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Am. J. Respir. Crit. Care Med., Volume 158, Number 4, October 1998, 1168-1172

Salmeterol Prevents Aspirin-induced Attacks of Asthma and Interferes with Eicosanoid Metabolism

ANDRZEJ SZCZEKLIK, RYSZARD DWORSKI, LUCYNA MASTALERZ, ANNA PROKOP, JAMES R. SHELLER, EWA NIZANKOWSKA, ADAM CMIEL, and JOHN A. OATES

Department of Medicine, Jagiellonian University School of Medicine, Cracow, Poland; and Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee

We determined the effect of a long acting beta 2-agonist, salmeterol, on aspirin-induced asthma (AIA) attacks and urinary release of eicosanoids in a double-blind, placebo-controlled, crossover study in 10 asthmatics sensitive to aspirin. The patients inhaled 50 µg of salmeterol or placebo 15 min prior to a cumulative challenge with increasing doses of lysine-aspirin (L-ASA) (Part I), and before a single, predetermined dose of L-ASA that caused a 20% fall in FEV1 (PD20) (Part II). Salmeterol significantly attenuated aspirin-precipitated bronchoconstriction and the increase in urinary LTE4. Salmeterol also prevented the decrease in blood eosinophils, and abolished the correlation between the urinary levels of LTE4 and provocative doses of aspirin. In addition, PGD-M, the major urinary metabolite of PGD2, increased after L-ASA inhalation in six of nine subjects; this increase was blocked in all six by salmeterol. The protective effect of salmeterol on aspirin-induced attacks and mediator release suggests that it may be efficacious in aspirin-sensitive asthma.




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Copyright © 1998 American Thoracic Society 		  ATS 2008 State of the Art Course