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Updated: Jun 8, 2026

Drug-Induced Sleep Endoscopy (DISE) with Target Controlled Infusion (TCI) and Bispectral Analysis in Obstructive Sleep Apnea
Published on: December 6, 2016
Upper airway structure and body fat composition in obese children with obstructive sleep apnea syndrome
Raanan Arens1, Sanghun Sin, Kiran Nandalike
1Division of Respiratory and Sleep Medicine, Children's Hospital at Montefiore, 3415 Bainbridge Avenue, Bronx, NY 10467, USA. rarens@montefiore.org.
Insights
Obese children with obstructive sleep apnea syndrome (OSAS) show enlarged upper airway lymphoid tissues, independent of obesity. Increased fat deposits were also noted but not directly linked to OSAS severity.
Area of Science:
- Pediatric Endocrinology
- Sleep Medicine
- Otolaryngology
Background:
- Obstructive sleep apnea syndrome (OSAS) in obese children lacks well-defined etiological mechanisms.
- Understanding anatomical risk factors is crucial for managing pediatric OSAS.
Purpose of the Study:
- To identify anatomical risk factors for OSAS in obese children.
- To compare these factors with obese children without OSAS.
Main Methods:
- Magnetic resonance imaging (MRI) assessed upper airway structures and body fat composition.
- Paired analysis compared subjects with and without OSAS.
- Regression models evaluated the effect of BMI Z-score as a modifier.
Main Results:
- Subjects with OSAS had smaller oropharynx and larger adenoids, tonsils, and retropharyngeal nodes compared to controls.
- Lymphoid tissue size correlated with OSAS severity; BMI Z-score did not modify this relationship.
- Parapharyngeal and abdominal visceral fat pads were larger in OSAS subjects, but not associated with OSAS severity or BMI Z-score.
Conclusions:
- Upper airway lymphoid hypertrophy is a significant factor in obese children with OSAS.
- The hypertrophy's independence from obesity suggests alternative causative mechanisms.
- While increased fat deposits were observed, their direct association with OSAS severity or obesity remains unclear.
Rationale:
Mechanisms leading to obstructive sleep apnea syndrome (OSAS) in obese children are not well understood.
Objectives:
The aim of the study was to determine anatomical risk factors associated with OSAS in obese children as compared with obese control subjects without OSAS.
Methods:
Magnetic resonance imaging was used to determine the size of upper airway structure, and body fat composition. Paired analysis was used to compare between groups. Mixed effects regression models and conditional multiple logistic regression models were used to determine whether body mass index (BMI) Z-score was an effect modifier of each anatomic characteristic as it relates to OSAS.
Measurements And Main Results:
We studied 22 obese subjects with OSAS (12.5 ± 2.8 yr; BMI Z-score, 2.4 ± 0.4) and 22 obese control subjects (12.3 ± 2.9 yr; BMI Z-score, 2.3 ± 0.3). As compared with control subjects, subjects with OSAS had a smaller oropharynx (P < 0.05) and larger adenoid (P < 0.01), tonsils (P < 0.05), and retropharyngeal nodes (P < 0.05). The size of lymphoid tissues correlated with severity of OSAS whereas BMI Z-score did not have a modifier effect on these tissues. Subjects with OSAS demonstrated increased size of parapharyngeal fat pads (P < 0.05) and abdominal visceral fat (P < 0.05). The size of these tissues did not correlate with severity of OSAS and BMI Z-score did not have a modifier effect on these tissues.
Conclusions:
Upper airway lymphoid hypertrophy is significant in obese children with OSAS. The lack of correlation of lymphoid tissue size with obesity suggests that this hypertrophy is caused by other mechanisms. Although the parapharyngeal fat pads and abdominal visceral fat are larger in obese children with OSAS we could not find a direct association with severity of OSAS or with obesity.
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