Migraine induction with calcitonin gene-related peptide in patients from erenumab trials.

Migraine induction with calcitonin gene-related peptide in patients from erenumab trials.
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DOI:
10.1186/s10194-018-0927-2
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发表时间:
2018-11-08
期刊:
The journal of headache and pain
影响因子:
--
通讯作者:
Ashina M
Ashina M
中科院分区:
其他
文献类型:
--
作者:
Christensen CE;Younis S;Deen M;Khan S;Ghanizada H;Ashina M

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用erenumab预防偏头痛和用降钙素基因相关肽(CGRP)诱导偏头痛都具有显著的个体差异。我们想探讨抗CGRP治疗的个体疗效与CGRP诱发偏头痛的易感性之间的可能联系。13名偏头痛患者,以前参加erenumab抗CGRP受体单克隆抗体试验,在双盲,安慰剂对照,随机交叉设计中接受CGRP,以研究他们对偏头痛诱导的易感性。使用标准化问卷评估既往抗体治疗的疗效。将患者分为高反应者和低反应者组。主要结果是输注CGRP和安慰剂后偏头痛样发作的发生率和头痛强度曲线下面积。所有访谈和实验均在丹麦头痛中心(丹麦,丹麦)的实验室中进行。包括10名高反应者和3名低反应者。CGRP在10名(77%)患者中诱导偏头痛样发作,其中2名为不良反应者,相比之下,安慰剂组无反应者(p = 0.002)。与安慰剂相比,CGRP治疗后0-90 min(p = 0.009)和2-12 h(p = 0.014)的头痛强度曲线下面积更大。CGRP治疗后头痛强度峰值评分中位数为5(5-9),安慰剂治疗后为2(0-4)(p = 0.004)。erenumab效果良好的患者对CGRP激发高度敏感。如果相关性是明显的,CGRP激发可以证明是预测抗体治疗效果的生物标志物。Retroperitoneal在clinicaltrials.gov注册,标识符为:NCT 03481400。
Migraine prevention with erenumab and migraine induction by calcitonin gene-related peptide (CGRP) both carry notable individual variance. We wanted to explore a possible association between individual efficacy of anti-CGRP treatment and susceptibility to migraine induction by CGRP. Thirteen migraine patients, previously enrolled in erenumab anti-CGRP receptor monoclonal antibody trials, received CGRP in a double-blind, placebo-controlled, randomized cross-over design to investigate their susceptibility to migraine induction. A standardized questionnaire was used to assess the efficacy of previous antibody treatment. The patients were stratified into groups of high responders and poor responders. Primary outcomes were incidence of migraine-like attacks and area under the curve of headache intensity after infusion of CGRP and placebo. All interviews and experiments were performed in laboratories at the Danish Headache Center, Copenhagen, Denmark. Ten high responders and three poor responders were included. CGRP induced migraine-like attacks in ten (77%) patients, whereof two were poor responders, compared to none after placebo (p = 0.002). The area under the curve for headache intensity was greater after CGRP, compared to placebo, at 0–90 min (p = 0.009), and 2–12 h (p = 0.014). The median peak headache intensity score was 5 (5–9) after CGRP, compared to 2 (0–4) after placebo (p = 0.004). Patients with an excellent effect of erenumab are highly susceptible to CGRP provocation. If an association is evident, CGRP provocation could prove a biomarker for predicting antibody treatment efficacy. Retrospectively registered at clinicaltrials.gov with identifier: NCT03481400.
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