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Peer-reviewedCC BY 4.0Liver International

Endohepatology in the Management of Portal Hypertension in Metabolic Dysfunction‐Associated Steatotic Liver Disease

  • Michael Praktiknjo1
  • Reiner Wiest2
  • Andres Cardenas3,4,5
  • Jonel Trebicka1
  • Wim Laleman1,6
6 affiliations
  1. 1Department of Medicine B University Hospital Münster Münster Germany
  2. 2Department of Visceral Surgery and Medicine Inselspital, Bern University Hospital, University of Bern Bern Switzerland
  3. 3GI/Liver Unit, Institute of Digestive Diseases & Metabolism Hospital Clínic Barcelona Spain
  4. 4Ciber de Enfermedades Hepáticas y Digestivas (CIBEREHD) Madrid Spain
  5. 5Institut d'Investigacions Biomèdiques August Pi‐Sunyer (IDIBAPS) Barcelona Spain
  6. 6Department of Gastroenterology and Hepatology, Section of Liver and Biliopancreatic Disorders and Liver Transplantation University Hospitals Leuven, KU Leuven Leuven Belgium
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Abstract

Portal hypertension is the principal driver of decompensation in advanced chronic liver disease, yet in metabolic dysfunction‐associated steatotic liver disease (MASLD) it deviates from the classical sinusoidal paradigm. Growing evidence points to a mixed sinusoidal–presinusoidal phenotype in which the hepatic venous pressure gradient (HVPG) may underestimate true portal pressure, and in which decompensation and varices can occur at lower HVPG values than in viral cirrhosis. This biology is compounded by a diagnostic gap: non‐invasive tests such as liver stiffness by vibration‐controlled transient elastography, FIB‐4, ANTICIPATE‐NASH, spleen stiffness and the NICER model, are degraded by obesity through technical limitations and altered diagnostic thresholds, even when test discrimination is preserved. Moreover, no non‐invasive rule‐in for clinically significant portal hypertension reaches a 90% positive predictive value in obese MASLD, leaving a clinically meaningful grey zone. Endohepatology addresses these diagnostic limitations by providing complementary hemodynamic, elastographic, and histological information. Within a single sedated session, EUS‐guided shear‐wave elastography and EUS‐guided liver biopsy can adjudicate F2–F3 fibrosis when treatment eligibility is uncertain; EUS‐guided portal pressure gradient measurement can provide a direct gradient when HVPG or non‐invasive tests are discordant with the clinical phenotype; and EUS‐based vascular assessment can characterize collateral and variceal anatomy. The same platform extends to therapy, including EUS‐guided gastric variceal obliteration and pre‐bariatric risk stratification. Current evidence is largely early‐phase and requires prospective validation. Rather than replacing established tools, endohepatology offers an integrated pathway tailored to the diagnostic and therapeutic problems most characteristic of MASLD.

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Cite

BibTeXRIS
BibTeX
@article{praktiknjo2026endohepatology,
  title = {{Endohepatology in the Management of Portal Hypertension in Metabolic Dysfunction‐Associated Steatotic Liver Disease}},
  author = {Michael Praktiknjo and Reiner Wiest and Andres Cardenas and Jonel Trebicka and Wim Laleman},
  journal = {Liver International},
  year = {2026},
  month = oct,
  doi = {10.1111/liv.70953},
  url = {https://doi.org/10.1111/liv.70953},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Endohepatology in the Management of Portal Hypertension in Metabolic Dysfunction‐Associated Steatotic Liver Disease
AU  - Michael Praktiknjo
AU  - Reiner Wiest
AU  - Andres Cardenas
AU  - Jonel Trebicka
AU  - Wim Laleman
PY  - 2026
DA  - 2026/10/26
JO  - Liver International
DO  - 10.1111/liv.70953
UR  - https://doi.org/10.1111/liv.70953
AB  - Portal hypertension is the principal driver of decompensation in advanced chronic liver disease, yet in metabolic dysfunction‐associated steatotic liver disease (MASLD) it deviates from the classical sinusoidal paradigm. Growing evidence points to a mixed sinusoidal–presinusoidal phenotype in which the hepatic venous pressure gradient (HVPG) may underestimate true portal pressure, and in which decompensation and varices can occur at lower HVPG values than in viral cirrhosis. This biology is compounded by a diagnostic gap: non‐invasive tests such as liver stiffness by vibration‐controlled transient elastography, FIB‐4, ANTICIPATE‐NASH, spleen stiffness and the NICER model, are degraded by obesity through technical limitations and altered diagnostic thresholds, even when test discrimination is preserved. Moreover, no non‐invasive rule‐in for clinically significant portal hypertension reaches a 90% positive predictive value in obese MASLD, leaving a clinically meaningful grey zone. Endohepatology addresses these diagnostic limitations by providing complementary hemodynamic, elastographic, and histological information. Within a single sedated session, EUS‐guided shear‐wave elastography and EUS‐guided liver biopsy can adjudicate F2–F3 fibrosis when treatment eligibility is uncertain; EUS‐guided portal pressure gradient measurement can provide a direct gradient when HVPG or non‐invasive tests are discordant with the clinical phenotype; and EUS‐based vascular assessment can characterize collateral and variceal anatomy. The same platform extends to therapy, including EUS‐guided gastric variceal obliteration and pre‐bariatric risk stratification. Current evidence is largely early‐phase and requires prospective validation. Rather than replacing established tools, endohepatology offers an integrated pathway tailored to the diagnostic and therapeutic problems most characteristic of MASLD.
SN  - 1478-3223
SN  - 1478-3231
ER  -