Risk Factors for Liver Decompensation and HCC in HCV-Cirrhotic Patients after DAAs: A Multicenter Prospective Study
Background: Prospective studies on predictors of liver-related events in cirrhotic subjects achieving SVR after DAAs are lacking. Methods: We prospectively enrolled HCV cirrhotic patients in four Italian centers between November 2015 and October 2017. SVR and no-SVR cases were compared according to...
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| Published in | Cancers Vol. 13; no. 15; p. 3810 |
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| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Basel
MDPI AG
29.07.2021
MDPI |
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| Online Access | Get full text |
| ISSN | 2072-6694 2072-6694 |
| DOI | 10.3390/cancers13153810 |
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| Abstract | Background: Prospective studies on predictors of liver-related events in cirrhotic subjects achieving SVR after DAAs are lacking. Methods: We prospectively enrolled HCV cirrhotic patients in four Italian centers between November 2015 and October 2017. SVR and no-SVR cases were compared according to the presence or absence of liver-related events during a 24-month follow-up. Independent predictors of liver-related events were evaluated by Cox regression analysis. Results: A total of 706 subjects started DAAs therapy. SVR was confirmed in 687 (97.3%). A total of 61 subjects (8.9%) in the SVR group and 5 (26.3%) in the no-SVR group had liver-related events (p < 0.03). The incidence rate x 100 p/y was 1.6 for HCC, 1.7 for any liver decompensation, and 0.5 for hepatic death. Baseline liver stiffness (LSM) ≥ 20 kPa (HR 4.0; 95% CI 1.1–14.1) and genotype different from 1 (HR 7.5; 95% CI 2.1–27.3) were both independent predictors of liver decompensation. Baseline LSM > 20 KPa (HR 7.2; 95% CI 1.9–26.7) was the sole independent predictor of HCC. A decrease in liver stiffness (Delta LSM) by at least 20% at the end of follow-up was not associated with a decreased risk of liver-related events. Conclusion: Baseline LSM ≥ 20 kPa identifies HCV cirrhotic subjects at higher risk of liver-related events after SVR. |
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| AbstractList | Simple SummaryThe present study explored the predictors of the development of liver-related events in HCV cirrhotic subjects achieving SVR following antiviral therapy with direct-acting antiviral agents (DAAs) during a follow-up of 24 months after SVR confirmation. Patients had a liver stiffness measurement (LSM) of ≥14 kPa at baseline. We found that baseline liver stiffness ≥ 20 kPa and HCV genotype different from 1 were both independent predictors of liver decompensation, while only LSM ≥ 20 kPa was an independent predictor of HCC.AbstractBackground: Prospective studies on predictors of liver-related events in cirrhotic subjects achieving SVR after DAAs are lacking. Methods: We prospectively enrolled HCV cirrhotic patients in four Italian centers between November 2015 and October 2017. SVR and no-SVR cases were compared according to the presence or absence of liver-related events during a 24-month follow-up. Independent predictors of liver-related events were evaluated by Cox regression analysis. Results: A total of 706 subjects started DAAs therapy. SVR was confirmed in 687 (97.3%). A total of 61 subjects (8.9%) in the SVR group and 5 (26.3%) in the no-SVR group had liver-related events (p < 0.03). The incidence rate x 100 p/y was 1.6 for HCC, 1.7 for any liver decompensation, and 0.5 for hepatic death. Baseline liver stiffness (LSM) ≥ 20 kPa (HR 4.0; 95% CI 1.1–14.1) and genotype different from 1 (HR 7.5; 95% CI 2.1–27.3) were both independent predictors of liver decompensation. Baseline LSM > 20 KPa (HR 7.2; 95% CI 1.9–26.7) was the sole independent predictor of HCC. A decrease in liver stiffness (Delta LSM) by at least 20% at the end of follow-up was not associated with a decreased risk of liver-related events. Conclusion: Baseline LSM ≥ 20 kPa identifies HCV cirrhotic subjects