Why the study?
Does obstructive sleep apnea and obesity associate with elevated Lp-PLA2 levels in children, and does adenotonsillectomy reduce these levels?
Does obstructive sleep apnea and obesity associate with elevated Lp-PLA2 levels in children, and does adenotonsillectomy reduce these levels?
Pediatric obstructive sleep apnea and obesity are associated with elevated Lp-PLA2, a marker of cardiovascular risk, which can be significantly reduced by adenotonsillectomy.
Lp-PLA2 may mark CV risk in obese OSA children; leaves open whether adenotonsillectomy improves outcomes.
Background Obstructive sleep apnea ( OSA ) is a highly prevalent condition, especially in obese children, and has been associated with increased risk for endothelial dysfunction and dislipidemia, which are precursors of atherosclerosis. Lipoprotein‐associated phospholipase A2 (Lp‐ PLA 2) is recognized as an independent risk factor for cardiovascular risk and atheromatous plaque activity. We hypothesized that Lp‐ PLA 2 levels would be elevated in children with OSA , particularly among obese children who also manifest evidence of endothelial dysfunction. Methods and Results One hundred sixty children (mean age 7.1±2.3 years), either nonobese with (n=40) and without OSA (n=40) or obese with (n=40) and without OSA (n=40) underwent overnight polysomnographic and postocclusive reperfusion evaluation and a fasting blood draw the morning after the sleep study. In addition to lipid profile, Lp‐ PLA 2 plasma activity was assessed using a commercial kit. Obese children and OSA children had significantly elevated plasma Lp‐ PLA 2 activity levels compared to controls. Furthermore, when both obesity and OSA were concurrently present or when endothelial function was present, Lp‐ PLA 2 activity was higher. Treatment of OSA by adenotonsillectomy resulted in reductions of Lp‐ PLA 2 activity (n=37; P <0.001). Conclusions Lp‐ PLA 2 plasma activity is increased in pediatric OSA and obesity, particularly when endothelial dysfunction is present, and exhibits decreases on OSA treatment. The short‐term and long‐term significance of these findings in relation to cardiovascular risk remain undefined.
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Philby et al. (2017) studied this question.
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