Intolerance to Aspirin: Clinical Studies and Consideration of its Pathogenesis

Abstract

Angioedema and rhinitis, nasal polyposis, and bronchial asthma of aspirin-sensitive patients are acquired diseases that develop, as a rule, after middle age in predominantly nonatopic patients. In many instances, nasal and bronchial symptoms precede the development of intolerance to aspirin by months or even by years. Salicylates other than acetylsalicylic acid fail to produce symptoms in aspirin-sensitive patients. Exposure to several chemicals, on the other hand, that are structurally unrelated to aspirin can induce comparable "aspirin-like" symptoms. The structural dissimilarity of these compounds is so pronounced that immunological cross-reactivity appears most unlikely. The substances that have been found to induce aspirin-like symptoms have one characteristic in common—they are strong minor analgesics and include pyrazolones and indomethacin as well as aspirin. Peripheral analgesics might act on peripheral chemoreceptors and initiate a series of reflexes that might produce either angioedema, or rhinitis and bronchial asthma, or all of these.