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Published ahead of print on May 18, 2006, doi:10.1164/rccm.200401-110OC
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American Journal of Respiratory and Critical Care Medicine Vol 174. pp. 455-460, (2006)
© 2006 American Thoracic Society
doi: 10.1164/rccm.200401-110OC


Original Article

Follow-up on Metabolic Markers in Children Treated for Obstructive Sleep Apnea

Karen A. Waters, Sinthu Sitha, Louise M. O'Brien, Sherryn Bibby, Carina de Torres, Silvano Vella and Roland de la Eva

Kosair Children's Hospital Research Institute, and Division of Pediatric Sleep Medicine, Department of Pediatrics, University of Louisville, Louisville, Kentucky; Department of Respiratory Medicine, The Children's Hospital at Westmead, Sydney, Australia; and Sleep Laboratory, Lindenhof Hospital, Bern, Switzerland

Correspondence and requests for reprints should be addressed to A/Prof. Karen A. Waters, M.B.B.S., F.R.A.C.P., Ph.D., Head, Respiratory Support Service, The Children's Hospital at Westmead, Locked Bag 4001, Westmead, Sydney, NSW 2145, Australia E-mail: kaw{at}med.usyd.edu.au

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.

Key Words: longitudinal • metabolic syndrome • obstructive sleep apnea • respiratory




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