Evidence map›Paper›PMID 40453976›Full record

ArticleJHEP reports : innovation in hepatology2025

Lipidomics-based plasma signature of alcohol-related hepatitis linked to short-term mortality.

Florent Artru, Stephen Atkinson, Francesca Trovato, Luke D Tyson, Vishal C Patel, Nikhil Vergis, Noora Kano, Robert Goldin, Alberto Quaglia, Alexandros Pechlivanis and 12 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JHEP reports : innovation in hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the 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.

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

3 citing papers in PubMed.

  1. Review
  2. Review
  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

22 authors.

Florent ArtruInstitute of Liver Studies, King's College Hospital London, London, UK.
Stephen AtkinsonInstitute of Liver Studies, School of Immunology and Microbial Sciences, Faculty of Life Sciences and Medicine, King's College London, London, UK.
Francesca TrovatoInstitute of Liver Studies, King's College Hospital London, London, UK.
Luke D TysonDepartment of Metabolism, Digestion and Reproduction, Division of Digestive Disease, Liver Unit, St Mary's and Hammersmith Hospitals, Imperial College London, London, UK Imperial College London, London, UK.
Vishal C PatelInstitute of Liver Studies, King's College Hospital London, London, UK.
Nikhil VergisDepartment of Metabolism, Digestion and Reproduction, Division of Digestive Disease, Liver Unit, St Mary's and Hammersmith Hospitals, Imperial College London, London, UK Imperial College London, London, UK.
Noora KanoDepartment of Metabolism, Digestion and Reproduction, Division of Digestive Disease, Liver Unit, St Mary's and Hammersmith Hospitals, Imperial College London, London, UK Imperial College London, London, UK.
Robert GoldinDepartment of Metabolism, Digestion and Reproduction, Division of Digestive Disease, Liver Unit, St Mary's and Hammersmith Hospitals, Imperial College London, London, UK Imperial College London, London, UK.
Alberto QuagliaDepartment of Metabolism, Digestion and Reproduction, Division of Digestive Disease, Liver Unit, St Mary's and Hammersmith Hospitals, Imperial College London, London, UK Imperial College London, London, UK.
Alexandros PechlivanisDepartment of Metabolism, Digestion and Reproduction, Division of Digestive Disease, Liver Unit, St Mary's and Hammersmith Hospitals, Imperial College London, London, UK Imperial College London, London, UK.
Phillip MorganInstitute of Liver Studies, King's College Hospital London, London, UK.
Salma MujibInstitute of Liver Studies, King's College Hospital London, London, UK.
Anna CavazzaInstitute of Liver Studies, King's College Hospital London, London, UK.
Ellen JeromeInstitute of Liver Studies, King's College Hospital London, London, UK.
Marc ZentarInstitute of Liver Studies, King's College Hospital London, London, UK.
Roosey ShethInstitute of Liver Studies, King's College Hospital London, London, UK.
Maura MorrisonInstitute of Liver Studies, King's College Hospital London, London, UK.
Evangelos TriantafyllouDepartment of Metabolism, Digestion and Reproduction, Division of Digestive Disease, Liver Unit, St Mary's and Hammersmith Hospitals, Imperial College London, London, UK Imperial College London, London, UK.
Elaine HolmesDepartment of Metabolism, Digestion and Reproduction, Division of Digestive Disease, Liver Unit, St Mary's and Hammersmith Hospitals, Imperial College London, London, UK Imperial College London, London, UK.
María Gómez-RomeroSection of Bioanalytical Chemistry, Division of Systems Medicine, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK.
Mark J McPhailInstitute of Liver Studies, King's College Hospital London, London, UK.
Mark ThurszDepartment of Metabolism, Digestion and Reproduction, Division of Digestive Disease, Liver Unit, St Mary's and Hammersmith Hospitals, Imperial College London, London, UK Imperial College London, London, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background & Aims: Severe alcohol-related hepatitis (sAH) is an inflammatory condition with high short-term mortality. Hypothesis-driven approaches have failed to identify effective treatments. Given the role of lipids as inflammatory mediators, this study aimed to identify lipidomic changes and lipid species associated with sAH and mortality risk. Methods: Untargeted lipidomics was performed on serum samples from two cohorts of patients with sAH and decompensated cirrhosis (DC). Principal component analysis and orthogonal partial least squares discriminant analysis were used to assess lipidome changes. Correlations were made with lipoproteins, lipid mediators, cytokines, cytokeratin fragments, and histological indices. Results: In the first part, 78 patients with sAH were matched on bilirubin levels with 23 patients with DC. Lipidomics identified a distinct sAH signature involving glycerophospholipids, including PC(34:2) (odds ratio [OR] 2.18, 95% confidence interval [CI] 1.45-7.05, Conclusions: Untargeted lipidomics identified a glycerophospholipid and sphingolipid signature distinguishing sAH from DC, implicating lipid species involved in liver regeneration and immune function. Acylcarnitine accumulation in patients with sAH and poor prognosis suggests mitochondrial dysfunction and warrants further investigation into therapeutic potential. Impact and implications: Lipids can act as mediators at the interface between the immune system and metabolism, potentially contributing to the pathogenesis and outcomes of patients with severe alcohol-related hepatitis, prompting us to investigate lipidomic changes in this population using untargeted approaches, compared with patients with decompensated cirrhosis. This study highlights a distinct lipidomic signature in patients with severe alcohol-related hepatitis compared with decompensated cirrhosis, primarily involving glycerophospholipids and sphingolipids. Specific lipid classes, such as acylcarnitines, suggest significant mitochondrial dysfunction and are associated with disease severity and short-term mortality in patients with severe alcohol-related hepatitis. These findings underscore the importance of targeted investigations into these lipid species, their pathways, and their links to disease severity and outcomes, particularly in this condition that currently lacks specific treatments.

Indexed as

Acute-on-chronic liver failureAcylcarnitinesAlcohol-related hepatitisCirrhosisGlycerophospholipidsLipidomicsLysophospholipidsMitochondrial dysfunction

Identifiers

PMID40453976
PMCPMC12123345

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Registered trials

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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.