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Airways inflammation has been associated with increased NO in the exhaled breath (Barnes, ERJ (6), 1993). We therefore questioned whether exhaled NO could act as an indicator of the severity of airways inflammation in the suppurative lung diseases, cystic fibrosis (CF) and bronchiectasis (Br). Methods: Single exhalation NO levels were measured using the chemiluminescence NO analyser (Logan Research, Kent); detection limit 0.3ppb. Upper airway NO production was excluded by maintaining a constant mouth pressure (4-5 cm H2O) during exhalation. This pushes back the soft palate and excludes air originating from the nose during exhalation. Values quoted are plateau levels at the end of exhalation, against a flow restrictor. Patients. All patients were recruited from our outpatient clinics. All except 3 CF patients have fully defined genotypes. Br was diagnosed by CT or classical CXR changes. All subjects were non smokers. 6 asthmatics were on inhaled steroids. All levels were taken when patients were stable. Results: normal CF Br Br+ster Asthma n=17 n=31 n=6 n=5 n=7 NO 5.5 (3.6) 4.5(2.6) 6.6(3.4) 5.9(1.4) 15.0(6.1) Age 32.8(16.1) 27.2(8.7) 49.3(8.4) 57.8(13.3) 39.6(16.3) FEV1 - 54.4(24.1) 61.0(22.8) 57.8(13.3) (All values are mean (SD), NO in ppb. Br= Bronchiectasis, Ster= inhaled fluticasone, budesonide or beclomethasone, FEV1 = % predicted.) These data suggest that NO in the exhaled breath of patients with CF and Br, in contrast to asthma, are not elevated. Explanations include a) poor diffusion of NO across increased and viscous airway secretion b) down regulation of iNOS in chronic suppurative conditions. Our findings in bronchiectasis contrast with those of Kharitonov et al (AJRCCM (151) 1995). This may be due to different methodologies.


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