缓激肽代谢与药物性血管性水肿。

Department of Clinical Immunology, Wroclaw Medical University, 50-368 Wroclaw, Poland.

Servicio de Alergia, Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), 28034 Madrid, Spain.

Int J Mol Sci. 2023 Jul 19;24(14):11649. doi: 10.3390/ijms241411649.

Bradykinin (BK) metabolism and its receptors play a central role in drug-induced angioedema (AE) without urticaria through increased vascular permeability. Many cardiovascular and diabetic drugs may cause BK-mediated AE. Angiotensin-converting enzyme inhibitors (ACEIs) and neprilysin inhibitors impair BK catabolism. Dipeptidyl peptidase-IV (DPP-IV) inhibitors reduce the breakdown of BK and substance P (SP). Moreover, angiotensin receptor blockers, thrombolytic agents, and statins may also induce BK-mediated AE. Understanding pathophysiological mechanisms is crucial for preventing and treating drug-induced AE.

缓激肽（BK）代谢及其受体在无荨麻疹的药物诱导性血管水肿（AE）中通过增加血管通透性起核心作用。许多心血管和糖尿病药物可能引起 BK 介导的 AE。血管紧张素转换酶抑制剂（ACEIs）和 Neprilysin 抑制剂损害 BK 的代谢。二肽基肽酶-IV（DPP-IV）抑制剂减少 BK 和 P 物质（SP）的分解。此外，血管紧张素受体阻滞剂、溶栓剂和他汀类药物也可能引起 BK 介导的 AE。了解病理生理学机制对于预防和治疗药物诱导性 AE 至关重要。