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sTWEAK 在急性缺血性脑卒中中的诊断价值。

The Diagnostic Value of sTWEAK in Acute Ischemic Stroke.

机构信息

Department of Emergency Medicine, Kırıkkale University School of Medicine, Kırıkkale, Turkey

Department of Emergency Medicine, Bozok University School of Medicine, Yozgat, Turkey

出版信息

Balkan Med J. 2020 Oct 23;37(6):336-340. doi: 10.4274/balkanmedj.galenos.2020.2020.2.45. Epub 2020 Aug 28.

Abstract

BACKGROUND

Considering the critical role of early diagnosis and management of acute ischemic stroke, biomarkers that can reliable assist in the diagnosis are still needed. These biomarkers should rapidly analyze, have high specificity for brain damage, and be available in the emergency settings for early diagnosis and exclusion of other conditions that mimic acute ischemic stroke. Soluble tumor necrosis factor-like weak inducer of apoptosis, a protein involved in the regulation of several biological functions, could be a potential acute ischemic stroke biomarker.

AIMS

To investigate the diagnostic value of soluble tumor necrosis factor-like weak inducer of apoptosis in patients with acute ischemic stroke and examine the relationship between ischemic area volume determined at diffusion-weighted magnetic resonance imaging and soluble tumor necrosis factor-like weak inducer of apoptosis.

STUDY DESIGN

A prospective, case-control study.

METHODS

This case-control prospective study included 36 patients with acute ischemic stroke and 36 healthy volunteers. Information on age, sex, presence of chronic disease, neurological examination findings, times of presentation to the emergency department after acute ischemic stroke, soluble tumor necrosis factor-like weak inducer of apoptosis levels, ischemic area volumes at diffusion-weighted magnetic resonance imaging, and 6-month mortality rates after stroke were recorded. The results were analyzed on SPSS 22.0 software (SPSS Inc., Chicago, IL, USA), and p<0.05 was considered statistically significant.

RESULTS

A soluble tumor necrosis factor-like weak inducer of apoptosis cut-off value of 995.5 pg/mL exhibited a sensitivity of 80.5% and a positive predictive value of 82.5% with an area under the curve of 0.84 (95% confidence interval: 0.74-0.94; p<0.001). The mean soluble tumor necrosis factor-like weak inducer of apoptosis levels in the acute ischemic stroke group (1968.08±1441.99 μg/L) were significantly higher than those in the control group (704.81±291.72 μg/L) (p<0.001). No correlation was observed between soluble tumor necrosis factor-like weak inducer of apoptosis levels and ischemic area volume measured at diffusion-weighted magnetic resonance imaging (r=-0.008; p=0.07). The mean ischemic area volume was 505.68±381.10 and 60.96±80.89 mm in the nonsurviving and surviving patients, respectively (p=0.002).

CONCLUSION

Soluble tumor necrosis factor-like weak inducer of apoptosis can be used in the diagnosis of acute ischemic stroke. However, it is inconclusive in estimating ischemic area volume and early mortality following acute ischemic stroke. Ischemic area volume measured at diffusion-weighted magnetic resonance imaging is a marker of poor prognosis and can be used in predicting early mortality.

摘要

背景

考虑到急性缺血性脑卒中的早期诊断和治疗至关重要,因此仍需要可靠的辅助诊断的生物标志物。这些生物标志物应能快速分析,对脑损伤具有高度特异性,并可在急诊环境中用于早期诊断和排除其他类似急性缺血性脑卒中的病症。可溶性肿瘤坏死因子样弱凋亡诱导因子是一种参与多种生物学功能调节的蛋白质,可能是一种有潜力的急性缺血性脑卒中生物标志物。

目的

研究可溶性肿瘤坏死因子样弱凋亡诱导因子在急性缺血性脑卒中患者中的诊断价值,并探讨扩散加权磁共振成像(DWI)确定的缺血面积与可溶性肿瘤坏死因子样弱凋亡诱导因子之间的关系。

研究设计

前瞻性病例对照研究。

方法

这项前瞻性病例对照研究纳入了 36 例急性缺血性脑卒中患者和 36 名健康志愿者。记录了年龄、性别、慢性疾病的存在、神经检查结果、从急性缺血性脑卒中发病到就诊于急诊的时间、可溶性肿瘤坏死因子样弱凋亡诱导因子水平、DWI 确定的缺血面积以及脑卒中后 6 个月的死亡率等信息。使用 SPSS 22.0 软件(SPSS Inc.,美国芝加哥)对结果进行分析,p<0.05 为统计学显著差异。

结果

可溶性肿瘤坏死因子样弱凋亡诱导因子的截断值为 995.5 pg/mL 时,其灵敏度为 80.5%,阳性预测值为 82.5%,曲线下面积为 0.84(95%置信区间:0.74-0.94;p<0.001)。急性缺血性脑卒中组的可溶性肿瘤坏死因子样弱凋亡诱导因子平均水平(1968.08±1441.99 μg/L)显著高于对照组(704.81±291.72 μg/L)(p<0.001)。可溶性肿瘤坏死因子样弱凋亡诱导因子水平与 DWI 确定的缺血面积之间无相关性(r=-0.008;p=0.07)。在非存活患者和存活患者中,平均缺血面积分别为 505.68±381.10 和 60.96±80.89 mm(p=0.002)。

结论

可溶性肿瘤坏死因子样弱凋亡诱导因子可用于急性缺血性脑卒中的诊断。但是,它在评估急性缺血性脑卒中后的缺血面积和早期死亡率方面尚无定论。DWI 确定的缺血面积是预后不良的标志物,可用于预测早期死亡率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62a7/7590550/f800b84392c4/BMJ-37-336-g1.jpg

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