Bradykinin Metabolism and Drug-Induced Angioedema

被引:13
作者
Smolinska, Sylwia [1 ]
Antolin-Amerigo, Dario [2 ]
Popescu, Florin-Dan [3 ]
机构
[1] Wroclaw Med Univ, Dept Clin Immunol, PL-50368 Wroclaw, Poland
[2] Hosp Univ Ramon y Cajal, Serv Alergia, Inst Ramon y Cajal Invest Sanitaria IRYCIS, Madrid 28034, Spain
[3] Carol Davila Univ Med & Pharm, Dept Allergol Nicolae Malaxa Clin Hosp, Bucharest 022441, Romania
关键词
bradykinin metabolism; drug-induced angioedema; CONVERTING-ENZYME-INHIBITOR; DIPEPTIDYL PEPTIDASE-IV; INCREASED RISK; AMINOPEPTIDASE-P; ACE-INHIBITORS; EDEMA; DEFICIENCY; EXPRESSION; MANAGEMENT; ICATIBANT;
D O I
10.3390/ijms241411649
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
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页数:15
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