Persistent sleep‐disordered breathing independently contributes to metabolic syndrome in prepubertal children

• Published in: Pediatric pulmonology 2024-01, Vol.59 (1), p.111-120
• Main Authors: Armañac‐Julián, Pablo, Martín‐Montero, Adrián, Lázaro, Jesús, Hornero, Roberto, Laguna, Pablo, Kheirandish‐Gozal, Leila, Gozal, David, Gil, Eduardo, Bailón, Raquel, Gutiérrez‐Tobal, Gonzalo
• Format: Article
• Language: English
• Subjects: cardiovascular risk and obesity; Metabolic syndrome; obstructive sleep apnea; Sleep apnea; sleep‐disordered breathing
• ISSN: 8755-6863; 1099-0496
• DOI: 10.1002/ppul.26720

Background Obstructive sleep apnea (OSA) is a risk factor for metabolic syndrome (MetS) in adults, but its association in prepubertal children is still questionable due to the relatively limited cardiometabolic data available and the phenotypic heterogeneity. Objective To identify the role of OSA as a potential mediator of MetS in prepubertal children. Methods A total of 255 prepubertal children from the Childhood Adenotonsillectomy Trial were included, with standardized measurements taken before OSA treatment and 7 months later. MetS was defined if three or more of the following criteria were present: adiposity, high blood pressure, elevated glycemia, and dyslipidemia. A causal mediation analysis was conducted to assess the effect of OSA treatment on MetS. Results OSA treatment significantly impacted MetS, with the apnea–hypopnea index emerging as mediator (p = .02). This mediation role was not detected for any of the individual risk factors that define MetS. We further found that the relationship between MetS and OSA is ascribable to respiratory disturbance caused by the apnea episodes, while systemic inflammation as measured by C‐reactive protein, is mediated by desaturation events and fragmented sleep. In terms of evolution, patients with MetS were significantly more likely to recover after OSA treatment (odds ratio = 2.56, 95% confidence interval [CI] 1.20–5.46; risk ratio = 2.06, 95% CI 1.19–3.54) than the opposite, patients without MetS to develop it. Conclusion The findings point to a causal role of OSA in the development of metabolic dysfunction, suggesting that persistent OSA may increase the risk of MetS in prepubertal children. This mediation role implies a need for developing screening for MetS in children presenting OSA symptoms.