Chest
Volume 118, Issue 3, September 2000, Pages 580-586
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Clinical Investigation
Sleep
Serum Leptin and Vascular Risk Factors in Obstructive Sleep Apnea

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Study objectives

To define the metabolic profilerelevant to vascular risks in obstructive sleep apnea (OSA) and therole of leptin resistance in this risk profile.

Design

Case control study.

Setting

Sleep Laboratory, Queen Mary Hospital, University of Hong Kong, China.

Methods

Thirty OSA subjects were matched with 30 non-OSAsubjects for body mass index (BMI), age, sex, and menopausal status. Neck, waist, and hip girth, skinfold thickness, and fasting serumlevels of lipids, glucose, insulin, and leptin were compared betweenthese two groups.

Results

Compared with controlsubjects with a similar BMI but without OSA, the OSA group had asignificantly more adverse vascular risk factor profile, includingdyslipidemia, higher diastolic BP, insulin resistance, and greateradiposity reflected by skinfold thickness. OSA subjects also had highercirculating leptin levels (9.18 ± 4.24 ng/mL vs 6.54 ± 3.81ng/mL, mean ± SD, p = 0.001). Serum leptin levels correlatedpositively with BMI, skinfold thickness, serum cholesterol, low-densitylipoprotein cholesterol, insulin, insulin/glucose ratio, apnea-hypopneaindex, and oxygen desaturation time; multiple stepwise regressionanalysis identified skinfold thickness, waist/hip ratio, serumlow-density lipoprotein cholesterol, and diastolic BP as independentcorrelates, while only serum insulin and diastolic BP were independentcorrelates in OSA subjects. After treatment with nasal continuouspositive airway pressure for 6 months, there was a significant decreasein circulating leptin (p = 0.01) and triglyceride levels (p = 0.02)without change in other parameters.

Conclusion

Despite controlling for BMI, OSA subjects showed distinct profiles withclustering of vascular risk factors. Hyperleptinemia was present in the, OSA subjects, but it can be normalized by treatment with nasalcontinuous positive airway pressure, suggesting that increased leptinresistance was not the cause of OSA or its associated vascularrisks.

Section snippets

Subjects

Subjects were recruited from those who were referred forsuspected sleep apnea to the Sleep Clinic, Department of Medicine, The University of Hong Kong, and from those who participated in aterritory-wide study on prevalence of sleep apnea. The study wasapproved by the institutional Ethics Committee. All subjects underwentan overnight sleep study to document sleep-disordered breathing, and fasting morning venous blood samples were taken with informed consent. Adult subjects with documented OSA,

Results

Thirty subjects with documented OSA syndrome(AHI = 35.7 ± 18) were compared with 30 subjects without OSA (AHI=1.8 ± 1.9), matched for sex, age, BMI, and in female subjects, for menopausal status. Their demographic and anthropometriccharacteristics are shown in Table 1. There were no significant differences between the two groups in theirbody habitus measurements of neck, waist, and hip circumference, butthere was significantly more subcutaneous fat in the OSA group, as indicated by skinfold

Discussion

OSA is now known to affect at least 2 to 4% of the middle-agedpopulation in white262728 as well as some Asianpopulations.29 The major concerns about the adverse healtheffects of OSA, apart from symptoms of excessive daytime sleepiness, are its association with cardiovascular and cerebrovascular morbidityand mortality from coronary heart disease and stroke.123While controversy and research are ongoing as to whether thisassociation is comorbid or causal, it is well appreciated thatindependent

ACKNOWLEDGMENTS

The authors thank Ms. Audrey Ip, Ms. Rosa Wong, and Mr. K.M. Lo for technical assistance, Dr. K.N. Chan for statisticaladvice, and Ms. Wendy Mok for statistical analysis.

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  • Cited by (0)

    This study was partially supported by Earmarked Competitive Grant no. HKU 457/96M, Research Grants Council, University Grants Committee, Hong Kong, China.

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