Evidence map›Paper›PMID 39411649›Full record

ArticleJHEP reports : innovation in hepatology2024

Clinical and molecular characterization of steatotic liver disease in the setting of immune-mediated inflammatory diseases.

Enrique García-Nieto, Juan Carlos Rodriguez-Duque, Coral Rivas-Rivas, Paula Iruzubieta, María José Garcia, Laura Rasines, Ana Alvarez-Cancelo, Agustín García-Blanco, José Ignacio Fortea, Angela Puente and 12 more

Abstract read
In one paragraph

Article in JHEP reports : innovation in hepatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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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

22 authors.

Enrique García-NietoClinical and Translational Research in Digestive Diseases. Valdecilla Research Institute (IDIVAL). Santander, Spain.
Juan Carlos Rodriguez-DuqueClinical and Translational Research in Digestive Diseases. Valdecilla Research Institute (IDIVAL). Santander, Spain.
Coral Rivas-RivasClinical and Translational Research in Digestive Diseases. Valdecilla Research Institute (IDIVAL). Santander, Spain.
Paula IruzubietaClinical and Translational Research in Digestive Diseases. Valdecilla Research Institute (IDIVAL). Santander, Spain.
María José GarciaClinical and Translational Research in Digestive Diseases. Valdecilla Research Institute (IDIVAL). Santander, Spain.
Laura RasinesClinical and Translational Research in Digestive Diseases. Valdecilla Research Institute (IDIVAL). Santander, Spain.
Ana Alvarez-CanceloClinical and Translational Research in Digestive Diseases. Valdecilla Research Institute (IDIVAL). Santander, Spain.
Agustín García-BlancoClinical and Translational Research in Digestive Diseases. Valdecilla Research Institute (IDIVAL). Santander, Spain.
José Ignacio ForteaClinical and Translational Research in Digestive Diseases. Valdecilla Research Institute (IDIVAL). Santander, Spain.
Angela PuenteClinical and Translational Research in Digestive Diseases. Valdecilla Research Institute (IDIVAL). Santander, Spain.
Beatriz CastroClinical and Translational Research in Digestive Diseases. Valdecilla Research Institute (IDIVAL). Santander, Spain.
Maria Luisa CagigalPathological Anatomy Service. University Hospital Marqués de Valdecilla. Santander, Spain.
Javier Rueda-GotorDivision of Rheumatology. University Hospital Marqués de Valdecilla. Santander, Spain.
Ricardo BlancoDivision of Rheumatology. University Hospital Marqués de Valdecilla. Santander, Spain.
Montserrat RiveroClinical and Translational Research in Digestive Diseases. Valdecilla Research Institute (IDIVAL). Santander, Spain.
Susana ArmestoDermatology Department. University Hospital Marqués de Valdecilla. Santander, Spain.
Marcos Antonio González-LópezDermatology Department. University Hospital Marqués de Valdecilla. Santander, Spain.
Anna Esteve CodinaCNAG-CRG, Centre for Genomic Regulation (CRG), Barcelona Institute of Science and Technology (BIST); Universitat Pompeu Fabra (UPF), Barcelona, Spain.
Marta GutCNAG-CRG, Centre for Genomic Regulation (CRG), Barcelona Institute of Science and Technology (BIST); Universitat Pompeu Fabra (UPF), Barcelona, Spain.
Jose Pedro VaqueClinical and Translational Research in Digestive Diseases. Valdecilla Research Institute (IDIVAL). Santander, Spain.
Javier CrespoClinical and Translational Research in Digestive Diseases. Valdecilla Research Institute (IDIVAL). Santander, Spain.
María Teresa Arias-LosteClinical and Translational Research in Digestive Diseases. Valdecilla Research Institute (IDIVAL). Santander, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background & Aims: Growing evidence suggests an increased prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) in the context of immune-mediated inflammatory diseases (IMIDs). We aimed to clinically and mechanistically characterize steatotic liver disease (SLD) in a prospective cohort of patients with IMID compared to controls. Methods: Cross-sectional, case-control study including a subset of patients with IMID. Controls from the general population were age-, sex-, type 2 diabetes-, and BMI-matched at a 1:2 ratio. SLD was established using controlled attenuation parameter. Liver biopsies were obtained when significant liver fibrosis was suspected. Total RNA was extracted from freshly frozen cases and analyzed by RNA-seq. Differential gene expression was performed with 'limma-voom'. Gene set-enrichment analysis was performed using the fgsea R package with a preranked "limma t-statistic" gene list. Results: A total of 1,456 patients with IMID and 2,945 controls were included. Advanced SLD (liver stiffness measurement ≥9.7 kPa) (13.46% Conclusions: The prevalence of advanced SLD and MASLD is disproportionately elevated in IMID cohorts. Our findings suggest that IMIDs may catalyze a distinct MASLD pathway, divergent from classical metabolic routes, highlighting the need for tailored clinical management strategies. Impact and implications: The prevalence of steatotic liver disease with advanced fibrosis is increased in patients with immune-mediated inflammatory diseases, independent of classic metabolic risk factors or high-risk alcohol consumption. Transcriptomic analysis revealed a unique gene expression signature associated with cellular activities that are compatible with a liver condition leading to an accelerated and aggressive form of steatotic liver disease. Our findings underscore the importance of heightened screening for advanced liver disease risk across various medical disciplines overseeing patients with immune-mediated inflammatory diseases.

Indexed as

advanced fibrosisIMIDMASLDSLDtranscriptome

Identifiers

PMID39411649
PMCPMC11474426

What OpenQuestion holds

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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.