Sleep-Disordered Breathing and Uric Acid in Overweight and Obese Children and Adolescents

sleep-disordered breathingOverweight and obese children and adolescents have a higher risk of sleep-disordered breathing (SDB). Sleep apnea in obese children is often associated with oxygen desaturation, and this is proportional to the degree of obesity. This could hypothetically result in tissue hypoxia. Tissue hypoxia is commonly defined as inadequate oxygen supply against oxygen demand in the integrity of cellular metabolic processes. This results in an impaired formation of adenosine triphosphate from adenosine diphosphate and in a net degradation of adenosine triphosphate to adenosine diphosphate and monophosphate. This leads to the release of purine intermediates and the purine catabolic end product, uric acid (UA). Previous studies have shown that elevated levels of these degradation products provide good indexes of tissue hypoxia in, for instance, infants with respiratory distress syndrome.

Furthermore, increased urinary UA excretion has been shown in adult patients with obstructive sleep apnea syndrome (OSAS) with normalization following continuous positive airway pressure treatment. To the best of our knowledge, there have been no reports in children or adolescents with SDB that have attempted to examine tissue hypoxia by studying UA metabolism.

An increased level of UA can thus be viewed as a marker of oxidative stress. Only a single study evaluated the presence of oxidative stress, by determining urinary F2-isoprostane metabolites, in children with SDB, but found no relation between these metabolites and SDB. Since oxidative stress-related mechanisms are probably one of the most important contributors to cardiovascular morbidity in adult subjects with SDB it is therefore important to further investigate whether sleep apnea could lead to hypoxic stress in children and adolescents.

The aim of this study was therefore to examine whether the severity of SDB was associated with increased UA excretion both in serum and in urine, as a biological marker of tissue hypoxia and of oxidative stress, in a sample of overweight and obese subjects, irrespective of indexes of adiposity.

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