Published ahead of print on March 30, 2007, doi:10.1164/rccm.200610-1519OC
© 2007 American Thoracic Society doi: 10.1164/rccm.200610-1519OC
C-reactive Protein, Obstructive Sleep Apnea, and Cognitive Dysfunction in School-aged Children1 Kosair Children's Hospital Research Institute, and 2 Division of Pediatric Sleep Medicine, Department of Pediatrics, University of Louisville, Louisville, Kentucky Correspondence and requests for reprints should be addressed to David Gozal, M.D., Kosair Children's Hospital Research Institute, University of Louisville School of Medicine, 570 South Preston Street, Suite 204, Louisville, KY 40202. E-mail: david.gozal{at}louisville.edu Rationale: Obstructive sleep apnea (OSA) in children is associated with substantial neurobehavioral and cognitive dysfunction. However, not all children with OSA exhibit altered cognitive performance. Objectives: To assess the magnitude of the systemic inflammatory response, as measured by high-sensitivity C-reactive protein (hsCRP) serum levels which may identify children with OSA at higher susceptibility for cognitive morbidity. Methods: Habitually snoring children and nonsnoring children (total, 278; age range, 5–7 yr) were recruited from the community, and underwent overnight polysomnography and neurocognitive testing and a blood draw the next morning. Snoring children were divided into OSA and no-OSA groups, and children with OSA were further subdivided into those with two or more abnormal cognitive subtests and into those with normal cognitive scores. Serum levels of hsCRP were also measured. Measurements and Main Results: Among snoring children without OSA, mean hsCRP was 0.19 ± 0.07 mg/dl compared with 0.36 ± 0.11 mg/dl in those with OSA (p < 0.01). Furthermore, hsCRP was 0.48 ± 0.12 mg/dl in children with OSA and cognitive deficits, compared with 0.21 ± 0.08 mg/dl in children with OSA and normal cognitive scores (p < 0.002). Conclusions: hsCRP levels are higher in children with OSA, and particularly in those who develop neurocognitive deficits, suggesting that the magnitude of the inflammatory responses elicited by OSA is a major determinant of increased risk for neurocognitive dysfunction.
Key Words: sleep-disordered breathing • systemic inflammation • hypoxia • sleep fragmentation
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