4.7 Article

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

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CHEST
卷 141, 期 3, 页码 682-691

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ELSEVIER SCIENCE BV
DOI: 10.1378/chest.11-1777

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  1. Jazz Pharmaceuticals
  2. National Institutes of Health [HL65270]

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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. CHEST 2012; 141(3):682-691

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