Noninvasive Diagnosis of Portal Hypertension in Patients With Compensated Advanced Chronic Liver Disease

Mònica Pons(Universitat Autònoma de Barcelona), Salvador Augustín(Universitat Autònoma de Barcelona), Bernhard Scheiner(Medical University of Vienna), Maéva Guillaume(Université Toulouse III - Paul Sabatier), Matteo Rosselli(The Royal Free Hospital), Susana Rodrigues(University of Bern), Horia Ştefănescu, Mang Ma(University of Alberta), Mattias Mandorfer(Medical University of Vienna), Mayka Mergeay-Fabre(Université Toulouse III - Paul Sabatier), Bogdan Procopeț, Philipp Schwabl(Medical University of Vienna), Arnulf Ferlitsch(Hospital of the Brothers of St. John of God), Georg Semmler(Medical University of Vienna), Annalisa Berzigotti(University of Bern), Emmanuel Tsochatzis(The Royal Free Hospital), Christophe Bureau(Université Toulouse III - Paul Sabatier), Thomas Reiberger(Medical University of Vienna), Jaime Bosch(University of Bern), Juan G. Abraldeṣ(University of Alberta), Joan Genescà(Universitat Autònoma de Barcelona)
The American Journal of Gastroenterology
October 8, 2020
Cited by 237Open Access
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Abstract

INTRODUCTION: We aimed to explore the prevalence of portal hypertension in the most common etiologies of patients with compensated advanced chronic liver disease (cACLD) and develop classification rules, based on liver stiffness measurement (LSM), that could be readily used to diagnose or exclude clinically significant portal hypertension (CSPH) in clinical practice. METHODS: This is an international cohort study including patients with paired LSM/hepatic venous pressure gradient (HVPG), LSM ≥10 kPa, and no previous decompensation. Portal hypertension was defined by an HVPG >5 mm Hg. A positive predictive value ≥90% was considered to validate LSM cutoffs for CSPH (HVPG ≥10 mm Hg), whereas a negative predictive value ≥90% ruled out CSPH. RESULTS: A total of 836 patients with hepatitis C (n = 358), nonalcoholic steatohepatitis (NASH, n = 248), alcohol use (n = 203), and hepatitis B (n = 27) were evaluated. Portal hypertension prevalence was >90% in all cACLD etiologies, except for patients with NASH (60.9%), being even lower in obese patients with NASH (53.3%); these lower prevalences of portal hypertension in patients with NASH were maintained across different strata of LSM values. LSM ≥25 kPa was the best cutoff to rule in CSPH in alcoholic liver disease, chronic hepatitis B, chronic hepatitis C, and nonobese patients with NASH, whereas in obese NASH patients, the positive predictive value was only 62.8%. A new model for patients with NASH (ANTICIPATE-NASH model) to predict CSPH considering body mass index, LSM, and platelet count was developed, and a nomogram was constructed. LSM ≤15 kPa plus platelets ≥150 × 10/L ruled out CSPH in most etiologies. DISCUSSION: Patients with cACLD of NASH etiology, especially obese patients with NASH, present lower prevalences of portal hypertension compared with other cACLD etiologies. LSM ≥25 kPa is sufficient to rule in CSPH in most etiologies, including nonobese patients with NASH, but not in obese patients with NASH.


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