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.
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.
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.
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.