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与血管紧张素转换酶抑制剂、西他列汀以及3种分解缓激肽的酶缺乏相关的医源性血管性水肿。

Iatrogenic angioedema associated with ACEi, sitagliptin, and deficiency of 3 enzymes catabolizing bradykinin.

作者信息

Beaudouin E, Defendi F, Picaud J, Drouet C, Ponard D, Moneret-Vautrin D A

机构信息

Service d'Allergologie, Centre Hospitalier E Durkheim, Epinal, France.

French Reference Center for Angioedema, CREAK, Grenoble, France. Université Joseph Fourier, GREPI/AGIM CNRS FRE 3405, Grenoble, France.

出版信息

Eur Ann Allergy Clin Immunol. 2014 May;46(3):119-22.

Abstract

New concepts of idiopathic and iatrogenic angioedema underline the role of bradykinin, and the importance of catabolizing enzymes. A case is described of Angiotensin converting enzyme inhibitor (ACEi) and sitagliptin induced angioedema, where AO attacks decreased after the withdrawal of lisinopril but resolved only after the withdrawal of sitagliptin, an inhibitor of dipeptylpeptidase IV. ACE, aminopeptidase P and carboxypeptidase N were decreased down to 17%, 42%, 64% of median references values, and remained low one year after the interruption of these drugs: 56%, 28% and 50%, respectively. The combined deficiency of APP and CPN might enhance the inhibiting effect of the DPP IV inhibitor. The fact that this triple deficiency remained latent before and after the treatment indicates that searching for latent enzyme deficiencies should be carried out when there is intention to treat with a combination of drugs interfering with the bradykinin metabolism.

摘要

特发性和医源性血管性水肿的新概念强调了缓激肽的作用以及分解代谢酶的重要性。本文描述了一例血管紧张素转换酶抑制剂(ACEi)和西他列汀诱导的血管性水肿病例,停用赖诺普利后血管性水肿发作次数减少,但仅在停用二肽基肽酶IV抑制剂西他列汀后才得以缓解。ACE、氨肽酶P和羧肽酶N分别降至中位参考值的17%、42%和64%,在停用这些药物一年后仍维持在较低水平,分别为56%、28%和50%。氨肽酶P和羧肽酶N的联合缺乏可能增强二肽基肽酶IV抑制剂的抑制作用。治疗前后这种三重缺乏均处于潜伏状态,这一事实表明,当有意联合使用干扰缓激肽代谢的药物进行治疗时,应筛查潜在的酶缺乏情况。

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