ATTENUATION OF ASPIRIN-INDUCED BRONCHOCONSTRICTION BY SODIUM CROMOGLYCATE AND NEDOCROMIL SODIUM

The protective activity of nedocromil sodium and of sodium cromoglycat e against aspirin-induced asthma has never been investigated in contro lled studies. Because it has been reported that aspirin-induced platel et-mediated cytotoxic activity in vitro is inhibited after treatment i n vivo with nedocromil but not with cromoglycate, we investigated whet her these compounds also exhibit a different protective activity again st aspirin-induced bronchoconstriction. Ten patients with aspirin-indu ced asthma underwent three bronchial challenges with a single dose of lysine acetylsalicylate (LASA) that caused a decrease in FEV(1) of 25% or more in a preliminary dose-response test 30 min after inhalation o f 4 mg nedocromil sodium, 10 mg sodium cromoglycate, or placebo. FEV(1 ) and SRaw were recorded at intervals for 195 min. After placebo, LASA caused a maximal decrease in FEV(1) of 42 +/- 4% of baseline. After c romoglycate and nedocromil the maximal decrease in FEV(1) was reduced to 20 +/- 3% and 18 +/- 4%, respectively (p < 0.01 versus placebo for both treatments), without significant differences between the two trea tments. Similar results were observed with SRaw. We conclude that, at the recommended therapeutic doses, sodium cromoglycate and nedocromil sodium are equally effective in attenuating aspirin-induced bronchocon striction and that it is unlikely that platelet activation participate s in the pathogenesis of aspirin-induced asthma.