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      Noninvasive Risk Stratification After HCV Eradication in Patients With Advanced Chronic Liver Disease

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          Abstract

          Background and Aims

          Risk stratification after cure from hepatitis C virus (HCV) infection remains a clinical challenge. We investigated the predictive value of noninvasive surrogates of portal hypertension (liver stiffness measurement [LSM] by vibration‐controlled transient elastography and von Willebrand factor/platelet count ratio [VITRO]) for development of hepatic decompensation and hepatocellular carcinoma in patients with pretreatment advanced chronic liver disease (ACLD) who achieved HCV cure.

          Approach and Results

          A total of 276 patients with pretreatment ACLD and information on pretreatment and posttreatment follow‐up (FU)‐LSM and FU‐VITRO were followed for a median of 36.6 months after the end of interferon‐free therapy. FU‐LSM (area under the receiver operating characteristic curve [AUROC]: 0.875 [95% confidence interval [CI]: 0.796‐0.954]) and FU‐VITRO (AUROC: 0.925 [95% CI: 0.874‐0.977]) showed an excellent predictive performance for hepatic decompensation. Both parameters provided incremental information and were significantly associated with hepatic decompensation in adjusted models. A previously proposed combined approach (FU‐LSM < 12.4 kPa and/or FU‐VITRO < 0.95) to rule out clinically significant portal hypertension (CSPH, hepatic venous pressure gradient ≥10 mm Hg) at FU assigned most (57.3%) of the patients to the low‐risk group; none of these patients developed hepatic decompensation. In contrast, in patients in whom FU‐CSPH was ruled in (FU‐LSM > 25.3 kPa and/or FU‐VITRO > 3.3; 25.0% of patients), the risk of hepatic decompensation at 3 years following treatment was high (17.4%). Patients within the diagnostic gray‐zone for FU‐CSPH (17.8% of patients) had a very low risk of hepatic decompensation during FU (2.6%). The prognostic value of this algorithm was validated in an internal (n = 86) and external (n = 162) cohort.

          Conclusion

          FU‐LSM/FU‐VITRO are strongly and independently predictive of posttreatment hepatic decompensation in HCV‐induced ACLD. An algorithm combining these noninvasive markers not only rules in or rules out FU‐CSPH, but also identifies populations at negligible versus high risk for hepatic decompensation. FU‐LSM/FU‐VITRO are readily accessible and enable risk stratification after sustained virological response, and thus facilitate personalized management.

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          Most cited references 37

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          EASL Recommendations on Treatment of Hepatitis C 2015.

          (2015)
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            Expanding consensus in portal hypertension: Report of the Baveno VI Consensus Workshop: Stratifying risk and individualizing care for portal hypertension.

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              EASL Recommendations on Treatment of Hepatitis C 2018

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                Author and article information

                Contributors
                thomas.reiberger@meduniwien.ac.at
                Journal
                Hepatology
                Hepatology
                10.1002/(ISSN)1527-3350
                HEP
                Hepatology (Baltimore, Md.)
                John Wiley and Sons Inc. (Hoboken )
                0270-9139
                1527-3350
                16 March 2021
                April 2021
                : 73
                : 4 ( doiID: 10.1002/hep.v73.4 )
                : 1275-1289
                Affiliations
                [ 1 ] Division of Gastroenterology and Hepatology Department of Internal Medicine III Medical University of Vienna Vienna Austria
                [ 2 ] Vienna Hepatic Hemodynamic Laboratory Medical University of Vienna Vienna Austria
                [ 3 ] Internal Medicine IV Ordensklinikum Linz Barmherzige Schwestern Linz Austria
                [ 4 ] Gastroenterology and Multivisceral Transplant Unit Department of Surgery, Oncology, and Gastroenterology Padua University Hospital Padua Italy
                [ 5 ] General Internal Medicine and Thrombotic and Hemorrhagic Diseases Unit Department of Medicine Padua University Hospital Padua Italy
                Author notes
                [* ] ADDRESS CORRESPONDENCE AND REPRINT REQUESTS TO:

                Thomas Reiberger, M.D.

                Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna

                Währinger Gürtel 18‐20

                1090, Vienna, Austria

                E‐mail: thomas.reiberger@ 123456meduniwien.ac.at

                Tel.: +43 1 40400 47440

                Article
                HEP31462
                10.1002/hep.31462
                8252110
                32659847
                46c9f808-022a-4641-8dd5-5b0d88636227
                © 2020 The Authors. H epatology published by Wiley Periodicals LLC on behalf of American Association for the Study of Liver Diseases.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                Page count
                Figures: 3, Tables: 4, Pages: 0, Words: 8883
                Product
                Funding
                Funded by: Andrew K. Burroughs short‐term training fellowship of the European Association for the Study of the Liver
                Funded by: Medical Scientific Fund of the Major of the City of Vienna
                Award ID: 17035
                Categories
                Original Article
                Original Articles
                Viral Hepatitis
                Custom metadata
                2.0
                April 2021
                Converter:WILEY_ML3GV2_TO_JATSPMC version:6.0.4 mode:remove_FC converted:02.07.2021

                Gastroenterology & Hepatology

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