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Brendon J Yee

Publications and source records attributed to Brendon J Yee.

2 recordsLinked to original sources

Ethnicity and obstructive sleep apnoea.

There is a scarcity of adult prevalence studies of OSA outside the Caucasian populations of North America, Europe and Australia, and comparisons have been complicated by methodological differences in sleep study settings, respiratory events definition, measured risk factors and clinical outcomes, and the lack of objective parameters for the measurement of ethnicity itself. Comparing studies with the same methodological design and respiratory events definition, recent large-scale prevalence studies from Hong Kong, Korea and India show similar OSA rates to populations of mainly Caucasian composition. OSA is a very complex disorder determined by several phenotypes such as obesity, craniofacial structure and abnormalities in neuromuscular and ventilatory control. Genetics may partially explain some of the ethnic clustering of these phenotypes, modulated by cultural and environmental factors. The exact contribution of these component phenotypes to overall OSA risk will be determined by their varying prevalence and relative risk conferred across ethnic groups. For lesser degrees of obesity, Asians are at risk for a more severe degree of illness compared with Caucasians. Inter-ethnic studies suggests that African-American ethnicity may also be a significant risk factor for OSA. The increased prevalences of OSA among American Indians and Hispanic adults, and increased severity among Pacific Islanders and Maoris, were mainly explained by increased obesity parameters. Most cephalometric studies have largely been conducted without specific regard to ethnicity and comparisons of findings across studies have been mainly limited by differences in sampling methods and the varying selection and definition of measured cephalometric variables. The limited number of studies with inter-ethnic comparative data suggest cephalometric variables and their degree of contribution to OSA vary across ethnic groups.

Adult↗

Treatment of obesity hypoventilation syndrome and serum leptin.

BACKGROUND: Leptin is a protein produced by adipose tissue that circulates to the brain and interacts with receptors in the hypothalamus to inhibit eating. In obese humans, serum leptin is up to four times higher than in lean subjects, indicating that human obesity is associated with a central resistance to the weight-lowering effects of leptin. Although the leptin-deficient mouse (ob/ob) develops obesity hypoventilation syndrome (OHS), in humans with OHS, serum leptin is a better predictor of awake hypercapnia in obesity than the body mass index (BMI). This suggests that central leptin resistance may promote the development of OHS in humans. We speculated that the reversal of OHS by regular non-invasive ventilation (NIV) therapy decreases leptin levels. OBJECTIVES: The aim of this study was to investigate whether ventilatory treatment of OHS would alter circulating leptin concentrations. METHOD: We measured fasting serum leptin levels, BMI, spirometry and arterial blood gases in 14 obese hypercapnic subjects undergoing a diagnostic sleep study. RESULTS: The average age of the subjects was (mean +/- SE) 62 +/- 13 years, BMI 40.9 +/- 2.2 kg/m(2), PaCO(2) 6.7 +/- 0.2 kPa, PaO(2 )8.9 +/- 0.4 kPa and total respiratory disturbance index 44 +/- 35 events/hour. Subjects were clinically reviewed after a median of 2.3 years (range 1.6-3) with repeat investigations. Nine patients were regular NIV users and 5 were non-users. NIV users had a significant reduction in serum leptin levels (p = 0.001), without a change in BMI. In these patients, there was a trend towards an improved daytime hypercapnia and hypoxemia, while in the 5 non-users, no changes in serum leptin, BMI or arterial blood gases occurred. CONCLUSION: Regular NIV use reduces serum leptin in OHS. Leptin may be a modulator of respiratory drive in patients with OHS.

Body Mass Index↗