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本文引用的文献

1
Randomized Trial of Icatibant for Angiotensin-Converting Enzyme Inhibitor-Induced Upper Airway Angioedema.依替巴肽治疗血管紧张素转换酶抑制剂诱导的上呼吸道血管性水肿的随机试验。
J Allergy Clin Immunol Pract. 2017 Sep-Oct;5(5):1402-1409.e3. doi: 10.1016/j.jaip.2017.03.003. Epub 2017 May 25.
2
Effect of bradykinin receptor antagonism on ACE inhibitor-associated angioedema.缓激肽受体拮抗作用对血管紧张素转换酶抑制剂相关血管性水肿的影响。
J Allergy Clin Immunol. 2017 Jul;140(1):242-248.e2. doi: 10.1016/j.jaci.2016.09.051. Epub 2016 Nov 29.
3
A randomized trial of icatibant in ACE-inhibitor-induced angioedema.依替巴肽治疗血管性水肿的随机试验。
N Engl J Med. 2015 Jan 29;372(5):418-25. doi: 10.1056/NEJMoa1312524.
4
Ecallantide for the acute treatment of angiotensin-converting enzyme inhibitor-induced angioedema: a multicenter, randomized, controlled trial.依替巴肽治疗血管紧张素转换酶抑制剂诱导的血管性水肿的急性治疗：一项多中心、随机、对照试验。
Ann Emerg Med. 2015 Feb;65(2):204-13. doi: 10.1016/j.annemergmed.2014.07.014. Epub 2014 Aug 30.
5
High-molecular-weight kininogen cleavage correlates with disease states in the bradykinin-mediated angioedema due to hereditary C1-inhibitor deficiency.在由遗传性C1抑制物缺乏引起的缓激肽介导的血管性水肿中，高分子量激肽原的裂解与疾病状态相关。
Clin Exp Allergy. 2014 Dec;44(12):1503-14. doi: 10.1111/cea.12293.
6
Genetic variants associated with angiotensin-converting enzyme inhibitor-associated angioedema.与血管紧张素转化酶抑制剂相关的血管性水肿相关的遗传变异。
Pharmacogenet Genomics. 2013 Sep;23(9):470-8. doi: 10.1097/FPC.0b013e328363c137.
7
Icatibant, a new bradykinin-receptor antagonist, in hereditary angioedema.依卡替班，一种新型缓激肽受体拮抗剂，用于遗传性血管性水肿。
N Engl J Med. 2010 Aug 5;363(6):532-41. doi: 10.1056/NEJMoa0906393.
8
Bradykinin-mediated angioedema.缓激肽介导的血管性水肿。
N Engl J Med. 2002 Aug 22;347(8):621-2. doi: 10.1056/NEJM200208223470820.
9
Quantification of BK1-5, the stable bradykinin plasma metabolite in humans, by a highly accurate liquid-chromatographic tandem mass spectrometric assay.
Anal Biochem. 2001 May 1;292(1):87-93. doi: 10.1006/abio.2001.5073.

血管紧张素转化酶抑制剂相关性血管水肿期间的内源性缓激肽和 B1-B5。

Endogenous bradykinin and B1-B5 during angiotensin-converting enzyme inhibitor-associated angioedema.

机构信息

Department of Medicine, Vanderbilt University Medical Center, Nashville, Tenn.

Department of Biostatistics, Vanderbilt University Medical Center, Nashville, Tenn.

出版信息

J Allergy Clin Immunol. 2018 Nov;142(5):1636-1639.e5. doi: 10.1016/j.jaci.2018.06.037. Epub 2018 Jul 21.

DOI:10.1016/j.jaci.2018.06.037
PMID:30036596
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6226317/
Abstract

Bradykinin concentrations and the ratio of bradykinin to its stable metabolite BK1–5 (RPPGF) were significantly increased in patients presenting with angiotensin-converting enzyme (ACE) inhibitor-associated angioedema compared to ACE inhibitor-treated controls. Cleavage of high molecular weight kininogen was not increased in patients with ACE inhibitor-associated angioedema, indicating that increased bradykinin concentrations result from decreased degradation.

摘要

与接受血管紧张素转换酶（ACE）抑制剂治疗的对照组相比，出现 ACE 抑制剂相关性血管性水肿的患者体内缓激肽浓度及其稳定代谢产物 BK1–5（RPPGF）的比值显著升高。ACE 抑制剂相关性血管性水肿患者的高分子量激肽原裂解并未增加，表明缓激肽浓度升高是由于降解减少所致。