Background Biochemical analysis of expiratory breath condensate is an emerging non-invasive technique for assessment of airway inflammation.
Objective We wondered whether application of expiratory breath condensate could facilitate diagnosis of aspirin-intolerant asthma and reproduce eicosanoids mediators' abnormalities described in this disease.
Methods We measured prostaglandins (PGs) E2, F2α, 9α11βF2 and iso-F2 by gas-chromatography/mass-spectrometry and cysteinyl leukotrienes (cys-LTs) by radioimmunoassay in breath condensates of asthmatic patients undergoing oral aspirin challenge. Fourteen patients with aspirin-induced asthma and 20 aspirin-tolerating asthmatics, most of them on chronic inhaled corticotherapy, were studied and compared with 10 healthy subjects. Additionally, plasma 9α11βPGF2, the metabolite of PGD2 and urinary leukotriene (LT) E4 were measured before and following the challenge.
Results At baseline, PG did not differ between the groups, except for lower 9α11βPGF2 in aspirin-intolerant asthma. Their concentrations were not changed by the challenge. Breath condensate cys-LTs were similar in the groups studied at base, and after aspirin challenge increased only in aspirin-intolerant patients. Elevated baseline urinary LTE4 and its further increase following aspirin challenge was highly diagnostic for aspirin-intolerant asthma. The discriminatory value of cys-LTs increase in breath condensates was lower (72.8%) than either basal (99%) or post-challenge increase (94%) of urinary LTE4.
Conclusions In asthmatic patients on chronic corticotherapy measurement of urinary LTE4 excretion rather than cys-LTs in breath condensate is of greater value for diagnosis of aspirin hypersensitivity.