ArticleGut2021
Differential inflammasome activation predisposes to acute-on-chronic liver failure in human and experimental cirrhosis with and without previous decompensation.
Article in Gut, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. It is linked to trial NCT06523608 (Prediction of Decompensation and HCC Development in Patients With Advanced Chronic Liver Disease by the PLEASE and M10S20 Algorithms), which is not on this map. Cited by 55 papers.
What it found
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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.
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.
Prediction of Decompensation and HCC Development in Patients With Advanced Chronic Liver Disease by the PLEASE and M10S20 Algorithms
Who cites it
55 citing papers in PubMed, 87 citations in OpenAlex.
- Ursolic acid ameliorates metabolic dysfunction-associated fatty liver disease by regulating the NOX4/ROS/NLRP3 pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- [Research advances in immune and metabolic dysregulation in the diagnosis and treatment of acute-on-chronic liver failure].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Review
- Acute-on-chronic liver failure: pathophysiological mechanisms and clinical management.Nature reviews. Gastroenterology & hepatology · 2026Review
- Low muscle mass predicts liver-related outcomes in cirrhosis, independent of portal hypertension: A retrospective cohort study.Canadian liver journal · 2026Article
- Recompensation of Liver Cirrhosis: Definition, Mechanism, Etiological Differences, Prognosis, and Challenges.Canadian journal of gastroenterology & hepatology · 2026Review
- IL-1 family of cytokines in gastrointestinal and liver disorders.Nature reviews. Gastroenterology & hepatology · 2026Review
- IL-1 receptor antagonist as a diagnostic biomarker for bacterial infections in acute decompensation of cirrhosis.Scientific reports · 2025Article
- Interaction of inflammation and portal hypertension in cirrhosis progression.Nature reviews. Gastroenterology & hepatology · 2025Review
- Metabolic-dysfunction associated steatotic liver disease and atrial fibrillation: A review of pathogenesis.World journal of cardiology · 2025Review
- Potential therapies for acute-on-chronic liver failure.Liver international : official journal of the International Association for the Study of the Liver · 2025Review
- Targeted animal models for preclinical assessment of cellular and gene therapies in pancreatic and liver diseases: regulatory and practical insights.Cytotherapy · 2025Review
- The clinical relevance of acute-on-chronic liver failure in medical procedures: Endoscopy, interventions and surgery.Liver international : official journal of the International Association for the Study of the Liver · 2025Review
- Acute and non-acute decompensation of liver cirrhosis.Liver international : official journal of the International Association for the Study of the Liver · 2025Review
- Serum IL-17F as a biomarker of infection-independent cirrhosis progression.Frontiers in immunology · 2025Observational
- Risk factors and prognostic impact of new decompensated events in hospitalized patients with decompensated cirrhosis.BMC gastroenterology · 2024Article
- Inflammasomes in chronic liver disease: Hepatic injury, fibrosis progression and systemic inflammation.Journal of hepatology · 2024Review
- Liver Cirrhosis: The Immunocompromised State.Journal of clinical medicine · 2024Review
- Use of the CytoSorb adsorber in patients with acute-on-chronic liver failure.Scientific reports · 2024Observational
- Review
- Thrombospondin 1 enhances systemic inflammation and disease severity in acute-on-chronic liver failure.BMC medicine · 2024Article
Corrections and comments
- Commented on by
- Commented on by
- Erratum issuedCorrection:2024
Authors and funding
21 authors at 8 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveSystemic inflammation predisposes acutely decompensated (AD) cirrhosis to the development of acute-on-chronic liver failure (ACLF). Supportive treatment can improve AD patients, becoming recompensated. Little is known about the outcome of patients recompensated after AD. We hypothesise that different inflammasome activation is involved in ACLF development in compensated and recompensated patients.
design249 patients with cirrhosis, divided into compensated and recompensated (previous AD), were followed prospectively for fatal ACLF development. Two external cohorts (n=327) (recompensation, AD and ACLF) were included. Inflammasome-driving interleukins (ILs), IL-1α (caspase-4/11-dependent) and IL-1β (caspase-1-dependent), were measured. In rats, bile duct ligation-induced cirrhosis and lipopolysaccharide exposition were used to induce AD and subsequent recompensation. IL-1α and IL-1β levels and upstream/downstream gene expression were measured.
resultsPatients developing ACLF showed higher baseline levels of ILs. Recompensated patients and patients with detectable ILs had higher rates of ACLF development than compensated patients. Baseline CLIF-C (European Foundation for the study of chronic liver failure consortium) AD, albumin and IL-1α were independent predictors of ACLF development in compensated and CLIF-C AD and IL-1β in recompensated patients. Compensated rats showed higher IL-1α gene expression and recompensated rats higher IL-1β levels with higher hepatic gene expression. Higher IL-1β detection rates in recompensated patients developing ACLF and higher IL-1α and IL-1β detection rates in patients with ACLF were confirmed in the two external cohorts.
conclusionPrevious AD is an important risk factor for fatal ACLF development and possibly linked with inflammasome activation. Animal models confirmed the results showing a link between ACLF development and IL-1α in compensated cirrhosis and IL-1β in recompensated cirrhosis.
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