APASL-ACLF without previous decompensation is immunologically distinct from EASL-CLIF-ACLF with previous decompensation
- 1Department of Internal Medicine II, LMU University Hospital
- 2Department for Gastroenterology and Hepatology, University Hospital Essen, University Duisburg-Essen
- 3Department of Internal Medicine I, University Medical Center of the Johannes Gutenberg University Mainz
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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BibTeX
@article{langer2026apaslaclf,
title = {{APASL-ACLF without previous decompensation is immunologically distinct from EASL-CLIF-ACLF with previous decompensation}},
author = {Mona-May Langer and Marc J. Weiss and Alina Bauschen and Sabrina Guckenbiehl and Gerald Denk and Helena Stadler and Christian M. Lange},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1893968},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1893968/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - APASL-ACLF without previous decompensation is immunologically distinct from EASL-CLIF-ACLF with previous decompensation
AU - Mona-May Langer
AU - Marc J. Weiss
AU - Alina Bauschen
AU - Sabrina Guckenbiehl
AU - Gerald Denk
AU - Helena Stadler
AU - Christian M. Lange
PY - 2026
DA - 2026/10/06
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1893968
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1893968/full
AB - 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.
SN - 1664-3224
ER -