Evidence map›Paper›PMID 41737543›Full record

ArticleJHEP reports : innovation in hepatology2026

Fibrosis activity

Stine Johansen, Mads Israelsen, Katrine Holtz Thorhauge, Johanne Kragh Hansen, Camilla Dalby Hansen, Helle Lindholm Schnefeld, Peter Andersen, Ida Villesen, Katrine Tholstrup Bech, Sönke Detlefsen and 6 more

Abstract read
In one paragraph

Article in JHEP reports : innovation in hepatology, 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

16 authors.

Stine JohansenFibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark.
Mads IsraelsenFibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark.
Katrine Holtz ThorhaugeFibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark.
Johanne Kragh HansenFibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark.
Camilla Dalby HansenFibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark.
Helle Lindholm SchnefeldFibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark.
Peter AndersenFibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark.
Ida VillesenFibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark.
Katrine Tholstrup BechFibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark.
Sönke DetlefsenDepartment of Clinical Research, Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark.
Nikolaj TorpFibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark.
Diana LeemingNordic Bioscience A/S, Herlev Hovedgade, Herlev, Denmark.
Maja ThieleFibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark.
Aleksander KragFibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark.
Morten KarsdalNordic Bioscience A/S, Herlev Hovedgade, Herlev, Denmark.
GALAXY consortia

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background & Aims: Excessive alcohol consumption accelerates fibrosis progression in steatotic liver disease. Disease activity can be described by fibrogenic activity, of which collagen formation is a central process. Type III collagen formation (PRO-C3) is a biomarker of fibrosis activity. We aimed to evaluate whether PRO-C3 predicts clinical outcomes in alcohol-related liver disease (ALD) independent of fibrosis stage. Methods: We conducted a prospective cohort study including patients with prior or current excessive alcohol intake (men: ≥36 g/day; women: ≥24 g/day for >1 year) and no prior decompensation. At baseline, liver biopsies, clinical investigations, and non-invasive blood tests were performed. During follow-up, patients' electronic healthcare records were manually reviewed for decompensation events and all-cause mortality. Decompensation was defined according to Baveno VII recommendations. Results: We followed 458 patients with ALD (76% male; mean age 57 ± 10 years) for a median of 5.9 years (IQR 4.5-7.8). At baseline, fibrosis stages were F0-1 (n = 260), F2 (n = 107), and F3-4 (n = 91). During follow-up, 67 patients experienced decompensation and 100 died. PRO-C3 provided prognostic value beyond fibrosis stage as a predictor of decompensation, both in patients with no to moderate fibrosis (F0-2; subhazard ratio per unit increase in PRO-C3 1.05; 95% CI 1.03-1.07; Conclusions: In ALD, prognosis is determined by both baseline fibrosis stage and markers of fibrosis activity. PRO-C3, a biomarker of fibrosis activity, was more strongly associated with the risk of decompensation than Kleiner fibrosis stage and predicted decompensation across fibrosis stages. Impact and implications: This study shows that fibrosis activity measured by PRO-C3 captures dynamic disease processes in alcohol-related liver disease that are not fully reflected by histological fibrosis stage. These findings are important for clinicians and patients because PRO-C3 independently predicts decompensation and supports stratifying risk by fibrosis activity in addition to stage. Practically, incorporating fibrosis-activity biomarkers could guide earlier monitoring and interventions aimed at modulating fibrogenic activity.

Indexed as

Alcoholic liver diseaseFibrogenesisSteatotic liver diseaseSurrogate endpoints

Identifiers

PMID41737543
PMCPMC12926629

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 Socratic graph.