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卒中后高血糖对脑损伤及修复相关循环生物标志物水平的影响:急性卒中血糖研究 II。

The effect of post-stroke hyperglycaemia on the levels of brain damage and repair-related circulating biomarkers: the Glycaemia in Acute Stroke Study II.

机构信息

La Paz University Hospital, IdiPAZ Health Research Institute, Autonomous University of Madrid, Madrid, Spain.

Ramón y Cajal University Hospital, Alcalá de Henares University, Madrid, Spain.

出版信息

Eur J Neurol. 2019 Dec;26(12):1439-1446. doi: 10.1111/ene.14010. Epub 2019 Jun 17.

DOI:10.1111/ene.14010
PMID:31141256
Abstract

BACKGROUND AND PURPOSE

The aim was to identify whether post-stroke hyperglycaemia (PSH) influences the levels of circulating biomarkers of brain damage and repair, and to explore whether these biomarkers mediate the effect of PSH on the ischaemic stroke (IS) outcome.

METHODS

This was a secondary analysis of the Glycaemia in Acute Stroke II study. Biomarkers of inflammation, prothrombotic activity, endothelial dysfunction, blood-brain barrier rupture, cell death and brain repair processes were analysed at 24-48 h (baseline) and 72-96 h (follow-up) after IS. The associations of the biomarkers and stroke outcome (modified Rankin Scale score at 3 months) based on the presence of PSH were compared.

RESULTS

A total of 174 patients participated in this sub-study. Brain-derived neurotrophic factor (BDNF) at admission was negatively correlated with glucose levels. PSH was associated with a trend toward higher levels of endothelial progenitor cells (EPCs) at baseline. The EPCs in the PSH group then decreased in the follow-up samples (-8.5 ± 10.3) compared with the non-PSH group (4.7 ± 7.33; P = 0.024). However, neither BDNF nor EPC values had correlation with the 3-month outcome. Higher interleukin-6 at follow-up was associated with poor outcomes (modified Rankin Scale > 2) independently of PSH.

CONCLUSION

Post-stroke hyperglycaemia appears to be associated with a negative regulation of BDNF and a different reaction in EPC levels. However, neither BDNF nor EPCs showed significant mediation of the PSH association with IS outcome, and only higher interleukin-6 in the follow-up samples (72-96 h) was related to poor outcomes, independently of PSH status. Further studies are needed to achieve definite conclusions.

摘要

背景与目的

本研究旨在明确卒中后高血糖(PSH)是否影响脑损伤和修复的循环生物标志物水平,并探讨这些生物标志物是否介导了 PSH 对缺血性卒中(IS)结局的影响。

方法

本研究为急性卒中血糖研究 II (Glycaemia in Acute Stroke II)的二次分析。在 IS 后 24-48 小时(基线)和 72-96 小时(随访)检测炎症、促血栓形成活性、血管内皮功能障碍、血脑屏障破裂、细胞死亡和脑修复过程的生物标志物,并比较了基于 PSH 存在的生物标志物与卒中结局(3 个月时改良 Rankin 量表评分)的相关性。

结果

共有 174 例患者参与了本亚研究。入院时脑源性神经营养因子(BDNF)与血糖水平呈负相关。PSH 与基线时内皮祖细胞(EPC)水平升高趋势相关。与非 PSH 组(4.7±7.33)相比,PSH 组的 EPC 在随访样本中下降(-8.5±10.3)(P=0.024)。然而,BDNF 和 EPC 值均与 3 个月结局无相关性。随访时白细胞介素-6 水平升高与不良结局(改良 Rankin 量表评分>2)独立相关,与 PSH 无关。

结论

PSH 似乎与 BDNF 的负调控和 EPC 水平的不同反应有关。然而,BDNF 和 EPC 均未显示出 PSH 与 IS 结局相关的显著中介作用,只有随访样本中较高的白细胞介素-6(72-96 小时)与结局不良独立相关,与 PSH 状态无关。需要进一步的研究来得出明确的结论。

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