Concerning the nature of intolerance to aspirin

Abstract

(1) Intolerance to aspirin is not uncommon in individuals near middle age who, as a rule, do not have a history of atopy. It is characterized by changes in the skin and respiratory mucous membranes—angioedema, perennial rhinitis, formation of nasal polyps, and bronchial asthma—which precede the development of intolerance to aspirin. (2) While reactions induced by aspirin simulate an immunological discase evidence for an allergy to acetylsalicylic acid per se or acetylsalicylic acid as an antigenic determinant is unconvincing. Attempts to demonstrate antibodies to acetylsalicylic acid have been generally unsuccessful. (3) If an immunological etiology can be ruled out, aspirin must induce its effects by a direct action on effector organs. (4) Acetylsalicylic acid can inhibit at least one mediator-induced reflex, i.e., the kinin-induced vasodilatation in the skin of man and the kinin-induced bronchoconstriction of the guinea pig. (5) Patients who have an intolerance to aspirin have a comparable intolerance to other minor analgesics, e.g., pyrazolones and indomethacin. Reactions to these structurally dissimilar compounds occur after first administration. It appears reasonable to assume that they exert their effect on the same receptors. (6) It is proposed that aspirin produces characteristic symptoms in aspirin-sensitive patients by activating peripheral chemoreceptors which have been altered by a pre-existing disease. (7) A possible mechanism by which peripheral chemoreceptors might participate in the pathogenesis of bronchial asthma has been outlined and reviewed in the light of what is known about reflexes which control the vascular bed of the skin and the functional state of the respiratory mucous membranes.