Department of Anaesthesiology and Intensive Care, University of Pecs, Ifjusag u. 13, Pecs 7623, Hungary.
3rd Department of Internal Medicine, Semmelweis University, Budapest, Hungary.
J Stroke Cerebrovasc Dis. 2020 Aug;29(8):104951. doi: 10.1016/j.jstrokecerebrovasdis.2020.104951. Epub 2020 Jun 5.
Activation of both the L-arginine and the lectin pathway contributes to the pathophysiology and the outcome of acute ischemic stroke (AIS). However, the interplay between the two systems has not yet been examined.
A total of 44 patients with AIS were recruited into this study. Serial measurement of serum L-arginine, asymmetric and symmetric dimethylarginine (ADMA, SDMA), and hsCRP, ficolin-2, ficolin-3, MAP-1, MASP-3 and mannose-binding lectin (MBL) were analyzed within 6 h after onset of stroke and 72 h later. Outcomes were assessed as National Institutes of Health Stroke Scale (NIHSS) worsening by 24 h, poststroke infection, and death by 1 month.
In the hyperacute stage of AIS, ficolin-3, MAP-1 and MBL were positively correlated with L-arginine within 6 h after onset of symptoms (p<0.05 respectively). Significantly lower ficolin-3 and MASP-3 levels were found at 72 h in patients, who developed post-stroke infection after day 4, when compared to patients without post-stroke infections (p=0.03 and p=0.009). At 72 hours, ficolin-3 levels negatively correlated with S100B (p=0.01). Ficolin-3 at 72 post-stroke hours remained an independent predictor of post-stroke infection, while only hsCRP was an independent predictor of 30-day mortality.
Early consumption of ficolin-3 is associated with complications such as post-stroke infections. In the hyperacute phase of AIS, the positive correlation between ficolins and the NO donor L-arginine may reflect the protective role of L-arginine presumably by improving the cerebral microcirculation in a prothrombotic environment induced by complement activation.
精氨酸途径和凝集素途径的激活均有助于急性缺血性脑卒中(AIS)的病理生理学和结局。然而,这两个系统之间的相互作用尚未被研究。
共招募了 44 名 AIS 患者进入本研究。在发病后 6 小时内和 72 小时后,对血清 L-精氨酸、非对称和对称二甲基精氨酸(ADMA、SDMA)以及 hsCRP、ficolin-2、ficolin-3、MAP-1、MASP-3 和甘露糖结合凝集素(MBL)进行连续测量。结局评估为发病后 24 小时 NIHSS 恶化、脑卒中后感染和 1 个月内死亡。
在 AIS 的超急性期,在症状发作后 6 小时内,ficolin-3、MAP-1 和 MBL 与 L-精氨酸呈正相关(p<0.05)。与无脑卒中后感染的患者相比,在第 4 天以后发生脑卒中后感染的患者在 72 小时时发现 ficolin-3 和 MASP-3 水平显著降低(p=0.03 和 p=0.009)。在 72 小时时,ficolin-3 水平与 S100B 呈负相关(p=0.01)。72 小时时的 ficolin-3 水平仍然是脑卒中后感染的独立预测因子,而仅 hsCRP 是 30 天死亡率的独立预测因子。
早期消耗 ficolin-3 与脑卒中后感染等并发症相关。在 AIS 的超急性期,ficolins 与 NO 供体 L-精氨酸之间的正相关可能反映了 L-精氨酸的保护作用,可能通过改善补体激活诱导的血栓前环境中的脑微循环来实现。