Rakesh Bhattacharjee1, Jinkwan Kim2, Wadha H Alotaibi3, Leila Kheirandish-Gozal4, Oscar Sans Capdevila3, David Gozal5. 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.
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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