Elevated LPS is largely driven by time since symptom onset in acute ischemic stroke: the impact on clinical outcomes.

lipopolysaccharide protein carbonylation stroke thrombolysis zonulin

Journal

Journal of thrombosis and haemostasis : JTH
ISSN: 1538-7836
Titre abrégé: J Thromb Haemost
Pays: England
ID NLM: 101170508

Informations de publication

Date de publication:
07 Aug 2024
Historique:
received: 01 03 2024
revised: 06 06 2024
accepted: 24 06 2024
medline: 10 8 2024
pubmed: 10 8 2024
entrez: 9 8 2024
Statut: aheadofprint

Résumé

Gut dysbiosis leading to increased intestinal barrier permeability and translocation of lipopolysaccharide (LPS) in the circulation has been demonstrated in patients with acute myocardial infarction and pulmonary embolism. We investigated changes in circulating LPS concentrations in acute ischemic stroke (AIS) and their consequences, including prognosis. We studied 98 AIS patients, aged 74±12 years, including 74 (75.5%) thrombolysed individuals. We determined serum LPS and zonulin, a marker of gut permeability, along with protein carbonylation (PC), fibrin clot properties, and thrombin generation on admission, at 24 hours and 3 months. Stroke severity was assessed using the NIH Stroke Scale (NIHSS). Stroke functional outcome using modified Rankin Scale (mRS) and stroke-related mortality were evaluated at 3 months. Serum LPS and zonulin on admission were associated with time since symptom onset (r=0.57, p<0.0001 and r=0.40, p<0.0001). Baseline LPS correlated with PC (r=0.51, p<0.0001) but not with coagulation and fibrinolysis markers. LPS levels increased at 24 hours in thrombolysed patients (p<0.001) and correlated with the NIHSS score (r=0.31, p=0.002) and PC (r=0.32, p=0.0057). Both LPS and zonulin levels measured at 24 hours increased the odds of having unfavorable mRS (OR=1.22, 95%CI, 1.04-1.42 and 2.36, 95%CI, 1.24-4.49 per unit). Elevated LPS, but not zonulin, was associated with stroke-related mortality (OR=1.26, 95%CI, 1.02-1.55 per unit). In AIS patients intestinal permeability is mainly driven by increasing time since the symptom onset. Our findings suggest that LPS with a trend toward its further rise following thrombolysis adversely affect neurological functional outcomes and 3-month mortality.

Sections du résumé

BACKGROUND BACKGROUND
Gut dysbiosis leading to increased intestinal barrier permeability and translocation of lipopolysaccharide (LPS) in the circulation has been demonstrated in patients with acute myocardial infarction and pulmonary embolism.
OBJECTIVES OBJECTIVE
We investigated changes in circulating LPS concentrations in acute ischemic stroke (AIS) and their consequences, including prognosis.
PATIENTS/METHODS METHODS
We studied 98 AIS patients, aged 74±12 years, including 74 (75.5%) thrombolysed individuals. We determined serum LPS and zonulin, a marker of gut permeability, along with protein carbonylation (PC), fibrin clot properties, and thrombin generation on admission, at 24 hours and 3 months. Stroke severity was assessed using the NIH Stroke Scale (NIHSS). Stroke functional outcome using modified Rankin Scale (mRS) and stroke-related mortality were evaluated at 3 months.
RESULTS RESULTS
Serum LPS and zonulin on admission were associated with time since symptom onset (r=0.57, p<0.0001 and r=0.40, p<0.0001). Baseline LPS correlated with PC (r=0.51, p<0.0001) but not with coagulation and fibrinolysis markers. LPS levels increased at 24 hours in thrombolysed patients (p<0.001) and correlated with the NIHSS score (r=0.31, p=0.002) and PC (r=0.32, p=0.0057). Both LPS and zonulin levels measured at 24 hours increased the odds of having unfavorable mRS (OR=1.22, 95%CI, 1.04-1.42 and 2.36, 95%CI, 1.24-4.49 per unit). Elevated LPS, but not zonulin, was associated with stroke-related mortality (OR=1.26, 95%CI, 1.02-1.55 per unit).
CONCLUSIONS CONCLUSIONS
In AIS patients intestinal permeability is mainly driven by increasing time since the symptom onset. Our findings suggest that LPS with a trend toward its further rise following thrombolysis adversely affect neurological functional outcomes and 3-month mortality.

Identifiants

pubmed: 39122194
pii: S1538-7836(24)00439-2
doi: 10.1016/j.jtha.2024.06.028
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024 International Society on Thrombosis and Haemostasis. Published by Elsevier Inc. All rights reserved.

Auteurs

Michał Błaż (M)

Department of Neurology, St. John Paul II Hospital, Krakow, Poland.

Joanna Natorska (J)

Krakow Centre for Medical Research and Technologies, St. John Paul II Hospital, Kraków, Poland; Department of Thromboembolic Diseases, Institute of Cardiology, Jagiellonian University Medical College, Krakow, Poland.

Jan P Bembenek (JP)

Department of Clinical Neurophysiology, Institute of Psychiatry and Neurology, Warsaw, Poland.

Anna Członkowska (A)

2nd Department of Neurology, Institute of Psychiatry and Neurology, Warsaw, Poland.

Michał Ząbczyk (M)

Krakow Centre for Medical Research and Technologies, St. John Paul II Hospital, Kraków, Poland; Department of Thromboembolic Diseases, Institute of Cardiology, Jagiellonian University Medical College, Krakow, Poland.

Maciej Polak (M)

Department of Epidemiology and Population Studies, Institute of Public Health, Jagiellonian University Medical College, Krakow, Poland.

Anetta Undas (A)

Krakow Centre for Medical Research and Technologies, St. John Paul II Hospital, Kraków, Poland; Department of Thromboembolic Diseases, Institute of Cardiology, Jagiellonian University Medical College, Krakow, Poland. Electronic address: mmundas@cyf-kr.edu.pl.

Classifications MeSH