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Título

Levels of anti-inflammatory cytokines and neurological worsening in acute ischemic stroke

AutorVila, Nicolás; Castillo, José; Dávalos, Antoni; Esteve-Codina, Anna; Planas, Anna M. CSIC ORCID; Chamorro, Ángel
Palabras claveInterleukin-4
Interleukin-10
Neuroprotection
Stroke, ischemic
Inflammation
Cytokines
Fecha de publicación1-mar-2003
EditorLippincott Williams & Wilkins
CitaciónStroke, a journal of cerebral circulation 34(3): 671-675 (2003)
ResumenBackground - Mechanisms involved in stroke progression are incompletely understood. Ischemic brain injury is characterized by acute local inflammatory response mediated by cytokines. Anti-inflammatory cytokines act in a feedback loop to inhibit continued proinflammatory cytokine production. We assessed the implication of interleukin (IL)-10 and IL-4 in deteriorating ischemic stroke. Methods - Two hundred thirty-one patients with ischemic stroke within the first 24 hours from onset were included. Neurological worsening was defined when the Canadian Stroke Scale score fell at least 1 point during the first 48 hours after admission. Anti-inflammatory cytokines were determined in plasma obtained on admission. Results - Eighty-three patients (35.9%) worsened within the first 48 hours after stroke onset. Significantly lower concentrations of IL-10 were found in patients with neurological worsening (P<0.05), but IL-4 levels were similar in patients with or without deterioration. Lower plasma concentrations of IL-10 (<6 pg/mL) were associated with clinical worsening on multivariate analysis (odds ratio=3.1, 95% CI=1.1 to 8.9) independently of hyperthermia, hyperglycemia, or neurological condition on admission. Further analysis disclosed that early worsening was independently associated with lower IL-10 plasma levels in patients with subcortical infarcts or lacunar stroke but not in patients with cortical lesions. Conclusions - Anti-inflammatory cytokine IL-10 is associated with the early clinical course of patients with acute ischemic stroke, especially in patients with small vessel disease or subcortical infarctions.
Versión del editorhttp://dx.doi.org/10.1161/01.STR.0000057976.53301.69
URIhttp://hdl.handle.net/10261/116796
DOI10.1161/01.STR.0000057976.53301.69
Identificadoresdoi: 10.1161/01.STR.0000057976.53301.69
issn: 0039-2499
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