at higher risk of liver-related events after SVR. Prospective studies on predictors of liver-related events in cirrhotic subjects achieving SVR after DAAs are lacking.BACKGROUNDProspective studies on predictors of liver-related events in cirrhotic subjects achieving SVR after DAAs are lacking.We prospectively enrolled HCV cirrhotic patients in four Italian centers between November 2015 and October 2017. SVR and no-SVR cases were compared according to the presence or absence of liver-related events during a 24-month follow-up. Independent predictors of liver-related events were evaluated by Cox regression analysis.METHODSWe prospectively enrolled HCV cirrhotic patients in four Italian centers between November 2015 and October 2017. SVR and no-SVR cases were compared according to the presence or absence of liver-related events during a 24-month follow-up. Independent predictors of liver-related events were evaluated by Cox regression analysis.A total of 706 subjects started DAAs therapy. SVR was confirmed in 687 (97.3%). A total of 61 subjects (8.9%) in the SVR group and 5 (26.3%) in the no-SVR group had liver-related events (p < 0.03). The incidence rate x 100 p/y was 1.6 for HCC, 1.7 for any liver decompensation, and 0.5 for hepatic death. Baseline liver stiffness (LSM) ≥ 20 kPa (HR 4.0; 95% CI 1.1-14.1) and genotype different from 1 (HR 7.5; 95% CI 2.1-27.3) were both independent predictors of liver decompensation. Baseline LSM > 20 KPa (HR 7.2; 95% CI 1.9-26.7) was the sole independent predictor of HCC. A decrease in liver stiffness (Delta LSM) by at least 20% at the end of follow-up was not associated with a decreased risk of liver-related events.RESULTSA total of 706 subjects started DAAs therapy. SVR was confirmed in 687 (97.3%). A total of 61 subjects (8.9%) in the SVR group and 5 (26.3%) in the no-SVR group had liver-related events (p < 0.03). The incidence rate x 100 p/y was 1.6 for HCC, 1.7 for any liver decompensation, and 0.5 for hepatic death. Baseline liver stiffness (LSM) ≥ 20 kPa (HR 4.0; 95% CI 1.1-14.1) and genotype different from 1 (HR 7.5; 95% CI 2.1-27.3) were both independent predictors of liver decompensation. Baseline LSM > 20 KPa (HR 7.2; 95% CI 1.9-26.7) was the sole independent predictor of HCC. A decrease in liver stiffness (Delta LSM) by at least 20% at the end of follow-up was not associated with a decreased risk of liver-related events.Baseline LSM ≥ 20 kPa identifies HCV cirrhotic subjects at higher risk of liver-related events after SVR.CONCLUSIONBaseline LSM ≥ 20 kPa identifies HCV cirrhotic subjects at higher risk of liver-related events after SVR. Background: Prospective studies on predictors of liver-related events in cirrhotic subjects achieving SVR after DAAs are lacking. Methods: We prospectively enrolled HCV cirrhotic patients in four Italian centers between November 2015 and October 2017. SVR and no-SVR cases were compared according to the presence or absence of liver-related events during a 24-month follow-up. Independent predictors of liver-related events were evaluated by Cox regression analysis. Results: A total of 706 subjects started DAAs therapy. SVR was confirmed in 687 (97.3%). A total of 61 subjects (8.9%) in the SVR group and 5 (26.3%) in the no-SVR group had liver-related events (p < 0.03). The incidence rate x 100 p/y was 1.6 for HCC, 1.7 for any liver decompensation, and 0.5 for hepatic death. Baseline liver stiffness (LSM) ≥ 20 kPa (HR 4.0; 95% CI 1.1–14.1) and genotype different from 1 (HR 7.5; 95% CI 2.1–27.3) were both independent predictors of liver decompensation. Baseline LSM > 20 KPa (HR 7.2; 95% CI 1.9–26.7) was the sole independent predictor of HCC. A decrease in liver stiffness (Delta LSM) by at least 20% at the end of follow-up was not associated with a decreased risk of liver-related events. Conclusion: Baseline LSM ≥ 20 kPa identifies HCV cirrhotic subjects at higher risk of liver-related events after SVR. |
| Author | Federico, Alessandro Benigno, Rosa G. Cannavò, Mariarita Dallio, Marcello Begini, Paola Guarino, Maria Pontillo, Giuseppina Lombardo, Flavia L. Stroffolini, Tommaso Marignani, Massimo Morisco, Filomena |
