Long-Term Outcome of HBV-Infected Patients with Clinically Significant Portal Hypertension Achieving Viral Suppression
Background: Nucleos(t)ide analog (NA) treatment for hepatitis B virus (HBV) infection may improve clinically significant portal hypertension (CSPH). Data on hepatic venous pressure gradient (HVPG) and non-invasive tests (NITs) for risk re-stratification in virally suppressed HBV-infected patients wi...
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2022-02-01
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author | Mathias Jachs Lukas Hartl David Bauer Benedikt Simbrunner Albert Friedrich Stättermayer Robert Strassl Michael Trauner Mattias Mandorfer Thomas Reiberger |
author_facet | Mathias Jachs Lukas Hartl David Bauer Benedikt Simbrunner Albert Friedrich Stättermayer Robert Strassl Michael Trauner Mattias Mandorfer Thomas Reiberger |
author_sort | Mathias Jachs |
collection | DOAJ |
description | Background: Nucleos(t)ide analog (NA) treatment for hepatitis B virus (HBV) infection may improve clinically significant portal hypertension (CSPH). Data on hepatic venous pressure gradient (HVPG) and non-invasive tests (NITs) for risk re-stratification in virally suppressed HBV-infected patients with pre-treatment CSPH are limited. Methods: We retrospectively included patients with long-term (>12 months) suppression of HBV replication and pre-treatment CSPH (i.e., varices, collaterals on cross-sectional imaging, or ascites). Patients were monitored by on-treatment liver stiffness measurement (LSM) and HVPG assessment. The primary outcome was (further) hepatic decompensation (including liver-related mortality). Results: Forty-two patients (<i>n</i> = 12 (28.6%) with previous decompensation, HBeAg-negative: <i>n</i> = 36 (85.7%)) were included and followed for 2.1 (0.6; 5.3) years. The median HVPG (available in <i>n</i> = 17) was 15 (10; 22) mmHg and the median LSM 22.5 (12.5; 41.0) kPa. LSM correlated strongly with HVPG (Spearman’s ρ: 0.725, <i>p</i> < 0.001) and moderately with the model for end-stage liver disease (MELD) score (ρ: 0.459, <i>p</i> = 0.002). LSM, MELD and albumin levels had good prognostic value for decompensation (area under the receiver operated characteristics curve (AUROC) >0.850 for all). LSM predicted (further) decompensation in competing risk regression (subdistribution hazard ratio (SHR): 1.05 (95% confidence interval(CI) 1.03–1.06); <i>p</i> < 0.001), even after adjusting for other factors. An LSM cut-off at 25kPa accurately stratified patients into a low-risk (<i>n</i> = 23, zero events during follow-up) and a high-risk (<i>n</i> = 19; <i>n</i> = 12 (63.2%) developed events during follow-up) group. Conclusions: Patients with HBV-induced CSPH who achieved long-term viral suppression were protected from decompensation, if LSM was <25 kPa. LSM ≥ 25 kPa indicates a persisting risk for decompensation, despite long-term HBV suppression. |
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spelling | doaj.art-574bd0b7f725483ca419f51152fa9cdd2023-11-23T20:40:21ZengMDPI AGJournal of Personalized Medicine2075-44262022-02-0112223910.3390/jpm12020239Long-Term Outcome of HBV-Infected Patients with Clinically Significant Portal Hypertension Achieving Viral SuppressionMathias Jachs0Lukas Hartl1David Bauer2Benedikt Simbrunner3Albert Friedrich Stättermayer4Robert Strassl5Michael Trauner6Mattias Mandorfer7Thomas Reiberger8Department of Internal Medicine III, Division of Gastroenterology and Hepatology, Medical University of Vienna, A-1090 Vienna, AustriaDepartment of Internal Medicine III, Division of Gastroenterology and Hepatology, Medical University of Vienna, A-1090 Vienna, AustriaDepartment of Internal Medicine III, Division of Gastroenterology and Hepatology, Medical University of Vienna, A-1090 Vienna, AustriaDepartment of Internal Medicine III, Division of Gastroenterology and Hepatology, Medical University of Vienna, A-1090 Vienna, AustriaDepartment of Internal Medicine III, Division of Gastroenterology and Hepatology, Medical University of Vienna, A-1090 Vienna, AustriaDepartment