EICOSANOIDS IN BRONCHOALVEOLAR LAVAGE FLUID OF ASPIRIN-INTOLERANT PATIENTS WITH ASTHMA AFTER ASPIRIN CHALLENGE

We have recently shown that oral aspirin provocation leads to an incre ase in LTE(4) and a reduction in 11-dehydro-TXB(2) levels in urine of patients with aspirin induced-asthma (AIA). To test the hypothesis tha t cyclooxygenase inhibition and an enhancement of cysteinyl-leukotrien e production occurs in the lungs of patients with AIA, we examined the eicosanoid levels in bronchoalveolar lavage fluid obtained 30 min aft er lysine-aspirin or placebo inhalation in 10 patients with AIA. Eosin ophil cationic protein (ECP) levels were determined to evaluate eosino phil activation. Six asthmatics nonsensitive to aspirin (NA) underwent challenge with placebo. The dose of lysine-aspirin inhaled by patient s with AIA was equal to that which had produced greater than or equal to 20% fall in FEV(1). Compared with NA, patients with AIA had: (1) ei cosanoid levels, particularly PGE(2) and TXB(2), elevated and (2) high er number of eosinophils and ECP. The overproduction of eicosanoids co uld be related to a distinct eosinophilic inflammation in airways of p atients with AIA. Inhalation of lysine-aspirin had no effects on 12-HE TE and 15-HETE levels, but it markedly depressed cyclooxygenase produc ts and significantly enhanced leukotriene production in the lungs of p atients with AIA.