New insights in the diagnosis, pathophysiology and treatment of sleep-disordered breathing in pediatric obesity
16 December 2016
UAntwerpen, Campus Drie Eiken, Building O, Auditorium O.1 - Universiteitsplein 1 - 2610 Wilrijk (route: UAntwerpen, Campus Drie Eiken
Annelies Van Eyck
Prof S. Verhulst & Prof W. De Backer
PhD defence Annelies Van Eyck - Faculty of Medicine and Health Sciences
Childhood obesity is a major health problem with increasing prevalence worldwide. Obstructive sleep apnea (OSA) is a well-documented complication of obesity. The prevalence of OSA has been reported to be 13-59% in obese children, compared to 2–3% in normal-weight children. Several complications are associated with OSA in childhood, including cardiovascular and metabolic complications. However, the linking mechanism between OSA and these complications are mostly unknown, although several hypotheses have been made. In this dissertation several research topics concerning OSA in the setting of childhood obesity were explored.
Firstly, the role of pulmonary function in the pathophysiology of OSA in obese children was examined. We found that a decreased pulmonary function, both obstructive and restrictive patterns, contributed to the severity of OSA in obese children. Furthermore, this restrictive breathing pattern could be responsible for the more frequent oxygen desaturations seen in obese children with OSA.
Secondly, the role of nocturnal pulse oximetry as an alternative screening method for diagnosing OSA in obese children was explored. We found that oximetry alone was insufficient for a definite diagnose of OSA in a population of obese children, and other screening options need to be explored.
Thirdly, different linking mechanisms between OSA and its associated complications were investigated. Compared to studies in a normal-weight population, we couldn’t find any relationship between OSA and CRP levels, or adipokine secretion. The direct effect of obesity could be hidden by the independent effect of intermittent hypoxia on these systemic inflammatory markers. In contrast, OSA was associated with altered autonomic function, as shown by increased sympathetic activity on heart rate variability analysis. Especially, measures of hypoxia were related with an increased sympathetic tone, suggesting that intermittent hypoxia could be involved in autonomic dysfunction in OSA.
Fourthly, therapeutic aspects of OSA in obese adolescents were investigated. Adenotonsillectomy, which is the first-line treatment for OSA in children, is successful in less than 50% of obese children. Therefore, weight loss has been suggested as a potential treatment for OSA in obese children, and has proven to be more effective with a success percentage of 62-71%. However, this meant that 29-38% of the patients still dealt with residual OSA. Hence, possible clinical predictors for residual OSA after weight loss treatment were identified in a population of obese adolescents. We found that more severe OSA at baseline and the presence of respiratory allergies were associated with a higher risk for developing residual OSA.