Serum biomarkers of brain injury: a call for collaboration*.

Serum biomarkers of brain injury: a call for collaboration*.
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脑损伤的血清生物标志物:呼吁合作*。

DOI:
10.1097/pcc.0000000000000228
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发表时间:
2014
期刊:
Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies
影响因子:
--
通讯作者:
Fink,ErickaL
Fink,ErickaL
中科院分区:
--
文献类型:
--
作者:
Trakas,ErinV;Fink,ErickaL

文献摘要

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将高血糖症与脑损伤严重程度和结果联系起来的报告可以追溯到至少40年(2)。这导致了最近在重症儿童中实施积极的血糖控制的势头。然而,正如Elkon等人所指出的,围绕受损大脑中葡萄糖代谢的复杂问题质疑高血糖是否是TBI儿童的可行治疗目标。高血糖和不良结局之间的一致相关性提示了因果关系。理论上,高血糖症可能通过产生活性氧化物质、减少脑灌注、激活突触后谷氨酸受体和加重血脑屏障破坏而加重脑损伤(3)。除了治疗高血糖症,临床前数据表明胰岛素可能具有与血糖调节无关的额外神经保护作用。然而,使用胰岛素控制血糖的临床研究结果
Reports linking hyperglycemia to severity of brain injury and outcome can be traced back to at least 40 years (2). This has led to the recent momentum behind implementing aggressive glucose control in critically ill children. However, as Elkon et al point out, the complex issues around glucose metabolism in the injured brain question whether hyperglycemia is a feasible therapeutic target in children with TBI. Consistent correlation between hyperglycemia and poor outcome hints at causality. Theoretically, hyperglycemia may worsen brain injury through generation of reactive oxidative species, reduction in cerebral perfusion, activation of postsynaptic glutamate receptors, and exacerbation of blood-brain barrier breakdown (3). Beyond treating the hyperglycemia, preclinical data suggest that insulin may have additional neuroprotective effects unrelated to glucose regulation. However, results from clinical studies using insulin for glucose control