动脉瘤蛛网膜下腔出血后迟发性脑缺血患者血清水通道蛋白4、神经元特异性核蛋白水平及意义

丁大冬; 蒋宽; 吴达; 储亮

doi:10.7619/jcmp.20223873

动脉瘤蛛网膜下腔出血后迟发性脑缺血患者血清水通道蛋白4、神经元特异性核蛋白水平及意义

Levels and significance of serum aquaporin 4 and neuron specific nuclear protein in patients with delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage

摘要

摘要:
目的探讨动脉瘤蛛网膜下腔出血(aSAH)后迟发性脑缺血患者血清水通道蛋白4(AQP4)和神经元特异性核蛋白(NeuN)水平变化及临床意义。
方法选取100例aSAH患者为研究对象，根据aSAH后迟发性脑缺血发生情况将患者分为无迟发性脑缺血组(n=68)和迟发性脑缺血组(n=32)。血清中AQP4和NeuN水平采用酶联免疫吸附法(ELISA)检测，采用Pearson法分析血清AQP4与NeuN的相关性。采用受试者工作特征(ROC)曲线分析血清AQP4和NeuN水平对aSAH后迟发性脑缺血的预测价值。
结果与无迟发性脑缺血组相比，迟发性脑缺血组WFNS分级为Ⅲ~Ⅳ级患者占比、Hunt-Hess分级为Ⅲ~Ⅳ级占比以及血清AQP4水平较高，血清NeuN水平较低，差异有统计学意义(P < 0.05)。Pearson法分析显示，血清AQP4和NeuN呈负相关(P < 0.05)。Logistic回归分析显示, Hunt-Hess分级、AQP4是aSAH后迟发性脑缺血的危险因素, NeuN是aSAH后迟发性脑缺血的保护因素(P < 0.05)。ROC曲线显示, AQP4预测aSAH后迟发性脑缺血的曲线下面积(AUC)为0.862(95%CI: 0.781~0.942), 敏感度为76.50%, 特异度为83.82%, 截断值为1.19 ng/L; NeuN预测aSAH后迟发性脑缺血的AUC为0.771(95%CI: 0.672~0.870), 敏感度为78.10%, 特异度为76.50%, 截断值为0.47 μg/mL; AQP4联合NeuN预测aSAH后迟发性脑缺血的AUC为0.879(95%CI: 0.811~0.948), 敏感度为90.60%, 特异度为75.00%; 联合诊断的AUC值高于NeuN单独诊断(Z=2.476, P=0.013)。
结论 aSAH后迟发性脑缺血患者血清NeuN水平下调, AQP4水平上调, AQP4联合NeuN可作为预测aSAH后迟发性脑缺血的评估指标。

Abstract:
Objective To investigate the changes of serum aquaporin 4 (AQP4) and neuron specific nuclear protein (NeuN) levels in patients with delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage (aSAH) and their clinical significance.
Methods One-hundred patients with aSAH were selected as study objects, and were divided into non-delayed cerebral ischemia group (n=68) and delayed cerebral ischemia group (n=32) according to the occurrence of delayed cerebral ischemia after aSAH. The levels of serum AQP4 and NeuN were detected by enzyme-linked immunosorbent assay (ELISA), and the correlation between serum AQP4 and NeuN was analyzed by Pearson method. The predictive value of serum AQP4 and NeuN levels for delayed cerebral ischemia after aSAH was analyzed by using the ROC curve.
Results Compared with the non-delayed cerebral ischemia group, the proportions of patients with grade Ⅲ to Ⅳ of WFNS, those with grade Ⅲ to Ⅳ of Hunt-Hess, and serum AQP4 level in the delayed cerebral ischemia group were higher, while the serum NeuN level was lower (P < 0.05). Pearson analysis showed that serum AQP4 was negatively correlated with NeuN (P < 0.05); Logistic regression analysis showed that Hunt-Hess classification and AQP4 were risk factors for delayed cerebral ischemia after aSAH (P < 0.05), while NeuN was a protective factor of delayed cerebral ischemia after aSAH (P < 0.05). ROC curve showed that the area under the curve (AUC) of AQP4 in predicting delayed cerebral ischemia after aSAH was 0.862 (95%CI, 0.781 to 0.942), with sensitivity of 76.50%, specificity of 83.82%, and truncation of 1.19 ng/L; the AUC of NeuN in predicting delayed cerebral ischemia after aSAH was 0.771 (95%CI, 0.672 to 0.870), with sensitivity of 78.10%, specificity of 76.50%, and truncation of 0.47μg/mL; the AUC of delayed cerebral ischemia predicted by AQP4 combined with NeuN after aSAH was 0.879 (95%CI: 0.811 to 0.948), its sensitivity was 90.60% and specificity was 75.00%. The AUC value of combined diagnosis was higher than that of NeuN diagnosis alone (Z=2.476, P=0.013).
Conclusion The serum NeuN level is down-regulated and AQP4 level is up-regulated in patients with delayed cerebral ischemia after aSAH. AQP4 combined with NeuN can be used as an evaluation index to predict delayed cerebral ischemia after aSAH.

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