Knowles Sandra R, Drucker Aaron M, Weber Elizabeth A, Shear Neil H
Sunnybrook Health Sciences Centre, Department of Pharmacy and Drug Safety Clinic, Toronto, ON, Canada.
Ann Pharmacother. 2007 Jul;41(7):1191-200. doi: 10.1345/aph.1K023. Epub 2007 Jul 3.
To evaluate and provide management strategies for patients with aspirin or nonselective nonsteroidal antiinflammatory drug (NSAID) sensitivity.
Literature retrieval was accessed through MEDLINE (1966-March 2007) using the terms acetaminophen, aspirin, antiinflammatory agents nonsteroidal, urticaria, angioedema, asthma, leukotriene antagonists, desensitization, and tacrolimus. Article references retrieved were hand-searched for other relevant articles.
All studies published in English were evaluated. Studies, review articles, and commentaries on aspirin-induced asthma and aspirin- or NSAID-induced urticaria/angioedema were included in the review.
Aspirin sensitivity is most often manifested as respiratory reactions (eg, bronchospasm, profuse rhinorrhea, conjunctival injection) or urticaria/angioedema. The primary mechanism is believed to be inhibition of the cyclooxygenase 1 (COX-1) enzyme; as such, patients with aspirin sensitivity often display cross-reactions to nonselective NSAIDs that inhibit the COX-1 enzyme. Management strategies include avoidance of aspirin and cross-reacting nonselective NSAIDs. However, desensitization to aspirin is a viable option for patients with aspirin-induced respiratory reactions, especially for those who require aspirin for thromboembolic prophylaxis. Aspirin desensitization is maintained indefinitely with a daily aspirin dose. There is limited evidence of the use of leukotriene modifiers in preventing aspirin-induced asthma. COX-2 selective NSAIDs, especially in patients with aspirin-induced asthma, have not been found to cross-react. However, approximately 4% of patients with a history of aspirin-induced skin reactions may experience a cutaneous reaction following a challenge to a COX-2 selective NSAID. Since acetaminophen is a weak inhibitor of the COX-1 enzyme, patients with aspirin-induced asthma should not take more than 1000 mg of acetaminophen in a single dose.
Management of patients with aspirin/NSAID sensitivity includes avoidance of aspirin/nonselective NSAIDs, use of COX-2 selective NSAIDs, acetaminophen in doses less than 1000 mg, and desensitization. The role of leukotriene modifiers requires further study before they can be recommended for patients.
评估阿司匹林或非选择性非甾体抗炎药（NSAID）敏感患者的情况并提供管理策略。
通过MEDLINE（1966年 - 2007年3月）检索文献，使用的检索词为对乙酰氨基酚、阿司匹林、非甾体抗炎药、荨麻疹、血管性水肿、哮喘、白三烯拮抗剂、脱敏和他克莫司。对检索到的文章参考文献进行人工检索以查找其他相关文章。
评估所有以英文发表的研究。本综述纳入了关于阿司匹林诱发哮喘以及阿司匹林或NSAID诱发荨麻疹/血管性水肿的研究、综述文章和评论。
阿司匹林敏感最常表现为呼吸道反应（如支气管痉挛、大量流涕、结膜充血）或荨麻疹/血管性水肿。主要机制被认为是环氧合酶1（COX - 1）酶受到抑制；因此，阿司匹林敏感患者常对抑制COX - 1酶的非选择性NSAIDs出现交叉反应。管理策略包括避免使用阿司匹林和交叉反应的非选择性NSAIDs。然而，对于阿司匹林诱发呼吸道反应的患者，尤其是那些需要阿司匹林进行血栓栓塞预防的患者，阿司匹林脱敏是一种可行的选择。阿司匹林脱敏需每日服用阿司匹林剂量以无限期维持。白三烯调节剂用于预防阿司匹林诱发哮喘的证据有限。尚未发现COX - 2选择性NSAIDs会发生交叉反应，尤其是在阿司匹林诱发哮喘的患者中。然而，约4%有阿司匹林诱发皮肤反应病史的患者在使用COX - 2选择性NSAIDs激发试验后可能会出现皮肤反应。由于对乙酰氨基酚是COX - 1酶的弱抑制剂，阿司匹林诱发哮喘的患者单次服用对乙酰氨基酚不应超过1000mg。
阿司匹林/NSAID敏感患者的管理包括避免使用阿司匹林/非选择性NSAIDs、使用COX - 2选择性NSAIDs、服用剂量小于1000mg的对乙酰氨基酚以及脱敏。在推荐给患者之前，白三烯调节剂的作用需要进一步研究。
