Noninvasive Diagnosis of Portal Hypertension in Patients With Compensated Advanced Chronic Liver Disease
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 signi...
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| Vydáno v: | The American journal of gastroenterology Ročník 116; číslo 4; s. 723 - 732 |
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| Hlavní autoři: | , , , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
United States
Wolters Kluwer Health Medical Research, Lippincott Williams & Wilkins
01.04.2021
Lippincott, Williams & Wilkins |
| Témata: | |
| ISSN: | 0002-9270, 1572-0241, 1572-0241 |
| On-line přístup: | Získat plný text |
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| Abstract | 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.
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.
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.
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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| AbstractList | 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 × 109/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. 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 9 /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. 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. 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. 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. 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. 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.INTRODUCTIONWe 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.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.METHODSThis 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.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.RESULTSA 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.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.DISCUSSIONPatients 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. |
| Author | Schwabl, Philipp Rodrigues, Susana G. Ma, Mang M. Abraldes, Juan G. Stefanescu, Horia Scheiner, Bernhard Ferlitsch, Arnulf Procopet, Bogdan Mergeay-Fabre, Mayka Reiberger, Thomas Genescà, Joan Mandorfer, Mattias Semmler, Georg Tsochatzis, Emmanuel Augustin, Salvador Berzigotti, Annalisa Rosselli, Matteo Bureau, Christophe Guillaume, Maeva Bosch, Jaime Pons, Monica |
| Author_xml | – sequence: 1 givenname: Monica surname: Pons fullname: Pons, Monica organization: Liver Unit, Department of Internal Medicine, Hospital Universitari Vall d'Hebron, Vall d'Hebron Institut de Recerca (VHIR), Faculty of Medicine, Universitat Autònoma de Barcelona, Barcelona, Spain – sequence: 2 givenname: Salvador surname: Augustin fullname: Augustin, Salvador organization: Liver Unit, Department of Internal Medicine, Hospital Universitari Vall d'Hebron, Vall d'Hebron Institut de Recerca (VHIR), Faculty of Medicine, Universitat Autònoma de Barcelona, Barcelona, Spain;, Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain – sequence: 3 givenname: Bernhard surname: Scheiner fullname: Scheiner, Bernhard organization: Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria;, Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Vienna, Austria – sequence: 4 givenname: Maeva surname: Guillaume fullname: Guillaume, Maeva organization: Service d'Hépatologie CHU Toulouse Rangueil, Institut Cardiomet et Université Paul Sabatier, Toulouse, France – sequence: 5 givenname: Matteo surname: Rosselli fullname: Rosselli, Matteo organization: UCL Institute for Liver and Digestive Health and Sheila Sherlock Liver Centre, Royal Free Hospital and UCL, London, United Kingdom – sequence: 6 givenname: Susana G. surname: Rodrigues fullname: Rodrigues, Susana G. organization: Swiss Liver Center, UVCM, Inselspital, Department of Biomedical Research, University of Bern, Bern, Switzerland – sequence: 7 givenname: Horia surname: Stefanescu fullname: Stefanescu, Horia organization: Liver Unit, Regional Institute of Gastroenterology and Hepatology “Octavian Fodor,” University of Medicine and Pharmacy “Iuliu Hatieganu,” Cluj-Napoca, Romania – sequence: 8 givenname: Mang M. surname: Ma fullname: Ma, Mang M. organization: Division of Gastroenterology (Liver Unit), University of Alberta, Edmonton, Canada – sequence: 9 givenname: Mattias surname: Mandorfer fullname: Mandorfer, Mattias organization: Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria;, Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Vienna, Austria – sequence: 10 givenname: Mayka surname: Mergeay-Fabre fullname: Mergeay-Fabre, Mayka organization: Service d'Hépatologie CHU Toulouse Rangueil, Institut Cardiomet et Université Paul Sabatier, Toulouse, France – sequence: 11 givenname: Bogdan surname: Procopet fullname: Procopet, Bogdan organization: Liver Unit, Regional Institute of Gastroenterology and Hepatology “Octavian Fodor,” University of Medicine and Pharmacy “Iuliu Hatieganu,” Cluj-Napoca, Romania – sequence: 12 givenname: Philipp surname: Schwabl fullname: Schwabl, Philipp organization: Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria;, Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Vienna, Austria – sequence: 13 givenname: Arnulf surname: Ferlitsch fullname: Ferlitsch, Arnulf organization: Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria;, Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Vienna, Austria;, Division of Internal Medicine II, Krankenhaus Barmherzige Brüder, Vienna, Austria – sequence: 14 givenname: Georg surname: Semmler fullname: Semmler, Georg organization: Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria;, Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Vienna, Austria – sequence: 15 givenname: Annalisa surname: Berzigotti fullname: Berzigotti, Annalisa organization: Swiss Liver Center, UVCM, Inselspital, Department of Biomedical Research, University of Bern, Bern, Switzerland;, Liver Unit, Hospital Clinic, IDIBAPS, University of Barcelona, Barcelona, Spain – sequence: 16 givenname: Emmanuel surname: Tsochatzis fullname: Tsochatzis, Emmanuel organization: UCL Institute for Liver and Digestive Health and Sheila Sherlock Liver Centre, Royal Free Hospital and UCL, London, United Kingdom – sequence: 17 givenname: Christophe surname: Bureau fullname: Bureau, Christophe organization: Service d'Hépatologie CHU Toulouse Rangueil, Institut Cardiomet et Université Paul Sabatier, Toulouse, France – sequence: 18 givenname: Thomas surname: Reiberger fullname: Reiberger, Thomas organization: Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria;, Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Vienna, Austria – sequence: 19 givenname: Jaime surname: Bosch fullname: Bosch, Jaime organization: Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain;, Swiss Liver Center, UVCM, Inselspital, Department of Biomedical Research, University of Bern, Bern, Switzerland;, Liver Unit, Hospital Clinic, IDIBAPS, University of Barcelona, Barcelona, Spain – sequence: 20 givenname: Juan G. surname: Abraldes fullname: Abraldes, Juan G. organization: Division of Gastroenterology (Liver Unit), University of Alberta, Edmonton, Canada – sequence: 21 givenname: Joan surname: Genescà fullname: Genescà, Joan organization: Liver Unit, Department of Internal Medicine, Hospital Universitari Vall d'Hebron, Vall d'Hebron Institut de Recerca (VHIR), Faculty of Medicine, Universitat Autònoma de Barcelona, Barcelona, Spain;, Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33982942$$D View this record in MEDLINE/PubMed https://hal.science/hal-04868138$$DView record in HAL |
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article-title: Elastography, spleen size, and platelet count identify portal hypertension in patients with compensated cirrhosis publication-title: Gastroenterology doi: 10.1053/j.gastro.2012.10.001 – volume: 10 start-page: 1028 year: 2012 ident: R27-20250804 article-title: Prevalence and indicators of portal hypertension in patients with nonalcoholic fatty liver disease publication-title: Clin Gastroenterol Hepatol doi: 10.1016/j.cgh.2012.05.008 – volume: 17 start-page: 156 year: 2019 ident: R25-20250804 article-title: Vibration-controlled transient elastography to assess fibrosis and steatosis in patients with nonalcoholic fatty liver disease publication-title: Clin Gastroenterol Hepatol doi: 10.1016/j.cgh.2018.04.043 – volume: 33 start-page: 517 year: 2014 ident: R18-20250804 article-title: Graphical assessment of internal and external calibration of logistic regression models by using loess smoothers publication-title: Stat Med doi: 10.1002/sim.5941 – volume: 393 start-page: 1597 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