Neutrophil Elastase As A Predictive Biomarker For Post-Stroke Infection
Diaz, B.; Calleja, P.; Alzamora, L.; Ruiz, A.; Martinez-Salio, A.; Ostos, F.; Gutierrez-Sanchez, M.; Garcia-Culebras, A.; Moro, M. A.; Moraga, A.; Lizasoain, I.
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BACKGROUND.Ischemic stroke, a major cause of death and disability, triggers immune suppression and inflammation, increasing the risk of infections, particularly early post-stroke. These infections worsen outcomes, prolong hospitalization, and lack reliable predictive protocols. Current management with broad-spectrum antibiotics is not proven effective and may disrupt microbiota balance. Neutrophil elastase (NE), vital for immune defense, can exacerbate inflammation and infection susceptibility. The main objective of this study is to explore the role of NE in the development of infections after ischemic stroke. METHODS.This study enrolled 544 ischemic stroke patients to evaluate NE as a biomarker for post-stroke infections. Data regarding age, sex, cardiovascular risk factors, stroke etiology and severity were collected. Blood samples from eligible patients, meeting strict inclusion and exclusion criteria, were analyzed using ELISA and multiplex assays to measure NE, myeloperoxidase, and immune mediators. RESULTS.This study analyzed post-stroke infections in ischemic stroke patients, with 27.57% developing infections, respiratory (48.9%) and urinary (24.8%), mostly within three days. Infected patients were older, more often women, and diabetic, with higher NIHSS scores and larger infarct volumes. Elevated NE levels, higher leukocyte counts, and reduced lymphocytes at admission correlated with infection. Logistic regression showed NE, NIHSS, and diabetes as independent predictors. A matched case-control analysis confirmed higher NE levels in infected cases. Cytokine analysis revealed distinct immune profiles, with NE and IL-6 linked to respiratory infections. CONCLUSIONS.NE levels at admission may help identify stroke patients at high infection risk, guiding targeted treatment and supporting potential anti-NE therapies and prophylactic antibiotic strategies.
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