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Analgesic‐induced asthma
Author(s) -
Seale J. Paul
Publication year - 1983
Publication title -
medical journal of australia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 131
eISSN - 1326-5377
pISSN - 0025-729X
DOI - 10.5694/j.1326-5377.1983.tb136230.x
Subject(s) - bronchospasm , aspirin , cyclooxygenase , asthma , analgesic , medicine , pharmacology , bronchodilator , arachidonic acid , arachidonic acid metabolism , drug , anesthesia , chemistry , immunology , enzyme , biochemistry
The reported incidence of acute bronchospasm in patients with asthma who take aspirin varies from 2% to 28%, depending on the methods used to obtain data. Earlier surveys were conducted among adults, and recent studies have shown a similar incidence in children. Immunological mechanisms are unlikely to be responsible. A current hypothesis for the development of analgesic‐induced asthma is based upon the inhibitory effect of aspirin on the cyclooxygenase pathway for the metabolism of arachidonic acid. This theory is supported by the observation that any non‐steroidal anti‐inflammatory drug which inhibits cyclooxygenase activity may precipitate attacks in subjects with asthma who are sensitive to aspirin. Since most of these drugs are structurally dissimilar to aspirin, any immunological crossreactivity is unlikely. It is possible that the bronchospasm which follows inhibition of cyclooxygenase activity is due either to decreased formation of cyclooxygenase products with bronchodilator properties and inhibitory effects on mediator release, or to increased formation of lipoxygenase products with bronchoconstrictor properties.