Chest, Vol 80, 676-681, Copyright © 1981 by American College of Chest Physicians

ARTICLES

Clinical response and serum prostaglandin levels in aspirin idiosyncrasy. Effect of aspirin and a new nonsteroidal anti- inflammatory agent

SL Spector, HG Morris and JC Selner

Clinical measurements and serum prostaglandin concentrations were monitored in three normal subjects, three asthmatic controls and five asthmatic patients with aspirin (ASA) idiosyncrasy before and after oral challenge with small doses of aspirin. Additionally, in the latter group, the effects of ASA were compared with those of piroxicam, a new nonsteroidal anti-inflammatory agent. Challenge with either agent caused bronchospasm in patients with aspirin idiosyncrasy, but was more severe after piroxicam. Nasal stuffiness and/or rhinorrhea preceded or accompanied the changes in pulmonary function with both agents. Serum prostaglandin concentrations, which reflect synthesis by platelets during the clotting of blood, revealed significant decreases in PGE1, PGE2, and PGF2 alpha and thromboxane B2 within two to four hours after drug administration in all subjects with or without ASA idiosyncrasy. The change in serum PG concentration was presented when bronchospasm developed in patients with ASA idiosyncrasy, but persisted for a longer time, reflecting the irreversible effect of these agents on the cyclo- oxygenase enzyme in platelets. The results demonstrate that administration of minute doses of ASA and other nonsteroidal anti- inflammatory drugs alters prostaglandin synthesis in normal and asthmatic subjects with or without ASA idiosyncrasy. Alteration in arachidonate metabolism may be responsible for the induction of bronchospasm, and cautious use of cyclo-oxygenase inhibitors in patients with known or suspected ASA idiosyncrasy is indicated.