Abstract

Introduction

Bradykinin-mediated angioedema is a rare but potentially fatal adverse event. Angioedema induced by angiotensin-converting enzyme (ACE) inhibitors is generally attributed to an inhibition of bradykinin degradation following ACE inhibition. Clinical studies on ACE inhibitors mainly focus on their efficacy. Few examine their potential to generate undesirable adverse effects, particularly with regard to angioedema.

Case description

We report here a case of angioedema occurring after ramipril initiation in a patient chronically treated with quinapril. Angioedema subsided spontaneously after ramipril discontinuation and quinapril reintroduction.

Discussion and conclusions

Our clinical case suggests that despite similar pharmacodynamic properties, quinapril and ramipril do not have the same potential to generate angioedema. To explain this difference, we suggest a potentiation of the effect of bradykinin at the B2 receptor level by ramipril, which does not occur with quinapril. Consequently, angioedema may not always be a class effect of ACE inhibitors.

中文翻译：

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血管紧张素转换酶抑制剂诱发的血管性水肿：不总是一类效应？病例报告和简短叙述回顾

摘要

介绍

缓激肽介导的血管性水肿是一种罕见但可能致命的不良事件。血管紧张素转换酶 (ACE) 抑制剂诱导的血管性水肿通常归因于 ACE 抑制后缓激肽降解的抑制。ACE抑制剂的临床研究主要集中在其疗效上。很少有人检查它们产生不良副作用的可能性，特别是在血管性水肿方面。

案例说明

我们在此报告一例长期接受喹那普利治疗的患者在开始使用雷米普利后发生血管性水肿的病例。雷米普利停药和喹那普利重新引入后，血管性水肿自发消退。

讨论和结论

我们的临床案例表明，尽管药效学特性相似，但喹那普利和雷米普利没有相同的产生血管性水肿的潜力。为了解释这种差异，我们建议雷米普利增强缓激肽在 B2 受体水平的作用，而喹那普利不会发生这种情况。因此，血管性水肿可能并不总是 ACE 抑制剂的一类效应。