2006
DOI: 10.1378/chest.130.1.143
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Inflammatory Mediators in Exhaled Breath Condensate of Children With Obstructive Sleep Apnea Syndrome

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Cited by 160 publications
(103 citation statements)
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“…4,[23][24] The results we observed in our study are consistent with the current evidence showing elevated cytokines and inflammatory markers in exhaled breath as well as upper airway tissues of OSA patients. 4,[9][10][11][12][13][14][15][16][17]23,[25][26][27][28] Salerno et al and Devouassoux et al detected increased neutrophils and reduced macrophages in the induced sputum of OSA patients. 27,28 The latter study also observed a concurrent higher interleukin-8 concentration in the induced sputum specimen of these patients.…”
Section: Discussionmentioning
confidence: 99%
“…4,[23][24] The results we observed in our study are consistent with the current evidence showing elevated cytokines and inflammatory markers in exhaled breath as well as upper airway tissues of OSA patients. 4,[9][10][11][12][13][14][15][16][17]23,[25][26][27][28] Salerno et al and Devouassoux et al detected increased neutrophils and reduced macrophages in the induced sputum of OSA patients. 27,28 The latter study also observed a concurrent higher interleukin-8 concentration in the induced sputum specimen of these patients.…”
Section: Discussionmentioning
confidence: 99%
“…It has now become apparent that both nasal and oropharyngeal mucosal inflammation are present in children with OSA, and may contribute to increased adenotonsillar proliferation in children with OSA [8]. The recently reported increase in the expression of glucocorticoid receptors in upper airway lymphoid tissues would globally predict favourable outcomes when using intranasal corticosteroids (CS) in paediatric OSA [9], and indeed intranasal CS have shown promising efficacy in reducing the size of the upper airway lymphoid tissues [10][11][12][13][14].…”
mentioning
confidence: 99%
“…Upper airway inflammation is consistently present among children with either habitual snoring or OSA [34,35], and inflammatory processes within the upper airway are likely to exacerbate upper airway collapsibility, as well as promote the proliferation of adenotonsillar tissues. In this context, it has become apparent that short-term exposures to traffic-related air pollutants may increase airway inflammation and/or oxidative stress in urban children [36][37][38] and, therefore, such processes would be unlikely to be restricted to the lower airways and could, in fact, be even more prominent in the upper airways considering the relative concentrations of particles more likely to deposit in the upper segments of the airways [39,40].…”
Section: Discussionmentioning
confidence: 99%