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Increased Exhaled 8-Isoprostane in Childhood Asthma^*

^* From the Department of Pediatrics (Drs. Baraldi, Ghiro, Piovan, and Carraro), School of Medicine, University of Padova, Padova, Italy; Department of Drug Sciences (Dr. Ciabattoni), School of Pharmacy, University "G. d’Annunzio", Chieta, Italy; Department of Thoracic Medicine (Dr. Barnes), Imperial College, School of Medicine, National Heart and Lung Institute, London, UK; and Department of Pharmacology (Dr. Montuschi), School of Medicine, Catholic University of the Sacred Heart, Rome, Italy.

Correspondence to: Paolo Montuschi, MD, Department of Pharmacology, School of Medicine, Catholic University of the Sacred Heart, Largo F. Vito, 1, 00168 Rome, Italy;

Study objectives: To quantify lung oxidative stress in asthmatic children by measuring concentrations of 8-isoprostane, a marker of oxidative stress, in exhaled breath condensate (EBC), which is a noninvasive method of sampling airway secretions. Secondary objectives were as follows: (1) to measure levels of exhaled prostaglandin (PG) E₂, since impaired PGE₂ production has been implicated in the pathogenesis of asthma in adults; and (2) to measure levels of fractional exhaled nitric oxide (FeNO), which is a marker of airway inflammation.

Design: Single-center, cross-sectional study.

Patients: Twelve healthy children, 12 steroid-naïve asthmatic children, and 30 children in stable condition with mild-to-moderate persistent asthma who were being treated with inhaled corticosteroids (ICSs) [average dose, 300 µg per day] were studied.

Interventions: Subjects attended the outpatient clinic on one occasion for the collection of EBC and FeNO measurements.

Measurements and results: 8-Isoprostane and PGE₂ concentrations in EBC were measured with specific radioimmunoassays. FeNO was measured online by a chemiluminescence analyzer. 8-Isoprostane was detectable in the EBC of healthy children (mean [± SEM], 34.2 ± 4.5 pg/mL), and its concentrations were increased in both steroid-naïve asthmatic children (mean, 56.4 ± 7.7 pg/mL; p < 0.01) and steroid-treated asthmatic children (mean, 47.2 ± 2.3 pg/mL; p < 0.05). There was no difference in exhaled 8-isoprostane concentrations between the two groups of asthmatic children (p = 0.14). By contrast, exhaled PGE₂ concentrations were similar among the three study groups (p = 0.56). FeNO levels were higher in steroid-naïve children with asthma (49.2 ± 9.6 parts per billion [ppb]; p < 0.05) and, to a lesser extent, in steroid-treated asthmatic children (37.8 ± 6.6 ppb; p < 0.05) compared with healthy children (15.2 ± 1.7 ppb).

Conclusions: Lung oxidative stress is increased in children who are in stable condition with asthma, as reflected by increased exhaled 8-isoprostane concentrations. This increase seems to be relatively resistant to treatment with ICSs. Decreased PGE₂ lung production is unlikely to play a pathophysiologic role in childhood asthma.

Key Words: airway inflammation • asthma • 8-isoprostane • exhaled breath condensate • nitric oxide • noninvasive markers • oxidative stress • prostaglandin E₂

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