Weight Loss and Sleep‐Disordered Breathing in Childhood Obesity: Effects on Inflammation and Uric Acid

Abstract

Sleep‐disordered breathing (SDB) is prevalent in childhood obesity. It may be an independent risk factor for the metabolic syndrome. Possible mechanisms are inflammation and oxidative stress. Adenotonsillectomy in childhood obesity is associated with a high recurrence rate and risk of postoperative weight gain. Therefore, this study assessed the effects of SDB on inflammation and oxidative stress in childhood obesity before and after weight loss. We included 132 obese subjects between 10 and 18 years consecutively. Median age was 15.4 years (10.1–18.0). Mean BMI z‐score was 2.72 ± 0.42. Leukocytes and differentiation, high sensitivity C‐reactive protein (hs‐CRP), and uric acid (UA) were determined at baseline and subjects underwent a sleep assessment. SDB was diagnosed in 39%. Linear regression analysis showed an association between UAlog and oxygen desaturation indexlog (ODIlog) (r = 0.20; P = 0.03), between leukocyteslog and respiratory disturbance indexlog (RDIlog) (r = 0.23; P = 0.01), and between lymphocyteslog and RDIlog (r = 0.19; P = 0.04). Follow‐up was organized after 4–6 months of treatment. Median decrease in BMI z‐score was 32%. Laboratory measurements were repeated. Subjects with SDB at baseline underwent a second sleep study. Of these 49 subjects, 12 showed residual SDB. This corresponds with a treatment success rate of 71%. Unlike changes in inflammatory markers, improvements in UA were associated with improvements in RDI and ODI (respectively: r = 0.44; P = 0.007, r = 0.41; P = 0.01). In conclusion, weight loss is effective in treating obese children with SDB. At baseline, a link exists between inflammation and SDB. Oxidative stress is reflected by UA at baseline and the concentration decreases after treatment according to improvements in SDB.

Association Between Uric Acid Levels and Obstructive Sleep Apnea Syndrome in a Large Epidemiological Sample

“…Importantly, xanthine oxidase mediates intermittent hypoxia-induced vascular dysfunction and administration of allopurinol can prevent it by increasing intermediates, hypoxanthine and xanthine, and decreasing the final product uric acid [38], [39]. In fact, oxidative stress is reflected by uric acid levels, and its concentration decreases after treatment of sleep disordered breathing according to improvement of respiratory disturbance index and oxygen desaturation index [40]. Elevated serum uric acid levels are also associated with increased risk for cardiovascular mortality [21], [41], [42].…”

An Update on the Management of Pediatric Obstructive Sleep Apnea

“…Following weight loss, OSA resolved in 71 % of the patients. Adolescents with tonsillar hypertrophy were less likely to achieve resolution of OSA with weight loss [7,Class III]. & A recent review of OSA outcomes in obese adults that underwent bariatric surgery demonstrated improvement in OSA severity in the majority of patients.…”

Serum urate and obstructive sleep apnoea in severe obesity

“…7,22 Additionally, it has been suggested that elevated oxidative stress in OSA may be linked with uric acid production, and there is evidence implicating serum urate as an oxidative stress marker. 23,24 It is known that OSA is associated with cardiovascular disease and hypertension through mechanisms including intermittent hypoxia, leading to oxidative stress and inflammation. 20 Given our findings of an association between serum urate and OSA in females with severe obesity, there may be a possible role of uric acid in cardiovascular risk.…”