BRONCHIAL ASPIRIN CHALLENGE CAUSES SPECIFIC EICOSANOID RESPONSE IN ASPIRIN-SENSITIVE ASTHMATICS

We have shown that inhalation of lysine aspirin enhances leukotriene p roduction in the lungs of patients with aspirin-induced asthma (AIA). To assess the specificity of this reaction, we compared two well-match ed groups of patients: eleven with AIA versus 14 asthmatics tolerant t o aspirin (ATA). All subjects underwent bronchoalveolar lavage (BAL) w ith saline followed immediately by instillation of 10 mg of lysine asp irin, into a right middle lobe segmental bronchus, which was lavaged 1 5 min later. At baseline the two groups did not differ with respect to BAL fluid concentrations of cyclooxygenase products, peptido-leukotri enes, histamine, tryptase, interleukin-5 (IL-5), eosinophil cationic p rotein (ECP), or eosinophil number. Fifteen minutes after aspirin inst illation, there was a statistically significant rise in peptido-leukot rienes, ILS, and eosinophil number in AIA, but not in ATA patients. In the former, but not in the latter group, mean histamine concentration s rose in response to aspirin, approaching the level of statistical si gnificance. Tryptase and ECP levels showed no significant change. Aspi rin significantly depressed PGE(2) and thromboxane B-2 (TXB(2)) in bot h groups, however PGD(2), PGF(2 alpha), and 9 alpha, 11 beta-PGF(2) de creased only in ATA patients. A characteristic disturbance in eicosano id balance, produced by aspirin in patients intolerant to this drug, m ight explain precipitation of asthma attacks.