of Laboratory Medicine, Division of Clinical Virology, Medical University of Vienna, A-1090 Vienna, AustriaDepartment of Internal Medicine III, Division of Gastroenterology and Hepatology, Medical University of Vienna, A-1090 Vienna, AustriaDepartment of Internal Medicine III, Division of Gastroenterology and Hepatology, Medical University of Vienna, A-1090 Vienna, AustriaDepartment of Internal Medicine III, Division of Gastroenterology and Hepatology, Medical University of Vienna, A-1090 Vienna, AustriaBackground: Nucleos(t)ide analog (NA) treatment for hepatitis B virus (HBV) infection may improve clinically significant portal hypertension (CSPH). Data on hepatic venous pressure gradient (HVPG) and non-invasive tests (NITs) for risk re-stratification in virally suppressed HBV-infected patients with pre-treatment CSPH are limited. Methods: We retrospectively included patients with long-term (>12 months) suppression of HBV replication and pre-treatment CSPH (i.e., varices, collaterals on cross-sectional imaging, or ascites). Patients were monitored by on-treatment liver stiffness measurement (LSM) and HVPG assessment. The primary outcome was (further) hepatic decompensation (including liver-related mortality). Results: Forty-two patients (<i>n</i> = 12 (28.6%) with previous decompensation, HBeAg-negative: <i>n</i> = 36 (85.7%)) were included and followed for 2.1 (0.6; 5.3) years. The median HVPG (available in <i>n</i> = 17) was 15 (10; 22) mmHg and the median LSM 22.5 (12.5; 41.0) kPa. LSM correlated strongly with HVPG (Spearman’s ρ: 0.725, <i>p</i> < 0.001) and moderately with the model for end-stage liver disease (MELD) score (ρ: 0.459, <i>p</i> = 0.002). LSM, MELD and albumin levels had good prognostic value for decompensation (area under the receiver operated characteristics curve (AUROC) >0.850 for all). LSM predicted (further) decompensation in competing risk regression (subdistribution hazard ratio (SHR): 1.05 (95% confidence interval(CI) 1.03–1.06); <i>p</i> < 0.001), even after adjusting for other factors. An LSM cut-off at 25kPa accurately stratified patients into a low-risk (<i>n</i> = 23, zero events during follow-up) and a high-risk (<i>n</i> = 19; <i>n</i> = 12 (63.2%) developed events during follow-up) group. Conclusions: Patients with HBV-induced CSPH who achieved long-term viral suppression were protected from decompensation, if LSM was <25 kPa. LSM ≥ 25 kPa indicates a persisting risk for decompensation, despite long-term HBV suppression.https://www.mdpi.com/2075-4426/12/2/239cirrhosisportal hypertensionantiviralsnucleos(t)ide analogsdisease regressiontransient elastography |
spellingShingle | Mathias Jachs Lukas Hartl David Bauer Benedikt Simbrunner Albert Friedrich Stättermayer Robert Strassl Michael Trauner Mattias Mandorfer Thomas Reiberger Long-Term Outcome of HBV-Infected Patients with Clinically Significant Portal Hypertension Achieving Viral Suppression Journal of Personalized Medicine cirrhosis portal hypertension antivirals nucleos(t)ide analogs disease regression transient elastography |
title | Long-Term Outcome of HBV-Infected Patients with Clinically Significant Portal Hypertension Achieving Viral Suppression |
title_full | Long-Term Outcome of HBV-Infected Patients with Clinically Significant Portal Hypertension Achieving Viral Suppression |
title_fullStr | Long-Term Outcome of HBV-Infected Patients with Clinically Significant Portal Hypertension Achieving Viral Suppression |
title_full_unstemmed | Long-Term Outcome of HBV-Infected Patients with Clinically Significant Portal Hypertension Achieving Viral Suppression |
title_short | Long-Term Outcome of HBV-Infected Patients with Clinically Significant Portal Hypertension Achieving Viral Suppression |
title_sort | long term outcome of hbv infected patients with clinically significant portal hypertension achieving viral suppression |
topic | cirrhosis portal hypertension antivirals nucleos(t)ide analogs disease regression transient elastography |
url | https://www.mdpi.com/2075-4426/12/2/239 |
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