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S100B and NSE in Cluster Headache - Evidence for Glial Cell Activation?

丛集性头痛中的 S100B 和 NSE-胶质细胞活化的证据?

  • 影响因子:2.08
  • DOI:10.1111/head.13864
  • 作者列表:"Snoer AH","Vollesen ALH","Beske RP","Guo S","Hoffmann J","Jørgensen NR","Martinussen T","Ashina M","Jensen RH
  • 发表时间:2020-06-16
Abstract

OBJECTIVE:Neuronal-specific enolase (NSE) and protein S100B have gained considerable interest as the markers of CNS injury, glial cell activation, and/or blood-brain barrier (BBB) disruption. No studies have investigated NSE and S100B in cluster headache (CH), but these biomarkers could contribute to the understanding of CH. METHODS:Patients with episodic CH in bout (eCHa), in remission (eCHr), and chronic CH (cCH) were included in this randomized, double-blind, placebo-controlled, 2-way cross-over provocation study carried out at the Danish Headache Center. The primary endpoints included (1) differences of NSE and S100B in between groups (eCHa, eCHr, and cCH) at baseline; (2) differences over time in plasma concentrations of NSE and S100B between patient developing an attack and those who did not; (3) differences in plasma concentrations over time of NSE and S100B between active day and placebo day. Baseline findings were compared to the historical data on migraine patients and healthy controls and presented with means ± SD. RESULTS:Nine eCHa, 9 eCHr, and 13 cCH patients completed the study and blood samples from 11 CGRP-induced CH attacks were obtained. There were no differences in NSE levels between CH groups at baseline, but CH patients in active disease phase had higher levels compared with 32 migraine patients (9.1 ± 2.2 µg/L vs 6.0 ± 2.2 µg/L, P < .0001) and 6 healthy controls (9.1 ± 2.2 µg/L vs 7.3 ± 2.0 µg/L, P = .007). CGRP-infusion caused no NSE changes and, but a slight, non-significant, increase in NSE was seen in patients who reported a CGRP-induced CH attack (2.39 µg/L, 95% Cl [-0.26, 3.85], P = .061). At baseline S100B levels in eCHa patients were higher compared to cCH patients (0.06 ± 0.02 µg/L vs 0.04 ± 0.02 µg/L, P = .018). Infusion of CGRP and CGRP-induced attacks did not change S100B levels. Apart from induced CH-attacks no other adverse events were noted. CONCLUSIONS:At baseline eCHa patients had higher S100B plasma levels than cCH patients and there was a slight, however not significant, NSE increase in response to CGRP-induced CH attack. Our findings suggest a possible role of an ictal activation of glial cells in CH pathophysiology, but further studies are warranted.

摘要

目的: 神经元特异性烯醇化酶 (NSE) 和蛋白 S100B 作为 CNS 损伤、胶质细胞活化和/或血脑屏障 (BBB) 破坏的标志物已引起了人们的极大兴趣。没有研究调查丛集性头痛 (CH) 中的 NSE 和 S100B,但这些生物标志物可能有助于对 CH 的理解。 方法: 将发作性 CH (eCHa) 、缓解期 (eCHr) 和慢性 CH (cCH) 患者纳入本研究,随机、双盲、安慰剂对照,丹麦头痛中心开展的双向交叉激发研究。主要终点包括 (1) 基线时两组 (eCHa 、 eCHr 和 cCH) NSE 和 S100B 的差异; (2) 发生发作的患者与未发生发作的患者之间 NSE 和 S100B 血浆浓度随时间的差异; (3)活动日和安慰剂日 NSE 和 S100B 血浆浓度随时间的差异。将基线结果与偏头痛患者和健康对照的历史数据进行比较,并以平均值 ± SD 表示。 结果: 9 例 eCHa 、 9 例 eCHr 和 13 例 cCH 患者完成了研究,获得了 11 例 CGRP 诱导的 CH 发作的血液样本。基线时 CH 组之间 NSE 水平无差异,但与 32 例偏头痛患者相比,处于疾病活动期的 CH 患者水平更高 (9.1 ± 2.2 µ g/L vs 6.0 ± 2.2 µ g/L,P <.0001) 和 6 名健康对照 (9.1 ± 2.2 µ g/L vs 7.3 ± 2.0 µ g/L,P = .007)。CGRP-输注未引起 NSE 变化,在报告 CGRP 诱导的 CH 发作 (2.39 µ g/L, 95% Cl [-0.26,3.85],P = .061)。ECHa 患者基线 S100B 水平高于 cCH 患者 (0.06 ± 0.02 µ g/L vs 0.04 ± 0.02 µ g/L,P = .018)。输注 CGRP 和 CGRP 诱导的攻击没有改变 S100B 水平。除了诱导的 CH 发作外,未观察到其他不良事件。 结论: 基线时 eCHa 患者 S100B 血浆水平高于 cCH 患者,CGRP 诱导的 CH 发作引起 NSE 轻度升高,但不显著。我们的研究结果表明胶质细胞的发作性激活在 CH 病理生理学中的可能作用,但需要进一步的研究。

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