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1 Dept of Pathophysiology and 2 Clinical Chemistry, National Korányi Institute for Tuberculosis and Pulmonology, Budapest, Hungary
CORRESPONDENCE: É. Huszár, National Korányi Institute for Tuberculosis and Pulmonology, Department of Pathophysiology, Budapest Pihenö u1, PO Box 1, H-1529, Hungary. Fax: 36 12007060. E-mail: huszar@koranyi.hu
Keywords: adenosine, airway inflammation, bronchial asthma, exhaled breath condensate, exhaled nitric oxide
Received: January 23, 2002
Accepted July 30, 2002
This study was supported by the Hungarian National Scientific Research Fund (OTKA T-030340) and the Hungarian Ministry of Health Care (ETT T06-160).
Persistent airway inflammation may require the use of different markers for monitoring airway inflammation. In this study, the authors investigated whether adenosine, which may be produced in allergic inflammatory conditions, could be measured with good reproducibility in exhaled breath condensate (EBC), and whether its concentration was elevated in patients with asthma.
EBC adenosine and exhaled nitric oxide (eNO), a noninvasive marker of asthmatic airway inflammation, were measured in 40 healthy volunteers and 43 patients with allergic bronchial asthma. Repeatability of adenosine measurement was checked in 20 pairs of samples collected from healthy control subjects.
Adenosine was detectable in all EBC samples by the applied high-performance liquid chromatographic method. The mean difference between repeated measurements of adenosine was –0.1 nM and all differences were within the coefficient of repeatability. Adenosine concentration was higher in steroid-naive patients (n=23) compared with healthy control subjects and steroid-treated patients (n=20). In patients with worsening symptoms of asthma (n=23), adenosine concentration was elevated compared with those in a stable condition (n=20). Furthermore, adenosine concentrations were related to eNO levels in asthmatic patients.
These results, showing good reproducibility of adenosine measurements and increased adenosine concentrations in steroid-naive patients and in patients with worsening of asthmatic symptoms, indicate that adenosine measurement in exhaled breath condensate might be an acceptable novel method to investigate the role of local production of adenosine in the airways.
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