Amelioration of systemic inflammation in advanced chronic liver disease upon beta-blocker therapy translates into improved clinical outcomes
| Autor: | Mattias Mandorfer, David Bauer, Mathias Jachs, Lukas Hartl, Christopher Desbalmes, Dunja Schaufler, Albert Friedrich Stättermayer, Bernhard Scheiner, Benedikt Simbrunner, Theresa Bucsics, Rafael Paternostro, Philipp Schwabl, Thomas Reiberger, Matthias Pinter, Michael Trauner, Ernst Eigenbauer |
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| Rok vydání: | 2020 |
| Předmět: |
Male
medicine.medical_specialty Cirrhosis Portal venous pressure Adrenergic beta-Antagonists Systemic inflammation Chronic liver disease Gastroenterology Procalcitonin Leukocyte Count White blood cell Internal medicine medicine Humans Decompensation Retrospective Studies Inflammation biology business.industry Interleukin-6 C-reactive protein Acute-On-Chronic Liver Failure Middle Aged medicine.disease medicine.anatomical_structure C-Reactive Protein biology.protein Female medicine.symptom business |
| Zdroj: | Gut. 70(9) |
| ISSN: | 1468-3288 |
| Popis: | ObjectiveSystemic inflammation promotes the development of clinical events in patients with advanced chronic liver disease (ACLD). We assessed whether (1) non-selective beta blocker (NSBB) treatment initiation impacts biomarkers of systemic inflammation and (2) whether these changes in systemic inflammation predict complications and mortality.DesignBiomarkers of systemic inflammation, that is, white blood cell count (WBC), C reactive protein (CRP), interleukin-6 (IL-6) and procalcitonin (PCT) were determined at sequential hepatic venous pressure gradient (HVPG) measurements without NSBB and under stable NSBB intake. The influence of NSBB-related changes in systemic inflammation on the risk of decompensation and liver-related death was analysed using competing risk regression.ResultsOur study comprised 307 stable patients with ACLD (Child-A: 77 (25.1%), Child-B: 161 (52.4%), Child-C: 69 (22.5%), median HVPG: 20 (IQR 17–24) mm Hg) including 231 (75.2%) with decompensated disease.WBC significantly decreased upon NSBB therapy initiation (median: −2 (IQR −19;+13)%, p=0.011) in the overall cohort. NSBB-related reductions of WBC (Child-C: −16 (−30;+3)% vs Child-B: −2 (−16;+16)% vs Child-A: +3 (−7;+13)%, pAn NSBB-related decrease in systemic inflammation (ie, WBC reduction ≥15%) was achieved by n=91 (29.6%) patients and was found to be an independent protective factor of further decompensation (subdistribution HR, sHR: 0.694 (0.49–0.98), p=0.038) in decompensated patients and of liver-related mortality in the overall patient cohort (sHR: 0.561 (0.356–0.883), p=0.013).ConclusionNSBB therapy seems to exert systemic anti-inflammatory activity as evidenced by reductions of WBC and CRP levels. Interestingly, this effect was most pronounced in Child-C and independent of HVPG response. An NSBB-related WBC reduction by ≥15% was associated with a decreased risk of further decompensation and death. |
| Databáze: | OpenAIRE |
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