ArticleFrontiers in immunology2026
APASL-ACLF without previous decompensation is immunologically distinct from EASL-CLIF-ACLF with previous decompensation.
Article in Frontiers in immunology, 2026. 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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Abstract
Background and aims: Definitions of acute-on-chronic liver failure (ACLF) differ, with a focus on extrahepatic organ failures on the basis of previously compensated or decompensated cirrhosis in EASL-CLIF-ACLF versus hepatic failure in patients without previous decompensation in APASL-ACLF. Here, we explored whether patterns of systemic inflammation and immune cell alterations differ between these types of ACLF. Methods: Consecutive patients with acute decompensation, EASL-CLIF- or APASL-ACLF were recruited from two liver centres. Patterns of systemic inflammation were characterized by Olink analysis and changes in circulating immune cells by flow cytometry. Results: A total of 374 patients with acute decompensation (AD) were identified, of whom 56 fulfilled exclusively the EASL-CLIF-definition of ACLF (15% of all patients), while only 19 patients (5.1% of all patients) met exclusively the APASL-definition. APASL-ACLF was associated with higher bilirubin, lower creatinine, higher INR and higher hemoglobin concentrations compared to EASL-ACLF. Patterns of systemic inflammation differed between EASL-CLIF and APASL-ACLF. For example, FGF-23, IL-17 or VEGF-A were associated with EASL-CLIF-ACLF, while FGF-19 or low IL-12 were associated with APASL-ACLF. Moreover, patients with EASL-CLIF-ACLF had significantly lower counts of CD8+ T cells, while in APASL-ACLF a reduction of CD4+ T cell was characteristic. Detailed immune cell phenotyping revealed distinct expression of co-stimulatory molecules, inhibitory molecules and T cell activation markers in APASL-ACLF compared to patients with AD or EASL-CLIF-ACLF. Conclusion: We provide preliminary evidence that EASL-CLIF- and APASL-ACLF are associated with different changes in systemic inflammation patterns and immune cell phenotypes, suggesting that both types of ACLF might be pathophysiologically different.
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