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Original Research: SLEEP DISORDERS |

Endothelial Dysfunction in Children Without HypertensionEndothelial Dysfunction in Children: Potential Contributions of Obesity and Obstructive Sleep Apnea

Rakesh Bhattacharjee, MD; Jinkwan Kim, PhD; Wadha H. Alotaibi, MD; Leila Kheirandish-Gozal, MD; Oscar Sans Capdevila, MD; David Gozal, MD, FCCP
Author and Funding Information

From the Division of Pediatric Pulmonary Medicine (Drs Bhattacharjee and Gozal) and the Division of Pediatric Sleep Medicine (Drs Bhattacharjee, Kim, Kheirandish-Gozal, and Gozal), Department of Pediatrics, Pritzker School of Medicine, Comer Children’s Hospital, The University of Chicago, Chicago, IL; and the Division of Pediatric Sleep Medicine (Drs Bhattacharjee, Alotaibi, Kheirandish-Gozal, Capdevila, and Gozal), University of Louisville School of Medicine, Louisville, KY.

Correspondence to: Rakesh Bhattacharjee, MD, Division of Pediatric Pulmonology Medicine and Division of Pediatric Sleep Medicine, Department of Pediatrics, Comer Children’s Hospital, The University of Chicago, 5841 S Maryland Ave, MC 4064, Chicago, IL 60637; e-mail: rbhattac@bsd.uchicago.edu


Funding/Support: Dr Bhattacharjee was supported by a Sleep Fellowship Grant from Jazz Pharmaceuticals. This study was supported by the National Institutes of Health [Grant HL65270].

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2012 American College of Chest Physicians


Chest. 2012;141(3):682-691. doi:10.1378/chest.11-1777
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Background:  Endothelial dysfunction can develop in the context of both obesity and obstructive sleep apnea (OSA) in children. However, the potential interactions between OSA and obesity have not been defined.

Methods:  Children who were prepubertal and nonhypertensive were recruited. Endothelial function was assessed in a morning fasted state, using a modified hyperemic test involving cuff-induced occlusion of the radial and ulnar arteries, and blood was drawn for assessment of myeloid-related protein 8/14 (MRP8/14) levels using a commercial enzyme-linked immunosorbent assay. Overnight polysomnography defined the presence of OSA or absence of OSA (NOSA) in subjects investigated for sleep-disordered breathing. Anthropometric measurements were performed to assign subjects to obese (OB) and nonobese (NOB) categories.

Results:  Fifty-four children with OSA who were obese and nonobese (mean age, 7.90 ± 0.26 years; mean BMI z-score, 1.70 ± 0.3; obstructive apnea-hypopnea index [OAHI], 7.36 ± 1.09) were compared with 54 children without OSA who were obese and nonobese (mean age, 8.26 ± 0.24 years; mean BMI z-score, 1.41 ± 0.18; OAHI, 0.86 ± 0.07). Of those subjects, 62.5% of the OB-OSA category, 38.7% of the OB-NOSA category, and 20.0% of the NOB-OSA category had evidence of endothelial dysfunction, compared with 0.0% of the NOB-NOSA category (P < .01). The degree of endothelial dysfunction in all groups was associated with circulating MRP8/14 levels (r = 0.343, P < .001).

Conclusions:  Both obesity and OSA can independently increase the risk for endothelial dysfunction, and the concurrent presence of both markedly increases such risk. Although the mechanisms underlying endothelial dysfunction remain unclear, a potential role for MRP8/14 as an inflammatory biomarker of endothelial dysfunction is suggested.

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