Published ahead of print on May 18, 2006, doi:10.1164/rccm.200401-110OC Am. J. Respir. Crit. Care Med., Volume 174, Number 4, August 2006, 455-460 A more recent version of this article appeared on August 15, 2006
Submitted on January 25, 2004 Follow-up on Metabolic Markers in Children Treated for Obstructive Sleep ApneaKaren A Waters1*,1 Division of Pediatric Sleep Medicine, Department of Pediatrics, University of Louisville, Kosair Children's Hospital Research Institute, Louisville, KY, USA; Department of Respiratory Medicine, The Children's Hospital at Westmead, Westmead, Sydney NSW, Australia, 2 Department of Respiratory Medicine, The Children's Hospital at Westmead, Westmead, Sydney NSW, Australia, 3 Division of Pediatric Sleep Medicine, Department of Pediatrics, University of Louisville, Kosair Children's Hospital Research Institute, Louisville, KY, USA, 4 Department of Respiratory Medicine, The Children's Hospital at Westmead, Westmead, Sydney NSW, Australia; Sleep Laboratory, Lindenhof Hospital, Bern, Switzerland * To whom correspondence should be addressed. 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 years later. Measurements and main results: Forty-five children (34 males), aged 6.9±3.5 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; p=0.028), insulin/glucose ratio (23.7±14.3 vs 14.7±8.0; p=0.02) and significantly lower HDL cholesterol (1.3±0.2 vs 1.6±0.4; p=0.005) than non-obese children. Twenty children underwent surgical removal of adenotonsillar tissue while 12 children with OSA elected not to have treatment. OSA persisted after treatment in 5 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; p=0.005) and a trend for obese children with persisting OSA tended to have elevated insulin levels compared to obese children without OSA (p=0.07). Conclusion: Obesity appears to be the major influence on metabolic dysfunction in children with OSA, but this preliminary data also suggests that resolution or persistence of OSA may affect changes in metabolic function over time. Key words: respiratory, OSA, metabolic syndrome, longitudinal
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