Increased exhaled 8-isoprostane in childhood asthma.
OBJECTIVE
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) E(2), since impaired PGE(2) 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.


METHODS
Single-center, cross-sectional study.


METHODS
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 micro g per day] were studied.


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


RESULTS
8-Isoprostane and PGE(2) 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 PGE(2) 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 PGE(2) lung production is unlikely to play a pathophysiologic role in childhood asthma.
Baraldi
Eugenio
E
Department of Pediatrics (Drs. Baraldi, Ghiro, Piovan, and Carraro), School of Medicine, University of Padova, Padova, Italy.
Ghiro
Laura
L
Piovan
Vania
V
Carraro
Silvia
S
Ciabattoni
Giovanni
G
Barnes
Peter J
PJ
Montuschi
Paolo
P
D000293:Adolescent; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D001249:Asthma / Q000175:diagnosis / Q000188:drug therapy / Q000378:metabolism*; D001944:Breath Tests; D002648:Child; D002675:Child, Preschool; D003430:Cross-Sectional Studies; D015237:Dinoprost / Q000031:analogs & derivatives*; D015232:Dinoprostone / Q000378:metabolism; D028441:F2-Isoprostanes / Q000378:metabolism*; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D008163:Luminescent Measurements; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress; D011863:Radioimmunoassay; D012129:Respiratory Function Tests; D013256:Steroids
D000893:Anti-Inflammatory Agents; D028441:F2-Isoprostanes; D013256:Steroids; C075750:8-epi-prostaglandin F2alpha; D009569:Nitric Oxide; D015237:Dinoprost; D015232:Dinoprostone