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From the Authors

Dept of Pathophysiology, National Korányi Institute for Tuberculosis and Pulmonology, Budapest, Hungary

From the authors:

It is a pleasure to read the appreciation shown by L. Spicuzza and colleagues for our recent study on adenosine in exhaled breath condensate (EBC-adenosine).

We would like to comment on the possibility of using adenosine as a marker to assess the degree of airway inflammation. We agree with the comments made by L. Spicuzza and colleagues with regard to our results showing that EBC-adenosine levels are related to the degree of airway inflammation and are in line with previous findings, suggesting that adenosine may be a nonspecific marker of airway inflammation 1. In particular, it is worth noting that in the study by Driver et al. 1, no chronic obstructive pulmonary disease patients were included, only asymptotic smokers along side asthmatic patients. In a preliminary study we have shown that EBC-adenosine is also elevated in patients with cystic fibrosis, confirming that elevated adenosine levels may be a nonspecific indicator for ongoing airway inflammation 2.

Interestingly, not only is the increase in airway adenosine concentration related to other markers of airway inflammation but airway hyperresponsiveness to adenosine monophosphate also reflects the intensity of airway inflammation. Because both the release and indirect action of adenosine have been shown to be related to the number and/or activation of "primed" mast cells and other inflammatory cells present in the airways this could explain the observed relationships 1–5. It also seems to be obvious that the enhanced level of adenosine in the airways would lead to potentiated airway obstruction provoked by diverse bronchoconstrictor agents in asthma 6, 7.

Our results partly confirm the statement of the correspondents that exposure to aeroallergens may modulate airway inflammation in asthmatic patients. We found elevation in both EBC-adenosine concentrations and exhaled nitric oxide (eNO) levels in patients with worsening asthmatic symptoms. However, only eNO levels, not adenosine concentrations, were higher in patients in a stable condition than in healthy controls. This finding suggests that eNO may be a more sensitive marker of airway inflammation than EBC-adenosine in atopic asthmatics, showing even the hidden inflamed processes in the airways.

Furthermore, the notion concerning the potential effect of allergic rhinitis on mediator levels in the lower airways seems to be correct. In a pilot study, we measured EBC-adenosine levels in eight nonasthmatic patients with allergic rhinitis. At the time of the measurement all patients were exposed to natural allergens and had symptoms of rhinitis. Adenosine concentrations were significantly higher in samples from these patients than in samples from healthy subjects. This result confirms that active allergic inflammation, either of the upper or lower airways, may result in elevation in EBC-adenosine concentration as suggested. Furthermore, when EBC was collected with nasal inhalation adenosine levels were higher than in samples obtained with oral inhalation, suggesting that nasally produced adenosine may enter the lower airways which may, at least in part, be responsible for increases in the adenosine levels 8.

Finally, we agree with L. Spicuzza and colleagues that there is a need for further prospective studies on this topic. We believe these studies need to assess changes in the concentration of adenosine in exhaled breath condensate and also evaluate the relationship between adenosine in exhaled breath condensate and the degree of allergen exposure or deterioration in airway inflammation. Justification of the possible use of the concentration of adenosine in exhaled breath condensate to monitor chronic or acute airway inflammation also requires further investigation.

References

1. Driver AG, Kukoly CA, Ali S, Mustafa SJ. Adenosine in bronchoalveolar lavage fluid in asthma. Am Rev Respir Dis 1993;148:91–97.[Web of Science][Medline] [Order article via Infotrieve]
2. Barát E, Huszár É, Vass G, Csiszér E, Valyon M, Horváth I. Measurement of natrium chloride and adenosine concentration in exhaled breath condensate. Eur Respir J 2002;20:Suppl. 38, 281s.
3. Polosa R, Ciamarra I, Mangano G, et al. Bronchial hyperresponsiveness and airway inflammation markers in nonasthmatics with allergic rhinitis. Eur Respir J 2000;15:30–35.[Abstract]
4. Polosa R, Holgate ST. Adenosine bronchoprovocation: a promising marker of allergic inflammation in asthma?. Thorax 1997;52:919–923.[Web of Science][Medline] [Order article via Infotrieve]
5. van den Berge M, Meijer RJ, Kerstjens HA, et al. PC20 adenosine 5'-monohosphate is more closely associated with airway inflammation in asthma than PC20 methacholine. Am J Respir Crit Care Med 2000;163:1546–1550.
6. Huszár É, Horváth I, Barát E, Herjavecz I, Böszörményi-Nagy Gy, Kollai M. Elevated circulating adenosine level potentiates antigen-induced immediate bronchospasm and bronchoconstrictor mediator release in sensitized guinea pigs. J Allergy Clin Immunol 1998;102:687–691.[CrossRef][Web of Science][Medline] [Order article via Infotrieve]
7. Csoma Zs, Vizi É, Huszár É. Post-exercise changes in FEV1 values and in adenosine concentrations in exhaled-breath condensate in healthy subjects and patients with exercise-induced asthma. Eur Respir J 2002;20:Suppl. 38, 290s.
8. Vass G, Huszár É, Barát E, et al. Comparison of nasal and oral inhalation during exhaled breath condensate collection. Am J Respir Crit Care Med 2002;167:850–855.

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