Am. J. Respir. Crit. Care Med., Vol 154, No. 6, 12 1996, 1608-1614.
Bronchial aspirin challenge causes specific eicosanoid response in aspirin-sensitive asthmatics
A Szczeklik, K Sladek, R Dworski, E Nizankowska, J Soja, J Sheller and J Oates
Department of Medicine, Jagiellonian University School of Medicine, Cracow, Poland.
We have shown that inhalation of lysine aspirin enhances leukotriene
production in the lungs of patients with aspirin-induced asthma (AIA). To
assess the specificity of this reaction, we compared two well- matched
groups of patients: eleven with AIA versus 14 asthmatics tolerant to
aspirin (ATA). All subjects underwent bronchoalveolar lavage (BAL) with
saline followed immediately by instillation of 10 mg of lysine aspirin,
into a right middle lobe segmental bronchus, which was lavaged 15 min
later. At baseline the two groups did not differ with respect to BAL fluid
concentrations of cyclooxygenase products, peptido-leukotrienes, histamine,
tryptase, interleukin-5 (IL-5), eosinophil cationic protein (ECP), or
eosinophil number. Fifteen minutes after aspirin instillation, there was a
statistically significant rise in peptido-leukotrienes, IL-5, and
eosinophil number in AIA, but not in ATA, but not in ATA patients. In the
former, but not in the latter group, mean histamine concentrations rose in
response to aspirin, approaching the level of statistical significance.
Tryptase and ECP levels showed no significant change. Aspirin significantly
depressed PGE2 and thromboxane B2 (TXB2) in both groups, however PGD2, PGF2
alpha, and 9 alpha, 11 beta-PGF2 decreased only in ATA patients. A
characteristic disturbance in eicosanoid balance, produced by aspirin in
patients intolerant to this drug, might explain precipitation of asthma
attacks.
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Copyright © 1996 American Thoracic Society
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