title: Exhaled eicosanoids following oral aspirin challenge in asthmatic patients.
abstract: 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) E(2), F(2 alpha), 9 alpha 11 beta F(2) and iso-F(2) 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 9 alpha 11 beta PGF(2), the metabolite of PGD(2) and urinary leukotriene (LT) E(4) were measured before and following the challenge.
  
  
  RESULTS
  At baseline, PG did not differ between the groups, except for lower 9 alpha 11 beta PGF(2) 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 LTE(4) 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 LTE(4).
  
  
  CONCLUSIONS
  In asthmatic patients on chronic corticotherapy measurement of urinary LTE(4) excretion rather than cys-LTs in breath condensate is of greater value for diagnosis of aspirin hypersensitivity.
authors.affiliation: Department of Medicine, School of Medicine, Jagiellonian University, 31-066 Cracow, Poland.
authors.forename: M
authors.initials: M
authors.lastname: Sanak
authors.forename: B
authors.initials: B
authors.lastname: Kiełbasa
authors.forename: G
authors.initials: G
authors.lastname: Bochenek
authors.forename: A
authors.initials: A
authors.lastname: Szczeklik
mesh_terms: D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D019540:Area Under Curve; D001241:Aspirin / Q000009:adverse effects*; D001249:Asthma / Q000139:chemically induced* / Q000175:diagnosis; D015415:Biomarkers / Q000032:analysis / Q000097:blood / Q000652:urine; D001944:Breath Tests; D016022:Case-Control Studies; D015237:Dinoprost / Q000032:analysis / Q000097:blood; D015232:Dinoprostone / Q000032:analysis; D015777:Eicosanoids / Q000032:analysis*; D005260:Female; D008401:Gas Chromatography-Mass Spectrometry; D006801:Humans; D017999:Leukotriene E4 / Q000652:urine; D008168:Lung / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D012372:ROC Curve
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D015415:Biomarkers; D015777:Eicosanoids; D017999:Leukotriene E4; D015237:Dinoprost; D015232:Dinoprostone; D001241:Aspirin