-0.998), and 1-year FIB-4 score (HR 1.095; 95% CI 1.046-1.146) were independent factors associated with HCC. The TE-based HCC risk model predicted 0% of HCC occurrence at 3 years in patients with score 0 (baseline LSM ≤ 17.3 kPa, albumin >4.2 g/dL, and 1-year DeltaLSM > 25.5%) versus 5.2% in patients with score 1-3 (Harrell's C 0.779; log-rank 0.002). An alternative model with FIB-4 similarly predicted HCC risk. CONCLUSIONS: A combination of baseline and dynamic changes in noninvasive markers may help to identify patients with a very low risk of HCC development after SVR.
BACKGROUND AND AIMS: Patients with hepatitis C virus (HCV) and advanced fibrosis remain at risk of hepatocellular carcinoma (HCC) after sustained viral response (SVR) and need lifelong surveillance. Because HCC risk is not homogenous and may decrease with fibrosis regression, we aimed to identify patients with low HCC risk based on the prediction of noninvasive markers and its changes after SVR. APPROACH AND RESULTS: This is a multicenter cohort study, including patients with HCV and compensated advanced fibrosis that achieved SVR after direct antivirals. Clinical and transient elastography (TE) data were registered at baseline, 1 year, and 3 years after the end of treatment (EOT). All patients underwent liver ultrasound scan every 6 months. Patients with clinical evaluation 1 year after EOT were eligible. Univariate and multivariate Cox regression analysis were performed, and predictive models were constructed. HCC occurrence rates were evaluated by Kaplan-Meier. Nine hundred and ninety-three patients were eligible (56% male; 44% female; median age 62 years), 35 developed HCC (3.9%), and the median follow-up was 45 months (range 13-53). Baseline liver stiffness measurement (LSM) (HR 1.040; 95% CI 1.017-1.064), serum albumin (HR 0.400; 95% CI 0.174-0.923), 1-year DeltaLSM (HR 0.993; 95% CI 0.987-0.998), and 1-year FIB-4 score (HR 1.095; 95% CI 1.046-1.146) were independent factors associated with HCC. The TE-based HCC risk model predicted 0% of HCC occurrence at 3 years in patients with score 0 (baseline LSM ≤ 17.3 kPa, albumin >4.2 g/dL, and 1-year DeltaLSM > 25.5%) versus 5.2% in patients with score 1-3 (Harrell's C 0.779; log-rank 0.002). An alternative model with FIB-4 similarly predicted HCC risk. CONCLUSIONS: A combination of baseline and dynamic changes in noninvasive markers may help to identify patients with a very low risk of HCC development after SVR.
Authors: Jérémy Dana; Aïna Venkatasamy; Antonio Saviano; Joachim Lupberger; Yujin Hoshida; Valérie Vilgrain; Pierre Nahon; Caroline Reinhold; Benoit Gallix; Thomas F Baumert Journal: Hepatol Int Date: 2022-02-09 Impact factor: 9.029
Authors: Ângelo Zambam de Mattos; Jose D Debes; Andre Boonstra; Ju-Dong Yang; Domingo C Balderramo; Giovana D P Sartori; Angelo Alves de Mattos Journal: World J Gastroenterol Date: 2021-06-28 Impact factor: 5.742
Authors: Elton Dajti; Giovanni Marasco; Federico Ravaioli; Luigi Colecchia; Alberto Ferrarese; Davide Festi; Antonio Colecchia Journal: JHEP Rep Date: 2021-04-14