Obstructive Sleep Apnea in Children

Dayyat, Ehab; Kheirandish‐Gozal, Leila; Capdevila, Óscar Sans; Maarafeya, Muna; Gozal, David

doi:10.1378/chest.08-2568

Cited by 202 publications

(58 citation statements)

References 47 publications

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“…Furthermore, the apnea–hypopnea index (AHI) has not been shown to directly correlate with airway volume,7 and the coefficients of correlation between AHI and adenotonsillar size have been found to be usually relatively weak, albeit statistically significant,9,18 suggesting that other factors feature in the pathophysiology of pediatric OSA. The concept of airway collapsibility has thus been proposed to provide a more comprehensive and unified approach to this issue.…”

Section: Pathophysiology Of Osamentioning

confidence: 99%

Obstructive sleep apnea in children: a critical update

Tan¹,

Gozal²,

Kheirandish‐Gozal³

2013

NSS

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106

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Obstructive sleep apnea (OSA) in children is a highly prevalent disorder caused by a conglomeration of complex pathophysiological processes, leading to recurrent upper airway dysfunction during sleep. The clinical relevance of OSA resides in its association with significant morbidities that affect the cardiovascular, neurocognitive, and metabolic systems. The American Academy of Pediatrics recently reiterated its recommendations that children with symptoms and signs suggestive of OSA should be investigated with polysomnography (PSG), and treated accordingly. However, treatment decisions should not only be guided by PSG results, but should also integrate the magnitude of symptoms and the presence or absence of risk factors and signs of OSA morbidity. The first-line therapy in children with adenotonsillar hypertrophy is adenotonsillectomy, although there is increasing evidence that medical therapy, in the form of intranasal steroids or montelukast, may be considered in mild OSA. In this review, we delineate the major concepts regarding the pathophysiology of OSA, its morbidity, diagnosis, and treatment.

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Section: Pathophysiology Of Osamentioning

confidence: 99%

Obstructive sleep apnea in children: a critical update

Tan¹,

Gozal²,

Kheirandish‐Gozal³

2013

NSS

Self Cite

106

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“…Therefore, the magnitude of adenotonsillar effects on childhood OSA may be altered by age and obesity [14,15]. Tagaya et al [14] asserted that the correlation between adenoid size and OSA is more prominent in preschool children than in school-aged children.…”

Section: Introductionmentioning

confidence: 99%

“…Tagaya et al [14] asserted that the correlation between adenoid size and OSA is more prominent in preschool children than in school-aged children. Dayyat et al [15] reported a modest association between adenotonsillar sum scores and apnea index in non-obese children, but not in obese children. However, the relationships between adenotonsillar size and OSA in detailed age groups, and the respective effect of adenoid and tonsil size on OSA in obese and non-obese children, have not been well investigated.…”

Section: Introductionmentioning

confidence: 99%

Associations between Adenotonsillar Hypertrophy, Age, and Obesity in Children with Obstructive Sleep Apnea

et al. 2013

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ObjectiveTo investigate the contributions of adenoid and tonsil size to childhood obstructive sleep apnea (OSA) and the interactions between adenotonsillar hypertrophy, age, and obesity in children with OSA.MethodsIn total, 495 symptomatic patients were recruited. The patients were assigned to four groups according to age：toddler (age 1-3, n=42), preschool (age 3-6, n=164), school (age 6-12, n=200), and adolescence (age 12-18, n=89). All subjects had tonsil size graded by otolaryngologists, adenoid size determined on lateral radiographs (Fujioka method), and a full-night polysomnography. The apnea-hypopnea index (AHI), adenoid size, and tonsil size were compared in obese and non-obese children in the four age groups. Adjusted odds ratios (ORs) and 95% confidence interval (CI) of adenotonsillar hypertrophy and OSA risk were estimated by multi-logistic regression.ResultsThe AHI was positively related to tonsil grade (r=0.33, p <0.001) and adenoid size (r=0.24, p <0.01) in all patients. Tonsil grade was positively related to AHI in all four age groups. Adenoid size was positively related to AHI in the toddler, preschool, school groups, but not in the adolescent group (r=0.11, p=0.37). Tonsil grade and adenoid size were both positively related to AHI in obese and non-obese children. In the regression model, obesity (OR=2.89; 95% CI 1.47-5.68), tonsillar hypertrophy (OR=3.15; 95% CI 2.04-4.88), and adenoidal hypertrophy (OR=1.89; 95% CI 1.19-3.00) significantly increased OSA risk.ConclusionsAdenotonsillar hypertrophy and obesity are the major determinants of OSA in children. However, the influence of adenoid size decreases in adolescence.

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“…The basic pathological changes of obesity and OSAHS are closely related to insulin resistance and the metabolic syndrome of dyslipidemia [24,25]. OSAHS could be induced by the oxidative stress caused by repeatedly hypoxia and re-oxygenation during sleep.…”

Section: Discussionmentioning

confidence: 99%

Liver X Receptor Gene Expression is Enhanced in Children with Obstructive Sleep Apnea-Hyperpnoea Syndrome and Cyclooxygenase-2 (COX-2) is Correlated with Severity of Obstructive Sleep Apnea-Hypopnea Syndrome (OSAHS)

Chen

et al. 2017

Med Sci Monit

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BackgroundLiver X receptor (LXR) is a nuclear receptor presenting in macrophages; it works indispensably in lipid metabolism control and also negatively regulates the expression of inflammatory genes in macrophages. There are many LXR-related studies in adults with metabolic syndrome but rare reports in obese children with obstructive sleep apnea-hypopnea syndrome (OSAHS). The aim of this study was to investigate the expression of LXR, cholesterol ester transfer protein (CETP), and cyclooxygenase-2 (COX-2) genes in obese children with OSAHS compared with obese children without OSAHS and non-obese children.Material/MethodsSleep monitoring was conducted in 80 obese children with sleep disorders. Fasting morning blood samples from the 80 obese children and 51 normal children were collected and separated, so that macrophages were obtained after culture. Fluorescence quantitative real-time PCR (RT-PCR) was used to detect expression levels of the LXR, CETP, and COX-2 genes.ResultsLXR, COX-2, and CETP levels in the OSAHS group were higher than those in the other two groups (P<0.05), and the LXR levels in the group of obese children without OSAHS were higher than those in control group (P<0.05). COX-2 expression in the group with moderate to severe OSAHS was higher than that in the group with mild OSAHS (P<0.05). Meanwhile, there were no significant differences in the LXR and CETP levels between the moderate to severe OSAHS group and the mild OSAHS group (P>0.05).ConclusionsLXR gene expression was significantly increased in obese children with OSAHS. The severity of OSAHS was positively correlated with COX-2 levels.

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Obstructive Sleep Apnea in Children

Abstract: Background:The obesity epidemic has prompted remarkable changes in the proportion of obese children who are referred for habitual snoring. However, the contribution of obesity to adenotonsillar hypertrophy remains undefined.

Cited by 202 publications

References 47 publications

Obstructive sleep apnea in children: a critical update

Obstructive sleep apnea in children: a critical update

Associations between Adenotonsillar Hypertrophy, Age, and Obesity in Children with Obstructive Sleep Apnea

Liver X Receptor Gene Expression is Enhanced in Children with Obstructive Sleep Apnea-Hyperpnoea Syndrome and Cyclooxygenase-2 (COX-2) is Correlated with Severity of Obstructive Sleep Apnea-Hypopnea Syndrome (OSAHS)

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