Title: ACE inhibitor induced angioedema
题目：血管紧张素转化酶抑制剂（ACEI）导致的血管性水肿
Author 作者: Ellen Lemkin
 
Angioedema is induced by elevated levels of bradykinin.
血管性水肿是由缓激肽的升高造成。
Bradykinin is noramlly degraded by angiotensin-1 converting enzyme and several other enzymes (including aminipeptidase–P)
缓激肽在正常情况下是由血管紧张素－1转化酶和其它几个酶（如氨基酸肽酶－P）。
A deficiency in aminopeptidase-P likely leads to ACEI induced angioedema.
氨基酸肽酶缺乏很可能导致ACEI性血管性水肿。
Treatment typically starts with discontinuing ACE inhibitors, administering H1 and H2 antagonists, and corticosteroids (all Class indeterminate). 
治疗主要是停止ACEI的继续使用，给H1和H2拮抗剂，及类固醇激素（疗效级别都不定）。
Another consideration may be FFP 10-15 ml/kg IV or the off label use of icatibant (both Class II recommendations).
另外可考虑静脉应用新鲜冻干血浆（fresh frozen plasma，FFP）10－15ml／kg或者是非标记使用艾替班特（两个都是二类推荐药）。
Icatibant inhibits the bradykin B2 receptor. It is a sythetic decapeptide structurally similar to bradykin.
艾替班特抑制缓激肽B2受体，是在结构上与缓激肽相式的十肽。
Icatibant has been effective in case reports and case series in ACEI induced angioedema. There is a prospective, double blind randomized placebo controlled trial underway.
艾替班特在ACEI导致的血管性血肿中的效果已有个例和系列病例报道。现在正有一个前瞻性的，双盲随机，对照剂控制的临床试验在进行中。
 
References 参考文献
Wilerson G. Angioedema in the Emergency Department: An evidence-based review. Emergency Medicine Practice, Nov 2012.