Analgesic-induced asthma.
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 cyclo-oxygenase pathway for the metabolism of arachidonic acid. This theory is supported by the observation that any non-steroidal anti-inflammatory drug which inhibits cyclo-oxygenase 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 cyclo-oxygenase activity is due either to decreased formation of cyclo-oxygenase products with bronchodilator properties and inhibitory effects on mediator release, or to increased formation of lipoxygenase products with bronchoconstrictor properties.
D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects* / Q000494:pharmacology; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism; D001241:Aspirin / Q000009:adverse effects; D001249:Asthma / Q000139:chemically induced*; D001986:Bronchial Spasm / Q000139:chemically induced; D002648:Child; D016861:Cyclooxygenase Inhibitors; D006801:Humans; D008168:Lung / Q000187:drug effects; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism
D000894:Anti-Inflammatory Agents, Non-Steroidal; D001095:Arachidonic Acids; D016861:Cyclooxygenase Inhibitors; D016718:Arachidonic Acid; D011451:Prostaglandin-Endoperoxide Synthases; D001241:Aspirin