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PAP Therapy's Effect on Cardiometabolic Risk Markers in Pediatric Patients.

Journal of Clinical Sleep Medicine, Vol. 13, No. 9, 2017 A large body of data has accumulated in recent years showing that obstructive sleep apnea (OSA) poses an additive risk to disorders classically considered to be obesity-related comorbidities. In adults, OSA is fairly consistently associated with greater risk of having elements of metabolic syndrome, including insulin resistance (IR)1 and hypertension.2 As shown in studies of adults, treatment of OSA with continuous positive airway pressure (CPAP) improves insulin sensitivity in most,3 though not all,4 and several meta-analyses have found that CPAP therapy lowers blood pressure (BP) modestly but significantly.5 In children, the data regarding an association between OSA and metabolic syndrome risk factors are less consistent than in adults. Elevation of pro-inflammatory markers is frequent6; however, some studies have shown an association between OSA and IR,7,8 while others failed to find an association.9 Associations between OSA and IR are more likely to be seen in children that are obese than in those that are non-obese10,11 and in adolescents than in prepubertal children.8 Similarly, while many studies have shown that OSA is associated with elevated BP in children independent of obesity,12 some have found no such association.13 Relatively few studies have examined the metabolic impact of the treatment of OSA in pediatric patients. In these studies, results have been somewhat inconsistent, with some studies showing that treatment improves IR9,14 and BP,15 and others—including the multi-center randomized Childhood Adenotonsillectomy Trial (CHAT) study—finding no significant difference following treatment in either BP or IR from baseline.16 Levels of high-sensitivity C-reactive protein (hsCRP), an inflammatory marker, generally improve after adenotonsillectomy (T&A),6 and continuing hsCRP elevation may be a good marker for residual OSA following T&A.17 All of the pediatric treatment studies cited above utilized T&A as the treatment modality for OSA. T&A is generally the first-line treatment for OSA in children18; however, not all children with OSA have adenotonsillar hypertrophy, and therefore T&A is not always the appropriate therapeutic modality. Even among those who do have adenotonsillar hypertrophy and undergo T&A, residual OSA persists in a significant proportion of children following the surgery,19 especially in obese children,14,20 and therefore so may its sequelae. Thus, it is crucial to also examine the metabolic impact of the other mainstay of COMMENTARY