Prognostic performance of non-invasive tests for portal hypertension is comparable to that of hepatic venous pressure gradient.

BACKGROUND AND AIMS

Non-invasive tests (NIT) for assessing the probability of clinically significant portal hypertension (CSPH) including the ANTICIPATE±NASH models based on liver stiffness measurement (LSM), platelet count (PLT)±body mass index (BMI), and the von Willebrand factor antigen (VWF) to PLT ratio (VITRO) have fundamentally changed the management of compensated advanced chronic liver disease (cACLD). However, their prognostic utility has not been compared head-to-head against the hepatic venous pressure gradient (HVPG) as the gold standard.

METHODS

cACLD (LSM≥10 kPa) patients who underwent advanced characterization via same-day HVPG/NIT assessment from 2007-2022 were retrospectively included. Long-term follow-up data on hepatic decompensation was recorded.

RESULTS

Four hundred twenty cACLD patients (51.9% viral hepatitis, 20.5% ALD, 18.6% MASLD/MetALD, 9.0% other) with a CSPH prevalence of 67.6% were included. The cumulative incidence of hepatic decompensation at 1 and 2 years were 4.7% and 8.0%, respectively. HVPG, VITRO, and ANTICIPATE±NASH-CSPH-probability showed similar time-dependent prognostic value (AUROC 0.683-0.811 at 1 and 0.699-0.801 at 2 years). In competing risk analyses adjusted for MELD and albumin, HVPG (adjusted subdistribution hazard ratio [aSHR]:1.099 [95%CI:1.054-1.150) per mmHg; p<0.001), or VITRO (aSHR:1.134 [1.062-1.211] per unit; p<0.001), or ANTICIPATE±NASH-CSPH-probability (aSHR:1.232 [1.094-1.387] per 10%; p<0.001) all predicted first decompensation during follow-up. Previously proposed cut-offs (HVPG≥10mmHg vs.<10mmHg, VITRO≥2.5 vs.<2.5, and ANTICIPATE-CSPH probability≥60% vs.<60%) all accurately discriminated between patients at negligible risk and those at substantial risk of hepatic decompensation.

CONCLUSIONS

The prognostic performance of ANTICIPATE±NASH-CSPH-probability and VITRO is comparable to that of HVPG, supporting their utility for identifying patients who may benefit from medical therapies for preventing first hepatic decompensation.

IMPACT AND IMPLICATIONS

Non-invasive tests (NIT) have revolutionized the diagnosis and management of clinically significant portal hypertension (CSPH) in compensated advanced chronic liver disease (cACLD) patients. However, limited data exists regarding the prognostic utility of NIT in direct comparison to the gold standard for prognostication in cACLD, i.e., the hepatic venous pressure gradient (HVPG). In our study including 420 cACLD patients, HVPG and NIT, i.e., most importantly, the ANTICIPATE±NASH model based on platelet count (PLT) and liver stiffness measurement (LSM), and the von Willebrand factor (VWF) to PLT ratio (VITRO), yielded similar AUROC for hepatic decompensation within one to two years. Thus, NIT should be applied and updated in yearly intervals in clinical routine to identify patients at short-term risk, thereby identifying patients who may benefit from treatment aiming at the prevention of hepatic decompensation.

Informations de copyright

Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Conflict of interest The authors declare no conflict of interest regarding this study. Outside the submitted work, the authors declare the following potential conflicts of interest: M.J. served as a speaker and/or consultant for Gilead. B.Sim. received travel support from AbbVie and Gilead. D.B. received speaker fees from AbbVie and Siemens, as well as grant support form Gilead and Siemens, as well as travel support from AbbVie and Gilead. M.P. served as a speaker and/or consultant and/or advisory board member for Bayer, Bristol-Myers Squibb, Eisai, Ipsen, Lilly, MSD, and Roche, and received travel support from Bayer and Bristol-Myers Squibb. M.T. served as a speaker and/or consultant and/or advisory board member for Albireo, BiomX, Falk, Boehringer Ingelheim, Bristol-Myers Squibb, Falk, Genfit, Gilead, Intercept, Janssen, MSD, Madrigal, Novartis, Phenex, Pliant, Regulus, and Shire, and received travel support from AbbVie, Falk, Gilead, and Intercept, as well as grants/research support from Albireo, Alnylam, Cymabay, Falk, Gilead, Intercept, MSD, Takeda, and UltraGenyx. He is also co-inventor of patents on the medical use of 24-norursodeoxycholic acid filed by the Medical Universities of Graz and Vienna. T.R. served as a speaker and/or consultant and/or advisory board member for AbbVie, Bayer, Boehringer Ingelheim, Gilead, Intercept, MSD, Siemens, and W. L. Gore & Associates and received grants/research support from AbbVie, Boehringer Ingelheim, Gilead, Intercept, MSD, Myr Pharmaceuticals, Pliant, Philips, Siemens, and W. L. Gore & Associates as well as travel support from AbbVie, Boehringer Ingelheim, Gilead and Roche. M.M. served as a speaker and/or consultant and/or advisory board member for AbbVie, Ipsen, Echosens, Gilead, and W. L. Gore & Associates and received travel support from AbbVie and Gilead. L.H., G.S., L.B., B.H., M. Sch., and A.F.S. have nothing to disclose.