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急性缺血性卒中中的儿茶酚胺、感染与死亡

Catecholamines, infection, and death in acute ischemic stroke.

作者信息

Chamorro Angel, Amaro Sergio, Vargas Martha, Obach Víctor, Cervera Alvaro, Gómez-Choco Manuel, Torres Ferrán, Planas Anna M

机构信息

Stroke Unit, Hospital Clínic and Institut d' Investigacions Biomédiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Spain.

出版信息

J Neurol Sci. 2007 Jan 15;252(1):29-35. doi: 10.1016/j.jns.2006.10.001. Epub 2006 Nov 28.

DOI:10.1016/j.jns.2006.10.001
PMID:17129587
Abstract

Experimental studies have recently suggested that acute ischemia may facilitate the appearance of fatal infections as part of a brain-induced immunodepression syndrome. However, the mechanisms and neurological consequences of infections complicating acute ischemic stroke have received much less attention at the bedside. The incidence of infection and death after non-septic stroke was compared in this prospective study with longitudinal changes of cytokines, leukocytes, normetanephrine (NMN) and metanephrine (MN) in 75 consecutive patients. In multivariate analysis, infection, n = 13 (17%), was associated with the upper quartile of MN (OR 3.51, 95% CI 1.30-9.51), neurological impairment (NIHSS) on admission (OR 3.99, 95% CI 1.34-11.8), monocyte count (OR 1.78, 95% CI 1.13-2.79), and increased interleukin (IL)-10 (OR 1.54, 95% CI 1.00-2.38). Mortality at 3 months, n = 16 (21%), was associated with increased levels of NMN on admission (OR 2.34 95% CI 1.15-4.76), NIHSS score (OR 2.57, 95% CI 1.29-5.11), and higher IL-6 levels (OR 1.29, 95% 1.00-1.67). These findings suggest that acute ischemic stroke is associated with an early activation of the sympathetic adrenomedullar pathway that lowers the threshold of infection and increases the risk of death. Moreover, these findings are independent of the blood borne effects of pro- and anti-inflammatory cytokines, and circulating leukocytes.

摘要

近期的实验研究表明,急性缺血可能促使致命感染的出现,这是脑诱导免疫抑制综合征的一部分。然而,急性缺血性卒中并发感染的机制及神经学后果在临床床边受到的关注要少得多。在这项前瞻性研究中,对75例连续患者非脓毒性卒中后的感染及死亡发生率与细胞因子、白细胞、去甲变肾上腺素(NMN)和变肾上腺素(MN)的纵向变化进行了比较。多变量分析显示,13例(17%)发生感染与MN的上四分位数相关(比值比[OR] 3.51,95%置信区间[CI] 1.30 - 9.51)、入院时的神经功能缺损(美国国立卫生研究院卒中量表[NIHSS]评分)(OR 3.99,95% CI 1.34 - 11.8)、单核细胞计数(OR 1.78,95% CI 1.13 - 2.79)以及白细胞介素(IL)-10升高(OR 1.54,95% CI 1.00 - 2.38)。3个月时16例(21%)死亡与入院时NMN水平升高(OR 2.34,95% CI 1.15 - 4.76)、NIHSS评分(OR 2.57,95% CI 1.29 - 5.11)以及较高的IL-6水平(OR 1.29,95% CI 1.00 - 1.67)相关。这些发现提示,急性缺血性卒中与交感肾上腺髓质途径的早期激活有关,这降低了感染阈值并增加了死亡风险。此外,这些发现独立于促炎和抗炎细胞因子的血源性效应以及循环白细胞。

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