Association between serum NLRP3 and malignant brain edema in patients with acute ischemic stroke.
Association between serum NLRP3 and malignant brain edema in patients with acute ischemic stroke.
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DOI：
10.1186/s12883-021-02369-4
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发表时间：
2021-09-07
期刊：
影响因子：
2.6
通讯作者：
Wu S
中科院分区：
文献类型：
--
作者：
Wang Y;Huang H;He W;Zhang S;Liu M;Wu S
本研究旨在探讨急性缺血性脑卒中患者血清中核苷酸结合寡聚化结构域样受体家族pyrin domain-containing 3（NLRP 3）及其相关炎症标志物（缺氧诱导因子-1 α、组织蛋白酶B、caspase-1和基质金属蛋白酶-9）水平与恶性脑水肿（MBE）的关系。我们前瞻性招募了症状发作后24小时内入院的急性缺血性卒中患者。入院时进行脑部CT检查，并采集血液样本。入院后7天内重复进行脑部CT/MRI检查，以确定是否存在MBE，MBE定义为神经功能恶化伴中线移位或基底脑池受压的影像学体征。进行逻辑回归分析，以评估炎症生物标志物和MBE之间的关联，调整年龄和国立卫生研究院卒中量表（NIHSS）。纳入200例患者（69.3 ± 14.3岁;男性55%）进行分析，其中26例患者发生MBE（从卒中发作至MBE的中位时间为32.5 h）。MBE患者血清NLRP 3浓度高于非MBE患者（发病至采血中位时间3 h，1.85 ng/ml vs. 1.11 ng/ml，P = 0.026）。入院时NLRP 3水平与NIHSS呈正相关（斯皮尔曼ρ = 0.18，P = 0.01），校正年龄和NIHSS后，NLRP 3与MBE的相关性减弱（OR 1.47，95% CI 0.88-2.46，P = 0.138）。MBE组与非MBE组之间的其他生物标志物无显著差异。缺血性卒中后血清NLRP 3浓度升高与MBE风险增加之间存在相关趋势，可能受到卒中严重程度的混淆，值得在大型队列研究中进一步验证。
We aimed to explore the association of serum level of the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) and its related inflammatory biomarkers (hypoxia inducible factor-1α, cathepsin B, caspase-1 and matrix metalloproteinase-9) with malignant brain edema (MBE) in patients with acute ischemic stroke. We prospectively enrolled patients with acute ischemic stroke admitted < 24 h from onset of symptoms. Brain CT was performed on admission and blood samples were collected. Repeated brain CT/MRI was performed < 7 days of admission to identify the presence of MBE, defined as neurological deterioration with imaging signs of midline shift or compressed basal cisterns. Logistic regression analysis was performed to assess the association between inflammatory biomarkers and MBE, adjusted for age and National Institutes of Health Stroke Scale (NIHSS). 200 patients (69.3 ± 14.3 years; male 55 %) were included for analysis, of whom 26 patients developed MBE (median time from stroke onset to MBE 32.5 h). Compared with patients without MBE, those with MBE had higher level of serum concentration of NLRP3 (median time from onset to blood collection 3 h, 1.85 ng/ml vs. 1.11 ng/ml, P = 0.026). NLRP3 level was positively correlated with NIHSS on admission (Spearman ρ = 0.18, P = 0.01) and the association between NLRP3 and MBE was attenuated (OR 1.47, 95 % CI 0.88–2.46, P = 0.138) after adjusting for age and NIHSS. There was no significant difference in other biomarkers between MBE and non-MBE groups. There was a trend of association between a higher level of serum concentration of NLRP3 and an increased risk of MBE after ischemic stroke, possibly confounded by the severity of stroke, which is worth further validation in large cohort studies.
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