Abstract
Aspirin-induced asthma is a distinct clinical syndrome which affects about 10% of adult asthmatics. In these patients aspirin and several other analgesics precipitate asthmatic attacks. The idea that the attacks might result from the specific inhibition of a single enzyme, namely cyclooxygenase, has gained both experimental and clinical support. It stimulated a number of hypotheses on the mechanism of bronchoconstriction. All these hypotheses, here discussed, operate within the framework of the cyclooxygenase theory. Their major assumption is that inhibition of cyclooxygenase triggers specific biochemical reactions which lead to open asthma attacks.

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