Background. Obese adolescents with Obstructive Sleep Apnea (OSA) have a unique pathophysiology that combines adenotonsillar hypertrophy and increased visceral fat distribution. We hypothesized that in this population waist circumference (WC), as a clinical marker of abdominal fat distribution, correlates with the likelihood of response to AT. Methods. We conducted a retrospective cohort study of obese adolescents ( percentile) that underwent AT for therapy of severe OSA ( ). We contrasted WC and covariates in a group of subjects that had complete resolution of severe OSA after AT ( ) with those obtained in subjects with residual OSA after AT ( ). Multivariate linear and logistic models were built to control possible confounders. Results. WC correlated negatively with a positive AT response in young adolescents and the percentage of improvement in obstructive apnea-hypopnea index (OAHI) after AT ( ). Extended multivariate analysis demonstrated that the link between WC and AT response was independent of demographic variables, OSA severity, clinical upper airway assessment, obesity severity (BMI), and neck circumference (NC). Conclusion. The results suggest that in obese adolescents, abdominal fat distribution determined by WC may be a useful clinical predictor for residual OSA after AT. 1. Introduction Obstructive Sleep Apnea (OSA) is characterized by recurrent episodes of partial or complete upper airway obstruction, resulting in oxygen desaturation and sleep disruption [1]. A number of risk factors likely influence airway patency during sleep, and thus the susceptibility for OSA. Adenotonsillar enlargement is the most commonly recognized anatomic cause for pediatric OSA [1], and obesity is the major risk factor during adulthood [2, 3]. As a result, adenotonsillectomy (AT) is considered the first line of therapy in most cases of pediatric OSA [4] but it is seldom effective in the adult population [5, 6], particularly in those who are obese [6, 7]. Obesity also increases the risk of residual OSA after AT in the pediatric population [8], however, the obesity features associated with decreased response to AT in children and adolescents are largely unknown. The anatomic and functional risk factors relating obesity to OSA are complex. Obesity leads to upper airway narrowing due to enlargement of soft palate, lateral pharyngeal walls, tongue, and parapharyngeal fat pads [9–13]. Along with these upper airway changes, obesity causes restrictive respiratory physiology primarily attributed to abdominal visceral fat accumulation [14]. The combination of narrow
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