Angiotensin-converting Enzyme Inhibitor and Other Drug-associated Angioedema

被引:36
作者
Stone, Cosby, Jr. [1 ]
Brown, Nancy J. [2 ]
机构
[1] Vanderbilt Univ, Med Ctr, Div Allergy Pulm & Crit Care Med, Med Ctr Nouth, 1161 21st Ave South T-1218, Nashville, TN 37232 USA
[2] Vanderbilt Univ, Med Ctr, Dept Med, Med Ctr North, 1161 21st Ave South D-3100, Nashville, TN 37232 USA
关键词
Angioedema; ACE inhibitor; Bradykinin; NSAID; Leukotriene; Drug; Medication; TISSUE-PLASMINOGEN ACTIVATOR; ACUTE ISCHEMIC-STROKE; HYPERSENSITIVITY REACTIONS; HEREDITARY ANGIOEDEMA; PLASMA EXTRAVASATION; GENETIC-VARIANTS; IMMEDIATE HYPERSENSITIVITY; RADIOCONTRAST MEDIA; RECEPTOR ANTAGONIST; INDUCED ANAPHYLAXIS;
D O I
10.1016/j.iac.2017.04.006
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
Nonsteroidal antiinflammatory agents, beta-lectern antibiotics, non-beta lactam antibiotics, and angiotensin-converting enzyme inhibitors are the most common classes of drugs that cause angioedema. Drug-induced angioedema is known to occur via mechanisms mediated by histamine, bradykinin, or leukotriene, and an understanding of these mechanisms is crucial in guiding therapeutic decisions. Nonallergic angioedema occurs in patients with genetic variants that affect metabolism or synthesis of bradykinin, substance P, prostaglandins, or leukotrienes, or when patients are taking drugs that have synergistic mechanisms. The mainstay in treatment of nonallergic drug-induced angioedema is cessation of the offending agents.
引用
收藏
页码:483 / +
页数:14
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