Published ahead of print on February 14, 2008, doi:10.1164/rccm.200711-1670OC
Am. J. Respir. Crit. Care Med., Volume 177, Number 10, May 2008, 1142-1149
A more recent version of this article appeared on May 15, 2008
Submitted on November 12, 2007
Accepted on February 14, 2008
Metabolic Alterations in Obstructive Sleep Apnea among Non-Obese and Obese Prepubertal Children
David Gozal1*, Oscar Sans Capdevila1, and Leila Kheirandish-Gozal1
1 Division of Pediatric Sleep Medicine and Kosair Children's Hospital Research Institute, Department of Pediatrics, University of Louisville, Louisville, KY, USA
* To whom correspondence should be addressed. E-mail: david.gozal{at}louisville.edu.
Introduction: OSA has been associated with a higher prevalence and severity of the metabolic syndrome in adult patients, even after controlling for obesity. In contrast, OSA in pre-pubertal children does not appear to correlate with the magnitude of such metabolic derangements.
Methods: To further establish the potential mechanistic role of OSA in metabolic regulation in pre-pubertal children, fasting glucose, insulin, C-reactive protein , apolipoprotein B, and serum lipid concentrations were determined during the initial polysomnographic diagnosis of OSA and 6-12 months after adenotonsillectomy in both obese and non-obese children.
Results: Sixty-two children with OSA (37 obese and 25 non-obese) with a mean age 7.40±2.6 years [SD] completed the study. After adenotonsillectomy, significant improvements in apnea-hypopnea index and sleep fragmentation occurred, particularly among non-obese children. In non-obese children, adenotonsillectomy was associated with mild increases in body-mass-index z scores, no changes in either fasting glucose or insulin, significant increases in high density lipoprotein and reciprocal decreases in low density lipoprotein, and reductions in plasma C-reactive protein and apolipoprotein B levels. In obese children, adenotonsillectomy did not result in body-mass-index or glucose changes, but was associated with marked improvements in all other measures.
Conclusions: OSA does not appear to induce insulin resistance in non-obese pediatric patients but seems to play a significant role in obese patients. The significant improvements in lipid profiles, C-reactive protein, and apolipoprotein B followingadenotonsillecotmy in the 2 groups suggest a pathogenetic role for OSA in lipid homeostasis and systemic inflammation independently from the degree of adiposity.
Key words: obstructive sleep apnea, adenotonsillar hypertrophy; treatment; inflammation; atherosclerosis; snoring
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