SALMETEROL PREVENTS ASPIRIN-INDUCED ATTACKS OF ASTHMA AND INTERFERES WITH EICOSANOID METABOLISM

We determined the effect of a long acting beta(2)-agonist, salmeterol, on aspirin-induced asthma (AIA) attacks and urinary release of eicosa noids in a double-blind, placebo-controlled, crossover study in 10 ast hmatics sensitive to aspirin. The patients inhaled 50 mu g of salmeter ol or placebo 15 min prior to a cumulative challenge with increasing d oses of lysine-aspirin (L-ASA) (Part I), and before a single, predeter mined dose of L-ASA that caused a 20% fall in FEV1 (PD20) (Part II). S almeterol significantly attenuated aspirin-precipitated bronchoconstri ction and the increase in urinary LTE4. Salmeterol also prevented the decrease in blood eosinophils, and abolished the correlation between t he urinary levels of LTE4 and provocative doses of aspirin. In additio n, PGD-M, the major urinary metabolite of PGD(2), increased after L-AS A inhalation in six of nine subjects; this increase was blocked in all six by salmeterol. The protective effect of salmeterol on aspirin-ind uced attacks and mediator release suggests that it may be efficacious in aspirin-sensitive asthma.