Cromolyn sodium prevents bronchoconstriction and urinary LTE4 excretion in aspirin-induced asthma

Inhalation of cromolyn sodium protects against sulpyrine-induced bronchoconstriction and prevents urinary leukotriene E4 (u-LTE4) excretion in aspirin-induced asthma.

This study was designed 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 aspirin-induced urinary excretion of LTE4, a marker of the cysteinyl leukotriene overproduction that participates in the pathogenesis of aspirin-induced asthma.

We evaluated the effects of pretreatment with cromolyn sodium on bronchoconstriction precipitated by inhalation of sulpyrine in ten adult patients with mild aspirin-induced asthma. Those who were in stable clinical condition and were hyperresponsive to sulpyrine provocation test were allocated to this study. Urinary leukotriene E4 was measured using combined reverse phase high performance liquid chromatography (rp-HPLC)/enzyme immunoassay.

Inhaled cromolyn sodium protects against aspirin-induced attacks of asthma through mechanisms not related to the bronchodilator property, but related to the improvement of the bronchial hypersensitivity, almost completely in all patients (P < .001). By contrast, after cromolyn sodium the maximum level of u-LTE4 was significantly lower than control (P < .05).

Our results suggest for the first time that inhaled cromolyn sodium is one of the most useful inhibitors of aspirin-induced bronchoconstriction, probably acting by inhibiting the release of cysteinyl leukotrienes, and possibly other chemical mediators, by bronchial inflammatory cells.