BACKGROUND: In obese adults, sleep apnea is associated with excessive daytime sleepiness (EDS) and cardiometabolic risk factors. In children, on the other hand, sleep-disordered breathing (SDB) is primarily associated with anatomic abnormalities and neurocognitive impairment, whereas studies on potential concurrent metabolic aberrations and EDS have been limited and inconsistent. In this study, we examined the joint effect of SDB and obesity in EDS as well as proinflammatory and metabolic markers. METHODS: One hundred fifty children, aged 5-17 yr, were consecutively recruited from our sleep disorders clinic and a subset of the Penn State Children's Cohort. Every child had a thorough history and physical examination, 9-h polysomnographic study, and a single blood draw for the assessment of IL-6, TNFalpha, soluble IL-6 receptor, TNF receptor-1, hypersensitive C-reactive protein, leptin, and adiponectin. In addition, parents completed a subjective questionnaire to assess EDS. Analysis of covariance was performed on four groups that were separated by SDB severity and body mass index. RESULTS: EDS frequency increased progressively and significantly in the four groups. There was a significant linear trend in plasma IL-6, TNF receptor-1, hypersensitive C-reactive protein, and leptin concentrations, with lowest levels observed in lean controls and highest in overweight/obese with moderate SDB. Adiponectin followed the opposite pattern. CONCLUSIONS: This study suggests that in a clinical sample of obese children, SDB is associated with EDS, elevation of proinflammatory cytokines, increased leptin, and decreased adiponectin. All these changes point to an inflammatory/insulin resistance state, suggesting that SDB in obese children share many similarities with SDB in obese adults.
BACKGROUND: In obese adults, sleep apnea is associated with excessive daytime sleepiness (EDS) and cardiometabolic risk factors. In children, on the other hand, sleep-disordered breathing (SDB) is primarily associated with anatomic abnormalities and neurocognitive impairment, whereas studies on potential concurrent metabolic aberrations and EDS have been limited and inconsistent. In this study, we examined the joint effect of SDB and obesity in EDS as well as proinflammatory and metabolic markers. METHODS: One hundred fifty children, aged 5-17 yr, were consecutively recruited from our sleep disorders clinic and a subset of the Penn State Children's Cohort. Every child had a thorough history and physical examination, 9-h polysomnographic study, and a single blood draw for the assessment of IL-6, TNFalpha, soluble IL-6 receptor, TNF receptor-1, hypersensitiveC-reactive protein, leptin, and adiponectin. In addition, parents completed a subjective questionnaire to assess EDS. Analysis of covariance was performed on four groups that were separated by SDB severity and body mass index. RESULTS: EDS frequency increased progressively and significantly in the four groups. There was a significant linear trend in plasma IL-6, TNF receptor-1, hypersensitiveC-reactive protein, and leptin concentrations, with lowest levels observed in lean controls and highest in overweight/obese with moderate SDB. Adiponectin followed the opposite pattern. CONCLUSIONS: This study suggests that in a clinical sample of obesechildren, SDB is associated with EDS, elevation of proinflammatory cytokines, increased leptin, and decreased adiponectin. All these changes point to an inflammatory/insulin resistance state, suggesting that SDB in obesechildren share many similarities with SDB in obese adults.
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