Please use this identifier to cite or link to this item: https://hdl.handle.net/11000/31334
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dc.contributor.authorSimbrunner, Benedikt-
dc.contributor.authorCaparrós, Esther-
dc.contributor.authorNeuwirth, Teresa-
dc.contributor.authorSchwabl, Philipp-
dc.contributor.authorKönigshofer, Philipp-
dc.contributor.authorBauer, David-
dc.contributor.authorMarculescu, Rodrig-
dc.contributor.authorTrauner, Michael-
dc.contributor.authorScheiner, Bernhard-
dc.contributor.authorStary, Georg-
dc.contributor.authorMandorfer, Mattias-
dc.contributor.authorReiberger, Thomas-
dc.contributor.authorFrancés, Rubén-
dc.contributor.otherDepartamentos de la UMH::Medicina Clínicaes_ES
dc.date.accessioned2024-02-09T09:21:26Z-
dc.date.available2024-02-09T09:21:26Z-
dc.date.created2023-08-
dc.identifier.citationHepatology International (2023) 17:1045–1056es_ES
dc.identifier.issn1936-0541-
dc.identifier.issn1936-0533-
dc.identifier.urihttps://hdl.handle.net/11000/31334-
dc.description.abstractBackground: Experimental data suggest that bacterial translocation (BT) promotes systemic inflammation, portal hypertension, and circulatory dysfunction in advanced chronic liver disease (ACLD). Methods: Patients with ACLD undergoing hepatic venous pressure gradient (HVPG) measurement and absence of acute decompensation or infections were included (n = 249). Serum biomarkers of BT (lipopolysaccharide [LPS], lipoteichoic acid [LTA], bacterial DNA [bactDNA]), systemic inflammation and markers of circulatory dysfunction were assessed. T-cell subsets in intestinal biopsies (n = 7 ACLD, n = 4 controls) were analyzed by flow cytometry. Results: Patients had a median HVPG of 18 (12-21) mmHg and 56% had decompensated ACLD. LPS (0.04 [0.02-0.06] vs. 0.64 [0.30-1.06] EU/mL), LTA (4.53 [3.58-5.97] vs. 43.2 [23.2-109] pg/mL), and detection of bactDNA (≥ 5 pg/mL; 5% vs. 41%) were markedly higher in patients with ACLD than healthy controls (n = 40; p < 0.001) but were similar between different clinical stages of compensated and decompensated ACLD and displayed no meaningful correlation with HVPG and systemic hemodynamics. TNF-α and IL-10 correlated with LPS (Spearman's rs = 0.523, p < 0.001/rs = 0.143, p = 0.024) but not with LTA. Presence of bactDNA was associated with higher LPS (0.54 [0.28-0.95] vs. 0.88 [0.32-1.31] EU/mL, p = 0.001) and TNF-α (15.3 [6.31-28.1] vs. 20.9 [13.8-32.9] pg/mL). Patients with ACLD exhibited a decreased CD4:CD8-ratio and increased TH1-cells in the intestinal mucosa as compared to controls. During a median FU of 14.7 (8.20-26.5) months, bacterial antigens did not predict decompensation or liver-related death (in contrast to HVPG, IL-6, and MAP) as well as infections at 24 months. Conclusion: BT occurs already in early ACLD stages and triggers a systemic inflammatory response via TNF-α and IL-10. Interestingly, BT markers showed no clear correlation with portal hypertension and circulatory dysfunction in patients with stable ACLD.es_ES
dc.formatapplication/pdfes_ES
dc.format.extent12es_ES
dc.language.isoenges_ES
dc.publisherSpringeres_ES
dc.rightsinfo:eu-repo/semantics/openAccesses_ES
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectBacterial translocationes_ES
dc.subjectCirculatory dysfunctiones_ES
dc.subjectCirrhosises_ES
dc.subjectCytokinees_ES
dc.subjectEndotoxines_ES
dc.subjectGut–liver axises_ES
dc.subjectImmunityes_ES
dc.subjectInflammationes_ES
dc.subjectPAMPses_ES
dc.subjectPortal hypertensiones_ES
dc.titleBacterial translocation occurs early in cirrhosis and triggers a selective infammatory responsees_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.relation.publisherversionhttps://doi.org/10.1007/s12072-023-10496-yes_ES
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Artículos Medicina Clínica


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