Dorit Koren1, David Gozal2, Rakesh Bhattacharjee2, Mona F Philby2, Leila Kheirandish-Gozal3. 1. Section of Pediatric Sleep Medicine, Department of Pediatrics, Pritzker School of Medicine, Biological Sciences Division, University of Chicago, Chicago, IL; Section of Endocrinology and Metabolism, Department of Pediatrics, Pritzker School of Medicine, Biological Sciences Division, University of Chicago, Chicago, IL. 2. Section of Pediatric Sleep Medicine, Department of Pediatrics, Pritzker School of Medicine, Biological Sciences Division, University of Chicago, Chicago, IL; Section of Pulmonology, Department of Pediatrics, Pritzker School of Medicine, Biological Sciences Division, University of Chicago, Chicago, IL. 3. Section of Pediatric Sleep Medicine, Department of Pediatrics, Pritzker School of Medicine, Biological Sciences Division, University of Chicago, Chicago, IL. Electronic address: lgozal@peds.bsd.uchicago.edu.
Abstract
BACKGROUND: OSA associates with insulin resistance (IR), hyperglycemia, and dyslipidemia consistently in adults, but inconsistently in children. We set out to quantify the impact of OSA treatment upon obesity and metabolic outcomes and thus assess causality. METHODS: Sixty-nine children with OSA; mean age, 5.9 years (range, 3-12.6); 55% boys; and 68% nonobese (NOB) underwent baseline overnight polysomnography, anthropometric and metabolic measurements, adenotonsillectomy (T&A), and follow-up testing a mean 7.9 months (range, 2-20) later. RESULTS: Fifty-three children (77% of study cohort; 91% of obese children) had residual OSA (apnea-hypopnea index > 1 event/h) post-T&A. Fasting plasma insulin (FPI, 14.4 ± 9.4 → 12.6 ± 9.7 μIU/mL, P = .008), homeostasis model assessment-IR (3.05 ± 2.13 → 2.62 ± 2.22, P = .005), and high-density lipoprotein (HDL) (51.0 ± 12.9 → 56.5 ± 14.4 mg/dL, P = .007) improved despite increased BMI z score (1.43 ± 0.78 → 1.52 ± 0.62, P = .001); changes did not differ significantly between sexes or NOB and obese participants; however, post-T&A BMI z score rather than apnea-hypopnea index was the main predictor of levels of follow-up FPI, HDL, and other metabolic parameters. Higher baseline FPI and BMI-z predicted likelihood of residual OSA; conversely, on regression analysis, follow-up IR, HDL, and triglycerides were predicted by BMI z score, not residual OSA. CONCLUSIONS: T&A improved IR and HDL, and residual OSA is predicted by baseline FPI and BMI z score, indicating a causal relationship; however, following T&A, residual metabolic dysfunction related to underlying adiposity rather than remaining sleep-disordered breathing. Finally, T&A cured OSA in < 25% of all children and only 10% of obese children; post-T&A polysomnography is indicated to assess which children still require treatment.
BACKGROUND: OSA associates with insulin resistance (IR), hyperglycemia, and dyslipidemia consistently in adults, but inconsistently in children. We set out to quantify the impact of OSA treatment upon obesity and metabolic outcomes and thus assess causality. METHODS: Sixty-nine children with OSA; mean age, 5.9 years (range, 3-12.6); 55% boys; and 68% nonobese (NOB) underwent baseline overnight polysomnography, anthropometric and metabolic measurements, adenotonsillectomy (T&A), and follow-up testing a mean 7.9 months (range, 2-20) later. RESULTS: Fifty-three children (77% of study cohort; 91% of obesechildren) had residual OSA (apnea-hypopnea index > 1 event/h) post-T&A. Fasting plasma insulin (FPI, 14.4 ± 9.4 → 12.6 ± 9.7 μIU/mL, P = .008), homeostasis model assessment-IR (3.05 ± 2.13 → 2.62 ± 2.22, P = .005), and high-density lipoprotein (HDL) (51.0 ± 12.9 → 56.5 ± 14.4 mg/dL, P = .007) improved despite increased BMI z score (1.43 ± 0.78 → 1.52 ± 0.62, P = .001); changes did not differ significantly between sexes or NOB and obeseparticipants; however, post-T&A BMI z score rather than apnea-hypopnea index was the main predictor of levels of follow-up FPI, HDL, and other metabolic parameters. Higher baseline FPI and BMI-z predicted likelihood of residual OSA; conversely, on regression analysis, follow-up IR, HDL, and triglycerides were predicted by BMI z score, not residual OSA. CONCLUSIONS: T&A improved IR and HDL, and residual OSA is predicted by baseline FPI and BMI z score, indicating a causal relationship; however, following T&A, residual metabolic dysfunction related to underlying adiposity rather than remaining sleep-disordered breathing. Finally, T&A cured OSA in < 25% of all children and only 10% of obesechildren; post-T&A polysomnography is indicated to assess which children still require treatment.
Authors: Anton Mahne; Ghassan El-Haddad; Abass Alavi; Mohamed Houseni; Gul Moonis; Andrew Mong; Miguel Hernandez-Pampaloni; Drew A Torigian Journal: Semin Nucl Med Date: 2007-03 Impact factor: 4.446
Authors: D Koren; J A Chirinos; L E L Katz; E R Mohler; P R Gallagher; G F Mitchell; C L Marcus Journal: Int J Obes (Lond) Date: 2015-05-18 Impact factor: 5.095
Authors: Chun Ting Au; Kate Ching Ching Chan; Kin Hung Liu; Winnie Chiu Wing Chu; Yun Kwok Wing; Albert Martin Li Journal: J Clin Sleep Med Date: 2018-12-15 Impact factor: 4.062
Authors: P E Brockmann; F Damiani; D L Smith; A Castet; F Nuñez; L Villarroel; D Gozal Journal: Int J Obes (Lond) Date: 2016-08-01 Impact factor: 5.095
Authors: Sherri L Katz; Joanna E MacLean; Lynda Hoey; Linda Horwood; Nicholas Barrowman; Bethany Foster; Stasia Hadjiyannakis; Laurent Legault; Glenda N Bendiak; Valerie G Kirk; Evelyn Constantin Journal: J Clin Sleep Med Date: 2017-09-15 Impact factor: 4.062