急性可逆性脑血管收缩综合征伴低剂量双氢麦角胺,可能由丙戊酸和伊列单抗增强:1例报告

Hsiangkuo Yuan, S. Nahas, M. Berk
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引用次数: 3

摘要

二氢麦角胺(DHE),在多药的情况下,可能增加可逆性脑血管收缩综合征(RCVS)的可能性。一名64岁女性,患有慢性偏头痛和药物滥用性头痛(阿米替林、度洛西汀、伊瑞那单抗),选择性接受5天静脉注射氯胺酮(高达55 mg/h)治疗难治性偏头痛。第7天,患者第4次静脉注射DHE (0.25 mg)和第1次静脉注射丙戊酸(VPA) (500 mg)辅助治疗后,出现双侧急性视力下降、双颞区视野缺损和步态不稳。脑磁共振成像/磁共振血管造影(MRI/MRA)显示双侧融合型T2高信号伴枕叶点状扩散受限伴多节段狭窄,累及大脑前、中、后、基底动脉,与RCVS一致。开始使用维拉帕米,而停用DHE、神经抑制剂和血清素能药物。虽然患者持续出现非雷击性偏头痛,但其他神经系统症状在24小时内消失。同时使用VPA和erenumab与DHE可能导致RCVS。VPA可能会取代蛋白质结合的DHE,导致血清中游离DHE水平的短暂激增。Erenumab可能破坏了保护性的血管舒张机制,增强了DHE的血管收缩作用。本病例报告强调了这种药物-药物相互作用与DHE的重要性和认识。中华神经科学杂志,2020;10(1):20-24 doi: https://doi.org/10.14740/jnr558
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Acute Reversible Cerebral Vasoconstriction Syndrome With Low-Dose Dihydroergotamine Possibly Potentiated by Valproic Acid and Erenumab: A Case Report
Dihydroergotamine (DHE), in the setting of polypharmacy, may increase the possibility of reversible cerebral vasoconstriction syndrome (RCVS). A 64-year-old woman with chronic migraine and medication-overuse headache (on amitriptyline, duloxetine, erenumab) was electively admitted for 5 days of intravenous (IV) ketamine (up to 55 mg/h) to treat intractable migraine pain. On the seventh day, upon receiving her forth dose of IV DHE (0.25 mg) and the first of IV valproic acid (VPA) (500 mg) adjunctively, she developed acute bilateral decreased visual acuity, bitemporal visual field deficit, and unsteady gait. Brain magnetic resonance imaging/magnetic resonance angiography (MRI/MRA) showed confluent bilateral T2 hyperintensities with punctate restricted diffusion in the occipital lobes associated with multi-segmental narrowing involving anterior, middle, posterior cerebral, and basilar arteries consistent with RCVS. Verapamil was initiated, whereas DHE, neuroleptics, and serotonergic agents were discontinued. Though she continued to have constant, non-thunderclap migrainous headache, her other neurologic symptoms resolved in 24 h. Concomitant use of VPA and erenumab with DHE may result in RCVS. VPA likely displaces the protein-bound DHE causing a transient surge of free DHE level in the serum. Erenumab may have impaired the protective vasodilatory mechanism, augmenting DHE’s vasoconstrictive effect. This case report highlights the importance and awareness of such a drug-drug interaction with DHE. J Neurol Res. 2020;10(1):20-24 doi: https://doi.org/10.14740/jnr558
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