Hyperthermia is a surrogate marker of inflammation-mediated cause of brain damage in acute ischaemic stroke

Hyperthermia is a surrogate marker of inflammation-mediated cause of brain damage in acute ischaemic stroke
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DOI:
10.1111/j.1365-2796.2006.01694.x
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发表时间:
2006-10-01
影响因子:
11.1
通讯作者:
Castillo, J.
Castillo, J.
中科院分区:
医学1区
文献类型:
--
作者:
Leira, R.;Rodriguez-Yanez, M.;Castillo, J.

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在缺血性脑卒中实验模型中观察到的温度对结果的影响尚未在脑卒中患者中得到明确证实。白细胞介素-6 (IL-6)是重要的内源性热原,是脑缺血时自发体温的重要调节因子。本研究的目的是确定,在脑缺血的急性期,促炎细胞因子和高热之间的潜在关系,作为脑梗死的一个原因。患者和方法。我们研究了229例首次急性半球梗死患者,这些患者在症状出现后的第一个24小时内入院。入院时,记录腋窝温度,进行血液化学检查和颅脑计算机断层扫描。我们将体温分为两组:热疗(>= 37.5℃)和常温(< 37.5℃)。入院时我们检测了促炎标志物[IL-6,肿瘤坏死因子- α (tnf - α),细胞间粘附分子(ICAM-1)和血管细胞粘附分子]。评估两个结果变量:(i)梗死面积;(ii) 3个月时加拿大卒中量表(CSS) (css7良好结局)。热疗患者的梗死体积更高[46.5 (9.8-78.5)cm(3) vs. 19.1 (5.0-23.5) cm(3);P < 0.0001], 3个月时预后较差。热疗组血浆IL-6、tnf - α和ICAM-1水平明显高于常温组。入院时体温与梗死体积之间存在显著相关性(r = 0.302; P < 0.0001),促炎标志物(IL-6和tnf - α)与梗死体积之间存在显著相关性。促炎标志物(IL-6、tnf - α和ICAM-1)与不良预后之间也存在显著关联。然而,在调整了潜在的混杂因素后,热疗与3个月时较大的梗死面积或不良预后没有独立的相关性。炎症介质在急性缺血性脑损伤中发挥独立于热疗的作用。
The influence of temperature on the outcome observed in experimental models of ischaemic stroke has not been definitively proved in patients with stroke. Interleukin-6 (IL-6) acts as important endogenous pyrogen, and it is an important regulator of spontaneous body temperature during cerebral ischaemia. The objective of this study was to determine, during the acute phase of cerebral ischaemia, the potential relationship between proinflammatory cytokines and hyperthermia as a cause of larger cerebral infarcts.Patients and methods. We studied 229 patients with a first-ever acute hemispheric infarction admitted within the first 24 h from onset of symptoms. On admission, axillary temperature was recorded and blood chemistry studies and cranial computed tomography were performed. We classified body temperature into two groups: hyperthermia (>= 37.5 degrees C) and normothermia (< 37.5 degrees C). We determined proinflammatory markers [IL-6, tumour necrosis factor-alpha (TNF-alpha), intercellular adhesion molecule (ICAM-1) and vascular cellular adhesion molecule] on admission. Two outcome variables were evaluated: (i) infarct volume; (ii) Canadian Stroke Scale (CSS) at 3 months (CSS 7 good outcome).Results. Patients with hyperthermia had higher infarct volume [46.5 (9.8-78.5) cm(3) vs. 19.1 (5.0-23.5) cm(3); P < 0.0001], as well as poor outcome at 3 months. Plasma levels of IL-6, TNF-alpha and ICAM-1 were significantly higher in the group of patients with hyperthermia than in the normothermic group. There was a significant correlation between body temperature on admission and infarct volume (r = 0.302; P < 0.0001), and between proinflammatory markers (IL-6 and TNF-alpha) and infarct volume. A significant association was also found between proinflammatory markers (IL-6, TNF-alpha, and ICAM-1) and poor outcome. However, after adjustment for potential confounders, hyperthermia was not independently associated with either larger infarct volume or with poor outcome at 3 months.Conclusions. Inflammatory mediators play a role in acute ischaemic brain damage independently of hyperthermia.