Davin Laurent, Marechal Patrick, Lancellotti Patrizio, Martinez Christophe, Pierard Luc, Radermecker Regis
a University of Liege Hospital; CHU Sart Tilman Liege Belgium; Department of Cardiology.
b GIGA Cardiovascular Sciences University Hospital of Liege.
Acta Cardiol. 2019 Aug;74(4):277-281. doi: 10.1080/00015385.2018.1507477. Epub 2018 Oct 17.
The effects of angiotensin converting enzyme (ACE) inhibitors result from the inhibition of the ACE (kininase II) to ultimately influence both the renin-angiotensin system and the degradation of the bradykinin (BK) metabolism. ACE inhibitors block the degradation of BK and substance P by ACE. In addition, an active metabolite of BK (Des-Arg9-BK) is catalysed by kininase I and its degradation is controlled in part by the conversion enzyme. These molecules have been associated with increased plasma extravasation associated with ACE inhibitors. ACE inhibitors are the leading cause of drug-induced Angioedema (AE). Symptoms of AE mainly occur after the first month of treatment by ACE. However, very late onset cases, sometimes after several years of stable therapy, are also described in the literature. It has been observed that patients previously stable under ACE inhibitor will most likely develop AE soon after the addition of another medication, including the combination of aspirin or non-steroid anti-inflammatory drugs with ACE inhibitor which has proved to be the most common cause, accounting for close to 50% of all AE cases related to ACE inhibitors. This side effect of ACE inhibitors, sometimes very late and rare, deserves to be recalled.
血管紧张素转换酶（ACE）抑制剂的作用源于对ACE（激肽酶II）的抑制，最终影响肾素-血管紧张素系统以及缓激肽（BK）代谢的降解。ACE抑制剂可阻断ACE对BK和P物质的降解。此外，BK的一种活性代谢产物（去-精氨酸9-缓激肽）由激肽酶I催化，其降解部分受转换酶控制。这些分子与ACE抑制剂相关的血浆外渗增加有关。ACE抑制剂是药物性血管性水肿（AE）的主要原因。AE症状主要在ACE治疗的第一个月后出现。然而，文献中也描述了非常迟发的病例，有时是在数年稳定治疗之后。据观察，先前在ACE抑制剂治疗下病情稳定的患者，在加用另一种药物后很可能很快发生AE，包括阿司匹林或非甾体抗炎药与ACE抑制剂联合使用，这已被证明是最常见的原因，占所有与ACE抑制剂相关AE病例的近50%。ACE抑制剂的这种副作用，有时非常迟发且罕见，值得引起注意。
