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Chest. 2012 Mar;141(3):682-691. doi: 10.1378/chest.11-1777. Epub 2011 Oct 26.

Endothelial dysfunction in children without hypertension: potential contributions of obesity and obstructive sleep apnea.

Author information

1
Division of Pediatric Pulmonary Medicine, Department of Pediatrics, Pritzker School of Medicine, Comer Children's Hospital, The University of Chicago, Chicago, IL; Division of Pediatric Sleep Medicine, Department of Pediatrics, Pritzker School of Medicine, Comer Children's Hospital, The University of Chicago, Chicago, IL; Division of Pediatric Sleep Medicine, University of Louisville School of Medicine, Louisville, KY. Electronic address: rbhattac@bsd.uchicago.edu.
2
Division of Pediatric Sleep Medicine, Department of Pediatrics, Pritzker School of Medicine, Comer Children's Hospital, The University of Chicago, Chicago, IL.
3
Division of Pediatric Sleep Medicine, University of Louisville School of Medicine, Louisville, KY.
4
Division of Pediatric Sleep Medicine, Department of Pediatrics, Pritzker School of Medicine, Comer Children's Hospital, The University of Chicago, Chicago, IL; Division of Pediatric Sleep Medicine, University of Louisville School of Medicine, Louisville, KY.
5
Division of Pediatric Pulmonary Medicine, Department of Pediatrics, Pritzker School of Medicine, Comer Children's Hospital, The University of Chicago, Chicago, IL; Division of Pediatric Sleep Medicine, Department of Pediatrics, Pritzker School of Medicine, Comer Children's Hospital, The University of Chicago, Chicago, IL; Division of Pediatric Sleep Medicine, University of Louisville School of Medicine, Louisville, KY.

Abstract

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.

PMID:
22030801
PMCID:
PMC3296460
DOI:
10.1378/chest.11-1777
[Indexed for MEDLINE]
Free PMC Article
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