Evidence map›Paper›PMID 39708052›Full record

Observational studyUnited European gastroenterology journal2025

Inflammation remains a dynamic component of portal hypertension in regressive alcohol-related cirrhosis.

Benedikt Silvester Hofer, Benedikt Simbrunner, Philipp Königshofer, Ksenia Brusilovskaya, Oleksandr Petrenko, Vlad Taru, Thomas Sorz-Nechay, Kerstin Zinober, Katharina Regnat, Georg Semmler and 5 more

Registry-linked trialAbstract readObservational Study
In one paragraph

Observational study in United European gastroenterology journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03267615 (VICIS - Vienna Cirrhosis Study), which is not on this map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT03267615 recruitingnot on this map

VICIS - Vienna Cirrhosis Study

Typeobservational_patient_registrySponsorMedical University of ViennaRan2017 to 2027Enrolled10,000ConditionsLiver Cirrhosis, Portal Hypertension, Ascites, Variceal Hemorrhage
3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Observational
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors.

Benedikt Silvester HoferDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.ORCID 0000-0003-3403-3372
Benedikt SimbrunnerDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.ORCID 0000-0001-8181-9146
Philipp KönigshoferDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.ORCID 0000-0003-1279-1148
Ksenia BrusilovskayaDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.
Oleksandr PetrenkoDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.
Vlad TaruDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.ORCID 0000-0002-2313-7881
Thomas Sorz-NechayDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.
Kerstin ZinoberDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.
Katharina RegnatDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.
Georg SemmlerDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.ORCID 0000-0002-0411-166X
Carolin LacknerInstitute of Pathology, Medical University of Graz, Graz, Austria.
Michael TraunerDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.
Mattias MandorferDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.ORCID 0000-0003-2330-0017
Philipp SchwablDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.
Thomas ReibergerDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.ORCID 0000-0002-4590-3583

Funding

Austrian Federal Ministry for Digital and Economic Affairs, the National Foundation for Research, Technology and Development, the Christian Doppler Research Association, and Boehringer IngelheimBundesministerium für Digitalisierung und WirtschaftsstandortChristian Doppler ForschungsgesellschaftÖsterreichische Nationalstiftung für Forschung, Technologie und Entwicklung
6 · The paper itself

Abstract

backgroundPortal hypertension (PH) resulting from static and dynamic intrahepatic changes drives liver-related complications even after removing the underlying aetiological factor.

objectiveWe investigated the impact of inflammation on the dynamic component of PH during disease regression in animal models of toxin-induced cirrhosis and patients with alcohol-related cirrhosis.

methodsIn mice, cirrhosis was induced via toxin application for 12 weeks followed by toxin-withdrawal allowing for one or 2 weeks of regression. Furthermore, 128 patients with alcohol-related cirrhosis and alcohol abstinence undergoing same-day hepatic venous pressure gradient (HVPG) and liver stiffness measurement (LSM) were included. The influence of inflammation on the dynamic PH component was assessed using linear models. Specifically, we explored proinflammatory changes in mice/patients in whom the measured portal pressure (PP)/HVPG was significantly higher than the PP/HVPG expected from the static PH component (histological collagen proportionate area [CPA; %] in mice, LSM in patients).

resultsIn mice, toxin discontinuation induced a significant decrease in PP, CPA, histological hepatic inflammation and hepatic expression of proinflammatory genes (Tnfa, Il6, Cxcl1, Mcp1; all p < 0.05 for one/2 week regression vs. peak disease). Similarly, prolonged abstinence in alcohol-related cirrhosis was linked to lower HVPG/LSM and longer abstinence was correlated to lower C-reactive protein (CRP), IL-6, immunoglobulin A (IgA) and IgG levels (all p < 0.05). Nevertheless, the persistence of a low-grade proinflammatory state during regression was linked to a higher PP/HVPG than expected from static PH components. In regressive mice, higher hepatic proinflammatory gene expression (Tnfa, Il6, Il1b; all p < 0.05) was linked to higher-than-expected PP. Similarly, higher CRP, IL-6, IgA and IgG and lower complement factor C3c (all p < 0.05) were associated with higher-than-expected HVPG in abstinent patients with alcohol-related cirrhosis.

conclusionsAlthough removing the underlying aetiological factor resulted in significant improvements, a persistent hepatic proinflammatory environment remained a key driver of the dynamic PH component in regressive liver disease. CLINICAL TRIAL NUMBER: NCT03267615.

Indexed as

Hypertension, PortalInflammationLiver Cirrhosis, AlcoholicLiver Cirrhosis, ExperimentalAdultAlcohol AbstinenceAnimalsCarbon TetrachlorideDisease Models, AnimalElasticity Imaging TechniquesFemaleHumansLiverMaleMiceMiddle AgedCarbon Tetrachloridealcohol‐related cirrhosisdisease regressionimmune dysfunctionportal hypertensionsystemic inflammation

Identifiers

PMID39708052
PMCPMC11999040

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Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.