Drug Insight: Cyclo-Oxygenase-2 Inhibitors--A Critical Appraisal

Burkhard Hinz; Bertold Renner; Kay Brune


Nat Clin Pract Rheumatol. 2007;3(10):552-560. 

In This Article

Use of COX2 Inhibitors in Patients With Aspirin-Induced Asthma

Hypersensitivity to aspirin and other chemically unrelated NSAIDs affects 5–20% of patients with chronic asthma and an unknown fraction of patients with chronic urticaria–angioedema. These reactions seem to be caused by COX1 inhibition, which in turn leads to activation of the lipoxygenase pathway and production of cysteinyl leukotrienes that induce bronchospasm and nasal obstruction. Asthmatic patients who are intolerant of NSAIDs produce low levels of bronchodilatatory prostaglandin E2 (probably because of a lack of COX2), have increased levels of leukotriene C4 synthase and reduced levels of metabolites (i.e. lipoxins) released through the transcellular metabolism of arachidonic acid.[28] In accordance with an important role for COX1 in aspirin-induced asthma, COX2 inhibitors are well tolerated by aspirin-sensitive asthmatic patients in several re-exposure studies.[29,30,31,32] These findings, however, are not seen as proof, and the product information of all COX2 inhibitors still lists aspirin-induced asthma as a contraindication.


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