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. 2010;95:170-179.
doi: 10.1159/000315950. Epub 2010 Jun 1.




Andrzej Szczeklik. Chem Immunol Allergy. .


Aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) are often incriminated in hypersensitivity reactions leading to anaphylaxis. Two populations are at the high risk of developing such reactions: patients with asthma and those with urticaria. In a subset of asthmatics, NSAIDs that inhibit cyclooxygenase-1 (COX-1) precipitate non-allergic, hypersensitivity reactions, characterized by violent attacks of dyspnea. These patients suffer from a distinct clinical syndrome, called aspirin induced asthma (AIA), which includes chronic eosinophilic rhinusinusitis and persistent asthma. Inpatients with chronic idiopathic urticaria, and less commonly in patients without chronic urticaria, NSAIDs usually acting through inhibition of COX-1 can induce or exacerbate skin eruptions. While alterations in eicosanoid biosynthesis characterized both AIA and aspirin-triggered urticaria, other patients may rarely manifest IgE-mediated reactions.

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