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

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Autores de IDIVAL

Autores ajenos al IDIVAL

  • Codina, AE
  • Gut, M

Unidades

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% vs. 3.79%; p <0.001) and advanced MASLD (12.8% vs . 2.8%; p <0.001) prevalence were significantly higher among patients with IMID than controls. In multivariate analysis, concomitant IMID was an independent, and the strongest, predictor of advanced SLD (adjusted odds ratio 3.318; 95% CI 2.225-4.947; p <0.001). Transcriptomic data was obtained in 109 patients and showed 87 significant genes differentially expressed between IMID-MASLD and control-MASLD. IMID-MASLD cases displayed an enriched expression of genes implicated in pro-tumoral activities or the control of the cell cycle concomitant with a negative expression of genes related to metabolism. 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. (c) 2024 The Authors. Published by Elsevier B.V. on behalf of European Association for the Study of the Liver (EASL). This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Datos de la publicación

ISSN/ISSNe:
2589-5559, 2589-5559

JHEP REPORTS  ELSEVIER

Tipo:
Article
Páginas:
101167-101167
PubMed:
39411649

Citas Recibidas en Web of Science: 4

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Keywords

  • MASLD; SLD; IMID; advanced fibrosis; transcriptome

Campos de Estudio

Financiación

INSTITUTO DE SALUD CARLOS III. (PI18/01304)
INSTITUTO DE SALUD CARLOS III. (PI19/00204)
INSTITUTO DE SALUD CARLOS III. (PI20/01279)

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