Metabolic alterations and systemic inflammation in obstructive sleep apnea among nonobese and obese prepubertal children

David Gozal, Oscar Sans Capdevila, Leila Kheirandish-Gozal
American Journal of Respiratory and Critical Care Medicine 2008 May 15, 177 (10): 1142-9

RATIONALE: Obstructive sleep apnea (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 prepubertal children does not appear to correlate with the magnitude of such metabolic derangements.

OBJECTIVES: To further establish the potential mechanistic role of OSA in metabolic regulation in prepubertal children.

METHODS: 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 nonobese children.

MEASUREMENTS AND MAIN RESULTS: Sixty-two children with OSA (37 obese and 25 nonobese), age 7.40 +/- 2.6 years (mean +/- SD) completed the study. After adenotonsillectomy, significant improvements in apnea-hypopnea index and sleep fragmentation occurred, particularly among nonobese children. In nonobese 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 nonobese pediatric patients but seems to play a significant role in obese patients. The significant improvements in lipid profiles, C-reactive protein, and apolipoprotein B after adenotonsillectomy in the two groups suggest a pathogenic role for OSA in lipid homeostasis and systemic inflammation independent of the degree of adiposity.

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