RATIONALE: In adults, obstructive sleep apnea (OSA) is associated with metabolic dysfunction that improves with treatment of OSA. No equivalent studies exist in children. OBJECTIVE: To examine the relationship between metabolic markers and OSA with time and treatment in children. METHODS: Metabolic markers measured on a fasting morning blood sample at diagnostic polysomnography and follow-up 1.3 +/- 0.6 yr later. MEASUREMENTS AND MAIN RESULTS: Forty-five children (34 males), aged 6.9 +/- 3.5 yr, and including 12 obese subjects, were in the final analysis. There were no differences in metabolic markers between children with and without OSA at initial study; however, obese children had significantly higher insulin (106.1 +/- 72.1 vs. 66.7 +/- 37.6 pmol/L; p = 0.028), insulin/glucose ratio (23.7 +/- 14.3 vs. 14.7 +/- 8.0; p = 0.02), and significantly lower high-density lipoprotein cholesterol (1.3 +/- 0.2 vs. 1.6 +/- 0.4 nmol/L; p = 0.005) than nonobese children. Twenty children underwent surgical removal of adenotonsillar tissue, whereas 12 children with OSA elected not to have treatment. OSA persisted after treatment in five children, and resolved in 27. Thirteen children did not have OSA on initial or follow-up studies. At follow-up, there was a small but significant improvement in total cholesterol in those children whose OSA was resolved (4.8 +/- 0.8 to 4.7 +/- 0.6 nmol/L; p = 0.005) and a trend for obese children with persisting OSA to have elevated insulin levels compared with obese children without OSA (p = 0.07). CONCLUSION: Obesity appears to be the major influence on metabolic dysfunction in children with OSA, but these preliminary data also suggest that resolution or persistence of OSA may affect changes in metabolic function over time.
RATIONALE: In adults, obstructive sleep apnea (OSA) is associated with metabolic dysfunction that improves with treatment of OSA. No equivalent studies exist in children. OBJECTIVE: To examine the relationship between metabolic markers and OSA with time and treatment in children. METHODS: Metabolic markers measured on a fasting morning blood sample at diagnostic polysomnography and follow-up 1.3 +/- 0.6 yr later. MEASUREMENTS AND MAIN RESULTS: Forty-five children (34 males), aged 6.9 +/- 3.5 yr, and including 12 obese subjects, were in the final analysis. There were no differences in metabolic markers between children with and without OSA at initial study; however, obesechildren had significantly higher insulin (106.1 +/- 72.1 vs. 66.7 +/- 37.6 pmol/L; p = 0.028), insulin/glucose ratio (23.7 +/- 14.3 vs. 14.7 +/- 8.0; p = 0.02), and significantly lower high-density lipoprotein cholesterol (1.3 +/- 0.2 vs. 1.6 +/- 0.4 nmol/L; p = 0.005) than nonobese children. Twenty children underwent surgical removal of adenotonsillar tissue, whereas 12 children with OSA elected not to have treatment. OSA persisted after treatment in five children, and resolved in 27. Thirteen children did not have OSA on initial or follow-up studies. At follow-up, there was a small but significant improvement in total cholesterol in those children whose OSA was resolved (4.8 +/- 0.8 to 4.7 +/- 0.6 nmol/L; p = 0.005) and a trend for obesechildren with persisting OSA to have elevated insulin levels compared with obesechildren without OSA (p = 0.07). CONCLUSION: Obesity appears to be the major influence on metabolic dysfunction in children with OSA, but these preliminary data also suggest that resolution or persistence of OSA may affect changes in metabolic function over time.
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