| AuthorAffiliation | 4 Liver Unit, Department of Internal Medicine, ARNAS Garibaldi, 95100 Catania, Italy; mariaritac@alice.it (M.C.); r.benigno@ao-garibaldi.ct.it (R.G.B.) 6 Department of Tropical and Infectious Disease, Policlinico Umberto I, 00161 Rome, Italy; tommaso.stroffolini@hotmail.it 1 Gastroenterology and Hepatology Unit, Department of Clinical Medicine and Surgery, University of Naples “Federico II”, 80131 Naples, Italy; filomena.morisco@unina.it (F.M.); giu.pontillo@gmail.com (G.P.) 2 Hepato-Gastroenterology Unit, University of Campania Luigi Vanvitelli, 80131 Naples, Italy; alessandro.federico@unicampania.it (A.F.); marcello.dallio@gmail.com (M.D.) 5 National Center for Disease Prevention and Health Promotion, Italian National Institute of Health, 00161 Rome, Italy; flavia.lombardo@iss.it 3 Department of Liver Diseases Section, AOU Sant’Andrea Hospital, University of Hospital La Sapienza, 00189 Rome, Italy; massimo.marignani@uniroma1.it (M.M.); paolabegini@virgilio.it (P.B.) |
| AuthorAffiliation_xml | – name: 5 National Center for Disease Prevention and Health Promotion, Italian National Institute of Health, 00161 Rome, Italy; flavia.lombardo@iss.it – name: 3 Department of Liver Diseases Section, AOU Sant’Andrea Hospital, University of Hospital La Sapienza, 00189 Rome, Italy; massimo.marignani@uniroma1.it (M.M.); paolabegini@virgilio.it (P.B.) – name: 6 Department of Tropical and Infectious Disease, Policlinico Umberto I, 00161 Rome, Italy; tommaso.stroffolini@hotmail.it – name: 4 Liver Unit, Department of Internal Medicine, ARNAS Garibaldi, 95100 Catania, Italy; mariaritac@alice.it (M.C.); r.benigno@ao-garibaldi.ct.it (R.G.B.) – name: 2 Hepato-Gastroenterology Unit, University of Campania Luigi Vanvitelli, 80131 Naples, Italy; alessandro.federico@unicampania.it (A.F.); marcello.dallio@gmail.com (M.D.) – name: 1 Gastroenterology and Hepatology Unit, Department of Clinical Medicine and Surgery, University of Naples “Federico II”, 80131 Naples, Italy; filomena.morisco@unina.it (F.M.); giu.pontillo@gmail.com (G.P.) |
| Author_xml | – sequence: 1 givenname: Filomena surname: Morisco fullname: Morisco, Filomena – sequence: 2 givenname: Alessandro orcidid: 0000-0002-0885-0793 surname: Federico fullname: Federico, Alessandro – sequence: 3 givenname: Massimo surname: Marignani fullname: Marignani, Massimo – sequence: 4 givenname: Mariarita surname: Cannavò fullname: Cannavò, Mariarita – sequence: 5 givenname: Giuseppina orcidid: 0000-0001-8449-6362 surname: Pontillo fullname: Pontillo, Giuseppina – sequence: 6 givenname: Maria surname: Guarino fullname: Guarino, Maria – sequence: 7 givenname: Marcello orcidid: 0000-0003-4153-815X surname: Dallio fullname: Dallio, Marcello – sequence: 8 givenname: Paola surname: Begini fullname: Begini, Paola – sequence: 9 givenname: Rosa G. surname: Benigno fullname: Benigno, Rosa G. – sequence: 10 givenname: Flavia L. surname: Lombardo fullname: Lombardo, Flavia L. – sequence: 11 givenname: Tommaso surname: Stroffolini fullname: Stroffolini, Tommaso |
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| Snippet | Background: Prospective studies on predictors of liver-related events in cirrhotic subjects achieving SVR after DAAs are lacking. Methods: We prospectively... Simple SummaryThe present study explored the predictors of the development of liver-related events in HCV cirrhotic subjects achieving SVR following antiviral... Prospective studies on predictors of liver-related events in cirrhotic subjects achieving SVR after DAAs are lacking.BACKGROUNDProspective studies on... |
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| SubjectTerms | Antiviral agents Genotype & phenotype Genotypes Hypertension Liver Risk factors Serology Transplants & implants |
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| Title | Risk Factors for Liver Decompensation and HCC in HCV-Cirrhotic Patients after DAAs: A Multicenter Prospective Study |
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