ESPE Abstracts

Introduction: Hypothalamus is an important regulator of sleep onset, sleep maintenance and wakefulness as well as appetite control. Thus, hypothalamic damage can lead to both sleep dysregulation and severe morbid obesity. So, sleep apnea may be more prevalent and severe in obesity due to hypothalamic damage in comparison to exogenous obesity.

Aim: We aim to compare frequency and severity of obstructive sleep apnea (OSA) in children with hypothalamic and exogenous obesity in order to test the hypothesis that hypothalamic obese patients would be more prone to OSA than exogenous obese subjects.

Methods: Prospective, cross sectional, case control study consisted of 14 hypothalamic obese (4 males) children in study group (10 craniopharyngiomas, 2 suprasellar non-glial tumors, 1 septo-optic dysplasia and 1 patient with damaged hypothalamus and hydrocephalus due to sequela of meningoencephalitis), and 30 exogenous obese (11 males) children in control group. Informed consent was taken from all patients and families. Mallampati scores and scoring of sleepiness was carried out in all patients, and blood was withdrawn for fasting blood glucose, insulin, lipid profile, orexin-A, hsCRP, TNFα. All patients underwent full-night polysomnography.

Results: Mean age (13.08±3.6 vs 14.58±4.44, cases vs controls) as well as sex distribution were similar between the two groups. All patients with craniopharyngioma were operated at least once and all had multiple pituitary hormone deficiency. Body mass index (BMI) and z-score were higher in exogenous obesity group than hypothalamic obesity group. No difference was detected in frequency of hypertension, dyslipidemia, levels of fasting blood glucose, insulin, ratio of fasting blood glucose to insulin, orexin-A, hsCRP, TNFα, Mallampati scores and scoring of sleepiness between the two groups. Obstructive sleep apnea was not correlated to hypertension, insulin resistance, dyslipidemia, levels of inflammatory markers or orexin-A. The apnea-hypopnea index (AHI) of hypothalamic obesity group was higher than that of exogenous obesity group in full-night polysomnography. After adjusting for age, sex and BMI z-score; the odds of OSA increased 4.4-fold for hypothalamic obese subjects in multivariant analysis. As a result, risk of OSA is significantly increased in hypothalamic obesity group in comparison to exogenous obesity group.

Conclusion: Our findings show that polysomnography should be a part of routine investigation in hypothalamic obesity, even without any complaint suggesting a sleep disorder.