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脑损伤标志物:糖尿病酮症酸中毒患儿的 S100 钙结合蛋白 B、神经元特异性烯醇化酶和神经胶质纤维酸性蛋白。

Brain injury markers: S100 calcium-binding protein B, neuron-specific enolase and glial fibrillary acidic protein in children with diabetic ketoacidosis.

机构信息

Department of Pediatric Endocrinology, Faculty of Medicine, Izmir Katip Celebi University, Izmir, Turkey.

Department of Pediatric Endocrinology, Faculty of Medicine, Adnan Menderes University, Aydın, Turkey.

出版信息

Pediatr Diabetes. 2018 Aug;19(5):1000-1006. doi: 10.1111/pedi.12667. Epub 2018 Mar 13.

DOI:10.1111/pedi.12667
PMID:29484801
Abstract

BACKGROUND

To investigate serum levels of brain injury markers in diabetic ketoacidosis (DKA) and the relation of these markers with clinical and radiological findings of brain injury and laboratory results.

METHODS

Twenty-nine patients with DKA, 30 with type 1 diabetes mellitus (T1DM), and 35 healthy children were included. Clinical and laboratory findings, and the Glasgow Coma Scale (GCS) were recorded. In the DKA group, neuron-specific enolase (NSE), S100 calcium-binding protein B (S100B) and glial fibrillary acidic protein (GFAP) levels were measured at baseline and 6 and 12 hours after treatment. Magnetic resonance imaging was performed in the DKA group to demonstrate any brain injury.

RESULTS

No clinical or radiological findings of brain injury were found in any of the patients with DKA. In the DKA group, S100B was significantly higher than the healthy control and T1DM groups, while GFAP and NSE levels were not different from controls and T1DM patients. No significant differences were found in GFAP, NSE and S100B levels according to severity of DKA, diabetes duration and GCS.

CONCLUSION

NSE and GFAP levels do not increase in DKA patients without overt brain injury. Elevated levels of S100B, which is also synthesized from non-neuronal tissues, might arise from peripheral sources. A lack of concurrent increase in serum levels of these brain injury markers might result from the yet intact blood brain barrier or a true absence of neuronal damage. In order to reveal subclinical brain injury related to DKA, there is a need for studies concurrently assessing neurocognitive functions.

摘要

背景

研究糖尿病酮症酸中毒(DKA)患者血清脑损伤标志物水平及其与脑损伤临床和影像学表现及实验室结果的关系。

方法

纳入 29 例 DKA 患者、30 例 1 型糖尿病(T1DM)患者和 35 例健康儿童。记录临床和实验室检查结果及格拉斯哥昏迷量表(GCS)评分。DKA 组患者在治疗前及治疗后 6 小时、12 小时分别检测神经元特异性烯醇化酶(NSE)、S100 钙结合蛋白 B(S100B)和胶质纤维酸性蛋白(GFAP)水平。DKA 组患者行磁共振成像检查以明确有无脑损伤。

结果

DKA 患者均无临床或影像学脑损伤证据。DKA 组 S100B 水平显著高于健康对照组和 T1DM 组,而 GFAP 和 NSE 水平与对照组和 T1DM 患者无差异。根据 DKA 严重程度、糖尿病病程和 GCS 评分,GFAP、NSE 和 S100B 水平无显著差异。

结论

无脑损伤表现的 DKA 患者 NSE 和 GFAP 水平不升高。S100B 水平升高,而 S100B 也可由非神经元组织合成,可能来源于外周组织。这些脑损伤标志物血清水平无同步升高可能与血脑屏障完整或神经元无损伤有关。为了发现与 DKA 相关的亚临床脑损伤,需要同时评估神经认知功能的研究。

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引用本文的文献

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Serum Neuron-specific Enolase and S100 Calcium-binding Protein B in Pediatric Diabetic Ketoacidosis.小儿糖尿病酮症酸中毒患者血清神经元特异性烯醇化酶和S100钙结合蛋白B水平
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