Evidence map›Paper›PMID 41340228›Full record

ArticleAlimentary pharmacology & therapeutics2026

Serum Villin-1-A Novel Marker of Gut Barrier Damage in Acutely Decompensated Cirrhosis: A Cohort Study and Validation.

David Tornai, Boglarka Balogh, Aniko Csillag, Andras Budai, Andras Kiss, Peter Antal-Szalmas, Gabor Mehes, Lukacs Barath, Tamas Tornai, Istvan Tornai and 13 more

Abstract readValidation Study
In one paragraph

Article in Alimentary pharmacology & therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

23 authors.

David TornaiDivision of Gastroenterology, Department of Internal Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.ORCID https://orcid.org/0000-0002-1335-5498
Boglarka BaloghDivision of Gastroenterology, Department of Internal Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Aniko CsillagDivision of Gastroenterology, Department of Internal Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Andras BudaiDepartment of Pathology, Forensic and Insurance Medicine, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Andras KissDepartment of Pathology, Forensic and Insurance Medicine, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Peter Antal-SzalmasDepartment of Laboratory Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Gabor MehesDepartment of Pathology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Lukacs BarathDepartment of Pathology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Tamas TornaiInstitute of Pancreatic Diseases, Semmelweis University, Budapest, Hungary.
Istvan TornaiDivision of Gastroenterology, Department of Internal Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Zsuzsanna VitalisDivision of Gastroenterology, Department of Internal Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Nora SipekiDivision of Gastroenterology, Department of Internal Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Tamas DinyaDepartment of Surgery, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Attila EnyediDepartment of Surgery, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Florian A RosenbergerDepartment for Proteomics and Signal Transduction, Max-Planck Institute of Biochemistry, Martinsried, Germany.
Wim LalemanDivision of Liver & Biliopancreatic Disorders and Liver Transplantation, Department of Gastroenterology & Hepatology, University Hospitals Leuven, KU Leuven, Leuven, Belgium.
Minneke J CoenraadDepartment of Gastroenterology and Hepatology, Leiden University Medical Center, Leiden, the Netherlands.
Ferran AguilarEuropean Foundation for the Study of Chronic Liver Failure (EF CLIF), Barcelona, Spain.
Joan ClariaEuropean Foundation for the Study of Chronic Liver Failure (EF CLIF), Barcelona, Spain.
Richard MoreauEuropean Foundation for the Study of Chronic Liver Failure (EF CLIF), Barcelona, Spain.ORCID https://orcid.org/0000-0003-0862-403X
Jonel TrebickaDepartment of Internal Medicine B, University of Münster, Münster, Germany.ORCID https://orcid.org/0000-0002-7028-3881
Maria PappDivision of Gastroenterology, Department of Internal Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.ORCID https://orcid.org/0000-0003-3662-4010
MICROB‐PREDICT and PREDICT study group of the EASL‐CLIF consortium

Funding

Horizon 2020 Framework Programme 825694Magyar Tudományos AkadémiaMinistry for Culture and Innovation of Hungary ÚNKP-22-5Ministry of Innovation and Technology of Hungary 138041
6 · The paper itself

Abstract

backgroundGut barrier dysfunction contributes to acute decompensation (AD) of cirrhosis progression but, it is not acknowledged in severity or prognostic scores due to a lack of appropriate assessment tools.

aimWe investigated serum villin-1 (VIL1), an epithelial brush-border associated actin-binding protein, as a non-invasive marker for gut injury and prognosis in AD cirrhosis.

methodsSerum VIL1 was measured in 338 cirrhosis patients (discovery n = 130, validation n = 208, including acute-on-chronic liver failure [ACLF]) from MICROB-PREDICT cohorts and 50 healthy controls (HC). Duodenal biopsies (n = 49 patients, n = 11 HC) were assessed for tissue VIL1 via immunohistochemistry. Serum cytokine profiling linked serum VIL1 levels to systemic inflammation.

resultsCompared to HC, both serum and tissue VIL1 levels were lower in stable AD patients. However, serum VIL1 progressively increased with AD severity, peaking in ACLF. Serum VIL1 was associated with 90-day mortality (AUROC: 0.721, p < 0.001; similar to MELD: 0.722, p < 0.001). A cut-off > 12.79 ng/mL enhanced the prognostic accuracy provided by severe disease stage, defined as CLIF-C AD score ≥ 50 or ACLF (low VIL1: 17.5% vs. high VIL1: 53.6% mortality). This threshold was associated with increased systemic inflammation, suggesting enhanced bacterial translocation. VIL1 was an independent predictor of 90-day mortality (HR: 2.52, CI: 1.648-3.848, p < 0.001) in Cox regression. All findings were confirmed in the validation cohort.

conclusionSerum VIL1 is a non-invasive indicator of gut barrier damage and short-term mortality in AD cirrhosis. Incorporating VIL1 assessment into risk stratification methods improves prognostic accuracy by capturing an essential, yet previously overlooked component of disease progression.

Indexed as

Liver CirrhosisMicrofilament ProteinsAcute-On-Chronic Liver FailureAdultAgedBiomarkersCohort StudiesDisease ProgressionFemaleHumansMaleMiddle AgedPrognosisSeverity of Illness IndexBiomarkersMicrofilament Proteinsvillinacute‐on‐chronic liver failuregut barrier failureMICROB‐PREDICTprognosisserological biomarkershort‐term mortality

Identifiers

PMID41340228
PMCPMC12982645

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