CROMOLYN SODIUM PREVENTS BRONCHOCONSTRICTION AND URINARY LTE4 EXCRETION IN ASPIRIN-INDUCED ASTHMA

Background: Inhalation of cromolyn sodium protects against sulpyrine-i nduced bronchoconstriction and prevents urinary leukotriene E-4 (u-LTE 4) excretion in aspirin-induced asthma. Objective: This study was desi gned to investigate the protective effect of cromolyn sodium on airway responsiveness to the sulpyrine provocation test, and to investigate whether this protective activity is associated with a reduction in asp irin-induced urinary excretion of LTE4, a marker of the cysteinyl leuk otriene overproduction that participates in the pathogenesis of aspiri n-induced asthma. Methods: We evaluated the effects of pretreatment wi th cromolyn sodium on bronchoconstriction precipitated by inhalation o f sulpyrine in ten adult patients with mild aspirin-induced asthma. Th ose who were in stable clinical condition and were hyperresponsive to sulpyrine provocation test were allocated to this study. Urinary leuko triene E-4 was measured using combined reverse phase high performance liquid chromatography (rp-HPLC)/enzyme immunoassay. Results: Inhaled c romolyn sodium protects against aspirin-induced attacks of asthma thro ugh mechanisms not related to the bronchodilator property, but related to the improvement of the bronchial hypersensitivity, almost complete ly in all patients (P < .001). By contrast, after cromolyn sodium the maximum level of u-LTE4 was significantly lower than control (P < .05) , Conclusion: Our results suggest for the first time that inhaled crom olyn sodium is one of the most useful inhibitors of aspirin-induced br onchoconstriction, probably acting by inhibiting the release of cystei nyl leukotrienes, and possibly other chemical mediators, by bronchial inflammatory cells.