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危及生命的血管紧张素转换酶抑制剂所致血管性水肿的治疗

Treatment of Life-Threatening ACE-Inhibitor-Induced Angioedema.

作者信息

Hirschy RaeAnn, Shah Tanvi, Davis Tamara, Rech Megan A

机构信息

Department of Pharmacy, Loyola University Medical Center, Maywood, Illinois (Drs Hirschy, Shah, and Rech); and Department of Pharmacy, Novant Health-Forsyth Medical Center, Winston-Salem, North Carolina (Dr Davis).

出版信息

Adv Emerg Nurs J. 2018 Oct/Dec;40(4):267-277. doi: 10.1097/TME.0000000000000211.

Abstract

Incidence of angioedema associated with angiotensin-converting enzyme inhibitors (ACE-I) has been estimated at 0.1%-2.2% of patients receiving treatment. Despite the potential severity of this disease state, standardized treatment is lacking. Traditional pharmacotherapy options include medications that target inflammatory mediators and the angiotensin pathway. However, because ACE-I-induced angioedema is caused by accumulation of bradykinin, these medications fail to target the underlying pathophysiology. Recently, novel therapies that target the kallikrein-bradykinin pathway have been studied. These include icatibant, ecallantide, C1 esterase inhibitors, and fresh-frozen plasma. Recent randomized controlled trials exhibit contradictory results with the use of icatibant. This is a focused review on traditional and novel treatment strategies for ACE-I-induced angioedema.

摘要

据估计,接受血管紧张素转换酶抑制剂(ACE-I)治疗的患者中,血管性水肿的发生率为0.1%-2.2%。尽管这种疾病状态可能很严重,但缺乏标准化的治疗方法。传统的药物治疗选择包括针对炎症介质和血管紧张素途径的药物。然而,由于ACE-I诱导的血管性水肿是由缓激肽的积累引起的,这些药物未能针对潜在的病理生理学。最近,针对激肽释放酶-缓激肽途径的新型疗法已得到研究。这些疗法包括依替巴肽、艾卡拉肽、C1酯酶抑制剂和新鲜冷冻血浆。最近的随机对照试验显示,使用依替巴肽的结果相互矛盾。这是一篇关于ACE-I诱导的血管性水肿的传统和新型治疗策略的重点综述。

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