Nocturnal tissue hypoxia and associated cardiovascular risk factors in obstructive sleep apnoea syndrome assessed by overnight change in urine uric acid and metanephrine excretion in a New Zealand population
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Obstructive sleep apnoea syndrome (OSA) is caused by obstruction of the upper airway and is characterized by repetitive pauses in breathing during sleep, despite the effort to breathe. An apnoea is a period of time during which breathing stops or is markedly reduced, associated with reduced blood oxygen saturation (SaO2) level, called hypoxia. An individual with sleep apnoea is rarely aware of having difficulty in breathing, even upon awakening. If left untreated, it may cause high blood pressure, stroke and congestive heart failure. A hypopnoea is a decrease in breathing that is not as severe as an apnoea but is also associated with a low level of blood oxygen. The severity of OSA is measured by the apnoea-hypopnoea index (AHI/h) during sleep studies conducted at the “Sleep Laboratory” of Auckland City Hospital. Some studies suggest the pattern of overnight change in urinary uric acid to creatinine ratio significantly differ between OSA and healthy subjects and the use of overnight continuous positive airway pressure (CPAP) reverses the pattern. Low blood oxygen levels may hamper efficient formation of adenosine triphosphate (ATP), leading to increased release of the purine catabolic end product, uric acid. Thus, elevated uric acid in body fluids may be an indicator of tissue hypoxia. To the researcher’s knowledge, there have not been similar studies conducted in New Zealand which has high prevalence of gout, obesity and OSA. If delta urine uric acid over creatinine can prove to clearly distinguish normal from significant OSA, then with these tests’ easy availability and low cost compared with the relatively scarce availability of overnight sleep clinic assessment slots in Auckland, there is potential for these tests to be used for screening of OSA, prioritising the potentially higher yield referrals for confirmatory sleep studies. Therefore the current study investigated the diagnostic utility of urinary uric acid as a marker in identifying the possible relationship between hypoxia and sympathetic activity in a New Zealand population. Ninety subjects from the “Sleep Laboratory” participated in this study over six months. During the sleep study, each participant contributed urine samples before going to bed and in the morning after the sleep study. An additional sample was required if CPAP applied during duration of the sleep study. The urine samples of all the participants were tested for uric acid and metanephrine at LabPLUS, Auckland City Hospital. The results of these biochemical tests were compared to the AHI/h and other data obtained from the sleep study. Although the severity of OSA as measured by the AHI/h index correlated significantly with conventional risk factors associated with OSA such as Body Mass Index and neck circumference there was no significant correlation between change in urinary uric acid/creatinine ratio and AHI/h. Likewise there was no significant correlation between urinary metanephrine measured in the present study and AHI/h. Thus, at least in the population studied, measurements of changes in urinary uric acid and/or urinary metanephrine do not have diagnostic value in predicting severity of sleep apnoea.