© 2006 American Thoracic Society
Assessing the Role of Antiinflammatory Medications in Children with Mild Sleep-disordered BreathingFrom the Authors:We read with interest the comments of Dr. Kaditis and colleagues regarding our recent publication in the Journal (1). We certainly concur that inflammatory/immunologic mechanisms contribute to the pathogenesis of obstructive sleep apnea (OSA) in children. We have previously published evidence on the increased transcriptional and translational regulation of corticosteroid and leukotriene receptors in the upper airway lymphadenoid tissue of children with OSA (2, 3). In the study under discussion, we further found that leukotriene concentrations are increased in the lymphadenoid tissue taken from children with OSA (1). Taken together, these findings would suggest a favorable response to treatment with antiinflammatory agents such as intranasal steroids or leukotriene modifiers. To substantiate this hypothesis, a group from Greece reported recently how nasal budesonide ameliorated the severity of OSA in children with mild to moderate sleep-disordered breathing (4), thereby reproducing previous findings by Brouillette and colleagues (5). Furthermore, our group has now conclusively demonstrated that combination therapy with intranasal budesonide and oral montelukast effectively normalized sleep breathing patterns and sleep architecture in children with residual mild OSA after adenotonsillectomy (6). However, in all our studies we restricted our recruitment to a symptomatic group whose severity of disease would not routinely justify other available interventions such as surgery. In other words, we applied antiinflammatory therapy to the low end of severity and yet found significant improvements in sleep fragmentation and respiratory disturbance, even if these were comparatively minor. There is clearly a need to better establish the polysomnographic cut-off values for which antiinflammatory therapy is best indicated, the duration of such therapy, and the risk of recurrence on discontinuation of therapy. We wholeheartedly concur with Kaditis and colleagues that improved phenotypic characterization of study patients with OSA participating in any form of double-blind randomized trials of antiinflammatory therapy, including quality of life, levels of circulating inflammatory markers, and end-organ morbidity (neurobehavioral and cardiovascular), will be critical to better delineate the value of such interventions.
Kosair Children's Hospital and Research Institute, Louisville, Kentucky FOOTNOTES Conflict of Interest Statement: A.D.G. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. D.G. is currently the recipient of an investigator-initiated grant from AstraZeneca Ltd. for an unrelated research project on the effect of intranasal budesonide in mild sleep-disordered breathing in children. He serves on the national speaker bureau of Merck REFERENCES
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