The Correlation Among Obesity, Apnea-Hypopnea Index, and Tonsil Size in Children

Lam, Y.Y.; Chan, Eric Yat-Tung; Ng, Daniel; Chan, Chung-hong; Cheung, Josephine M.; Leung, Suet Yi; Chow, Pok-yu; Kwok, Ka‐li

doi:10.1378/chest.130.6.1751

Cited by 93 publications

(63 citation statements)

References 26 publications

(18 reference statements)

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“…In a retrospective review of 482 Chinese children referred for PSG and evaluated by using BMI and a tonsillar grading scale, the group of 111 obese children had a significantly higher median AHI and percentage with AHI >1.5/hour than did the nonobese group (level III). 171 In a regression analysis of log AHI as dependent variable, BMI and tonsil grade were predictors, but age and gender were not. In a large study of schoolchildren in e740…”

Section: Predictors Of Obesity-related Sdbmentioning

confidence: 96%

Diagnosis and Management of Childhood Obstructive Sleep Apnea Syndrome

Marcus¹,

Brooks²,

Ward³

et al. 2012

Pediatrics

1,416

1,464

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OBJECTIVE: This technical report describes the procedures involved in developing recommendations on the management of childhood obstructive sleep apnea syndrome (OSAS). METHODS: The literature from 1999 through 2011 was evaluated. RESULTS AND CONCLUSIONS: A total of 3166 titles were reviewed, of which 350 provided relevant data. Most articles were level II through IV. The prevalence of OSAS ranged from 0% to 5.7%, with obesity being an independent risk factor. OSAS was associated with cardiovascular, growth, and neurobehavioral abnormalities and possibly inflammation. Most diagnostic screening tests had low sensitivity and specificity. Treatment of OSAS resulted in improvements in behavior and attention and likely improvement in cognitive abilities. Primary treatment is adenotonsillectomy (AT). Data were insufficient to recommend specific surgical techniques; however, children undergoing partial tonsillectomy should be monitored for possible recurrence of OSAS. Although OSAS improved postoperatively, the proportion of patients who had residual OSAS ranged from 13% to 29% in low-risk populations to 73% when obese children were included and stricter polysomnographic criteria were used. Nevertheless, OSAS may improve after AT even in obese children, thus supporting surgery as a reasonable initial treatment. A significant number of obese patients required intubation or continuous positive airway pressure (CPAP) postoperatively, which reinforces the need for inpatient observation. CPAP was effective in the treatment of OSAS, but adherence is a major barrier. For this reason, CPAP is not recommended as first-line therapy for OSAS when AT is an option. Intranasal steroids may ameliorate mild OSAS, but follow-up is needed. Data were insufficient to recommend rapid maxillary expansion.

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Section: Predictors Of Obesity-related Sdbmentioning

confidence: 96%

Diagnosis and Management of Childhood Obstructive Sleep Apnea Syndrome

Marcus¹,

Brooks²,

Ward³

et al. 2012

Pediatrics

1,416

1,464

View full text Add to dashboard Cite

show abstract

“…2,3 As such, the severity of OSA correlates with adenoid and tonsillar size, and surgical excision of these tissues are consequently accompanied by significant clinical improvements. [4][5][6][7] In the past few years, we and others have shown 8,9 evidence of inflammation in both nasal and oropharyngeal mucosa in children with OSA, and we surmised that inflammatory processes may underlie increased adenotonsillar proliferation. Indeed, intranasal corticosteroids have shown favorable outcomes in children with OSA, and their use for periods of 4 to 6 weeks has been associated with improvements in the respiratory disturbance during sleep and partial involution of adenoidal hypertrophy.…”

mentioning

confidence: 99%

Leukotriene Pathways and In Vitro Adenotonsillar Cell Proliferation in Children With Obstructive Sleep Apnea

Dayyat

Serpero

Kheirandish‐Gozal

et al. 2009

Chest

106

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Introduction:The abundant expression of leukotrienes (LTs) and their receptors in adenotonsillar tissues of children with obstructive sleep apnea (OSA) suggest that LT antagonists could be useful in treating OSA. Methods: The effects of LTD4 and of LT receptor antagonists zileuton, montelukast, and BAY u9773 were examined on mixed cell cultures prepared from dissociated tonsils or adenoids harvested intraoperatively from children with polysomnographically diagnosed OSA. Proliferation was assessed by 3 [H]-thymidine incorporation, and inflammatory cytokine production (tumor necrosis factor [TNF]-␣, interleukin [IL]-6, IL-8, IL-10, and IL-12) was assessed in supernatants using enzyme-linked immunosorbent assay.Results: LTD4 elicited dose-dependent increases in adenotonsillar cell proliferation (p < 0.001; n ‫؍‬ 12). All LT antagonists exhibited dose-dependent reductions in adenotonsillar cellular proliferation rates, with montelukast more than BAY u9773 more than zileuton (n ‫؍‬ 14/group; p < 0.001). However, BAY u9773 showed partial agonist effects and increased cellular proliferation at higher concentrations (10 ؊4 mmol/L; p < 0.01; n ‫؍‬ 12). LTD4 effects were partially blocked by montelukast and BAY u9773 but not by zileuton. All three antagonists reduced TNF-␣, IL-6, and IL-12 concentrations, with selective changes in IL-8 and no effects on IL-10 levels. Conclusions: LT pathways mediate intrinsic proliferative and inflammatory signaling pathways in adenotonsillar tissues from children with OSA, and targeted pharmacologic disruption of these pathways may provide nonsurgical alternatives for prevention and treatment of this disease.

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“…[1][2][3][4][5][6] Although it is accepted overall that the primary pathophysiologic mechanism involved in pediatric OSA consists of hypertrophy of adenoid and tonsillar tissues in the upper airway, [7][8][9][10][11] several studies [12][13][14][15][16] have thus far failed to demonstrate the anticipated corollary to such findings, namely, a very strong association correlation between upper airway adenotonsillar size and OSA severity. These findings suggest that OSA represents the end point of the interactions between multiple factors contributing to upper airway collapsibility during sleep, which also include neuromotor responses as well as other important anatomic factors such as retrognathia and upper airway length.…”

mentioning

confidence: 99%