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Life sciences · Review
Liver International · October 26, 2026
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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.