SEARCH

SEARCH BY CITATION

Keywords:

  • Allergen challenge;
  • asthma;
  • breath analysis;
  • exhaled breath condensate;
  • exhaled nitric oxide

Eur J Clin Invest 2011; 41 (4): 411–416

Abstract

Background  Exhaled nitric oxide (NO), commonly accepted marker of airways inflammation, may be generated both by specific enzymes, NO synthases, as well as by nonenzymatic reduction in its metabolites. During asthma exacerbations, owing to lower airways pH, it has been reported that nitrite reduction may contribute to the increase in exhaled NO. Allergen exposure, an important cause of asthma exacerbations, is also known to increase exhaled NO.

Design  To investigate whether cat allergen exposure of cat-sensitized asthmatics leads to airway acidification, which could explain the expected increase in exhaled NO. Twelve nonsmoking, cat-sensitized patients (nine women) aged 33·5 (22–54) years with mild intermittent asthma performed a cat allergen challenge. Exhaled NO at 50–200 mL s−1, nasal NO, exhaled breath condensate (EBC) pH, nitrite and nitrate were measured before, 8 and 24 h after allergen challenge.

Results  A significant increase in FENO 50 was observed 24 h after allergen challenge compared to baseline: 110 ppb (34, 143) vs. 60 ppb (19, 122), P = 0·006. This was mainly explained by an increase in bronchial NO flux (P = 0·02), while no changes in EBC pH were observed (P = 0·35).

Conclusions  Allergen exposure is not associated with airways acidification, implying that the observed increase in exhaled NO is probably because of enzymatic NO production.