Z Gastroenterol 2020; 58(05): e90-e91
DOI: 10.1055/s-0040-1712291
Hepatologie

Non-invasive risk stratification by VCTE and VITRO after HCV eradication

G Semmler
1   Division of Gastroenterology & Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
2   Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Vienna, Austria.
,
T Binter
1   Division of Gastroenterology & Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
,
K Kozbial
1   Division of Gastroenterology & Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
,
P Schwabl
1   Division of Gastroenterology & Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
2   Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Vienna, Austria.
,
D Chromy
1   Division of Gastroenterology & Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
2   Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Vienna, Austria.
,
DJ Bauer
1   Division of Gastroenterology & Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
2   Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Vienna, Austria.
,
B Simbrunner
1   Division of Gastroenterology & Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
2   Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Vienna, Austria.
,
B Scheiner
1   Division of Gastroenterology & Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
2   Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Vienna, Austria.
,
T Bucsics
1   Division of Gastroenterology & Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
2   Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Vienna, Austria.
,
AF Stättermayer
1   Division of Gastroenterology & Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
2   Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Vienna, Austria.
,
M Pinter
1   Division of Gastroenterology & Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
2   Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Vienna, Austria.
,
P Steindl-Munda
1   Division of Gastroenterology & Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
,
M Trauner
1   Division of Gastroenterology & Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
,
P Ferenci
1   Division of Gastroenterology & Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
,
T Reiberger
1   Division of Gastroenterology & Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
2   Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Vienna, Austria.
,
M Mandorfer
1   Division of Gastroenterology & Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
2   Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Vienna, Austria.
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Background & Aims Risk stratification after cure from hepatitis C virus (HCV) infection remains a clinical challenge. We investigated the predictive value of non-invasive surrogates of portal hypertension (liver stiffness measurement (LSM) by vibration-controlled transient elastography (VCTE) and von Willebrand factor/platelet count ratio (VITRO)) for development of hepatic decompensation and hepatocellular carcinoma in patients with pre-treatment advanced chronic liver disease (ACLD) who achieved HCV-cure.

Methods 276 patients with pre-treatment ACLD and information on pre- and post-treatment (follow-up (FU)) LSM and VITRO were followed for a median of 36.6 months after the end of interferon-free therapy.

Results FU-LSM (AUROC: 0.875 (95 %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 models adjusted for previous hepatic decompensation and FU-MELD/-albumin.

A previously proposed combined approach (FU-LSM < 12.4kPa and/or FU-VITRO < 0.95) to rule-out clinically significant portal hypertension (CSPH, HVPG≥ 10mmHg) at FU assigned the majority (57.3 %) of 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 > 25.3kPa and/or FU-VITRO > 3.3; 25.0 % of patients), the risk of hepatic decompensation at 3-years post-treatment was high (17.4 %). Patients within the diagnostic grey-zone for FU-CSPH (17.8 % of patients) had a very low risk of hepatic decompensation during FU (2.6 %).

Finally, VITRO also predicted hepatocellular carcinoma development.

Conclusion FU-LSM/FU-VITRO are strongly and independently predictive of post-treatment hepatic decompensation in HCV-induced ACLD. An algorithm combining these non-invasive markers not only rules-in or rules-out FU-CSPH, but also identifies populations at negligible vs. high risk for hepatic decompensation. FU-LSM/FU-VITRO are readily accessible and enable risk stratification after SVR, and thus, facilitate personalized management.



Publication History

Article published online:
26 May 2020

© Georg Thieme Verlag KG
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