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| Journal of hepatology. 2021 Dec 3. pii: S0168-8278(21)02234-0. doi: 10.1016/j.jhep.2021.11.025 |
| HCC risk stratification after cure of hepatitis C in patients with compensated advanced chronic liver disease. |
| Semmler G1, Meyer EL2, Kozbial K3, Schwabl P4, Hametner-Schreil S5, Zanetto A6, Bauer D7, Chromy D8, Simbrunner B9, Scheiner B10, Stättermayer AF11, Pinter M12, Schöfl R13, Russo FP14, Greenfield H15, Schwarz M16, Schwarz C17, Gschwantler M18, Alonso López S19, Manzano ML20, Ahumada A21, Bañares R22, Pons M23, Rodriguez-Tajes S24, Genesca J25, Lens S26, Trauner M27, Ferenci P28, Reiberger T29, Mandorfer M30 |
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Abstract BACKGROUND&AIMS: Hepatocellular carcinoma (HCC) is a main cause of morbidity and mortality in patients with advanced chronic liver disease (ACLD) due to chronic hepatitis C and who have achieved sustained virologic response (SVR). We elaborated risk stratification algorithms for de-novo-HCC-development after SVR and validated them in an independent cohort. METHODS: Derivation cohort: 527 patients with pre-treatment ACLD and SVR to interferon-free therapy were evaluated for de-novo-HCC-development. Among others, alpha-fetoprotein (AFP) and non-invasive surrogates of portal hypertension including liver stiffness measurement (LSM) were assessed pre-/post-treatment. Validation cohort: 1500 patients with compensated ACLD (cACLD) from other European centers. RESULTS: During a median follow-up (FU) of 41 months, 22/475 cACLD (4.6%) (1.45/100patient-years)vs.12/52 decompensated patients (23.1%, 7.00/100patient-years, p<0.001) developed de-novo-HCC. Since decompensated patients were at substantial HCC-risk, we focused on cACLD for all further analyses. In cACLD, post-treatment-values showed a higher discriminative ability for patients with/without de-novo-HCC-development during FU than pre-treatment-values or absolute/relative changes. Models based on post-treatment AFP≥4.6ngxmL-3points, alcohol consumption (males:>30g/d/females:>20g/d)-2points (optional), age≥59year-2points, LSM≥19.0kPa-1point, and albumin<42gxL-1point, accurately predicted de-novo-HCC-development (bootstrapped Harrel's C with and without considering alcohol:0.893 and 0.836). Importantly, these parameters also provided independent prognostic information in competing risk analysis and accurately stratified patients into low-(0-3points; ≈2/3 of patients) and high-risk (≥4points; ≈1/3) groups in the derivation (algorithm with alcohol consumption; 4-year HCC-risk:0%vs.16.5%) and validation (3.3%/17.5%) cohorts. An alternative approach based on age/alcohol (optional)/FU-LSM/FU-albumin (i.e., without FU-AFP) also showed a robust performance. CONCLUSIONS: Simple algorithms based on post-treatment age/albumin/LSM, and optionally, AFP and alcohol, accurately stratified de-novo-HCC-risk in cACLD patients with SVR. Approximately 2/3 were identified as having an HCC-risk <1%/y in both the derivation and validation cohort, thereby clearly falling below the cost-effectiveness threshold for HCC-surveillance. LAY SUMMARY: Simple algorithms based on age, alcohol consumption, results of blood tests (albumin and α-fetoprotein), as well as liver stiffness measurement after the end of hepatitis C treatment identify a large proportion (approximately 2/3) of patients with advanced but still asymptomatic liver disease who are at very low risk (<1%/year) of liver cancer development, and thus, might not need to undergo 6-monthly liver ultrasound. |
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Copyright © 2021 The Author(s). Published by Elsevier B.V. All rights reserved. |
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KEYWORDS: SVR, cACLD, hepatitis C, hepatocellular carcinoma, surveillance |
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Publikations ID: 34871626 Quelle: öffnen |
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