Aspirin intolerance and the cyclooxygenase-leukotriene pathways.

PURPOSE OF REVIEW

In up to 10% of patients with bronchial asthma, aspirin and other nonsteroidal antiinflammatory drugs precipitate asthmatic attacks. This is a hallmark of a distinct clinical syndrome that develops according to a characteristic sequence of symptoms. Here we discuss its clinical picture and management as related to the abnormalities in arachidonic acid transformations.

RECENT FINDINGS

At the biochemical level, the characteristic feature is profound alteration in eicosanoid biosynthesis and metabolism. Major advances in the molecular biology of eicosanoids, exemplified by the cloning of cysteinyl-leukotriene receptors and discovery of a whole family of cyclooxygenase enzymes, offer new insights into mechanisms operating in aspirin-induced asthma. Clinical interest has been enhanced by the introduction into therapy of highly specific cyclooxygenase-2 inhibitors and antileukotriene drugs.

SUMMARY

Recent studies have improved our understanding of mechanisms operating in asthma and unvieled the role of eicosanoid mediators in pulmonary disease.