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Obesity, and not obstructive sleep apnea, is responsible for metabolic abnormalities in a cohort with sleep-disordered breathing.

机译:肥胖而非阻塞性睡眠呼吸暂停是导致睡眠呼吸异常的一组代谢异常的原因。

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OBJECTIVE: To assess the profile of metabolic abnormalities in subjects with obstructive sleep apnea (OSA). PATIENTS AND METHODS: In a case-control study conducted in two years, from April 2003 to March 2005, data obtained from polysomnography study, lipid profile, fasting blood sugar, serum insulin, insulin resistance, leptin and adiponectin levels, were compared between the various groups. Included in the study were OSA subjects from a sleep laboratory and matched controls from the community. Those with recent myocardial infarction, upper airway surgery, class III/IV heart failure, pregnancy, acromegaly, chronic renal failure, or who were on treatment for hyperthyroidism, on systemic steroid treatment, or on hormonal replacement therapy, were excluded from the study. RESULTS: Forty apneic obese subjects (AHI=32.19, range 13-52.75) were compared with 40 non-apneic obese controls (AHI=1.3, range 0-2.45) and 40 normal weight control subjects (AHI=0.7, range 0-1). No significant difference was noted in levels of fasting blood sugar, insulin resistance (obese apneics 61.9, obese controls 47.8, non-obese controls 19.1), leptin (obese apneics 10.65 microg/L, obese controls 8.52 microg/L, non-obese controls 2.83 microg/L) or adiponectin (obese apneics 4959.3 ng/ml, obese controls 5706 ng/ml, non-obese controls 7412 ng/ml) in the OSA group compared to obese controls. CONCLUSIONS: OSA has no independent association with lipid abnormalities, insulin resistance, serum leptin and adiponectin levels. In multivariate analysis, obesity was the major determinant of metabolic abnormalities in this cohort.
机译:目的:评估阻塞性睡眠呼吸暂停(OSA)患者的代谢异常情况。患者与方法:在2003年4月至2005年3月的两年中进行的病例对照研究中,比较了多导睡眠图研究,血脂,空腹血糖,血清胰岛素,胰岛素抵抗,瘦素和脂联素水平的数据。各种团体。该研究包括来自睡眠实验室的OSA受试者和来自社区的匹配对照。近期患有心肌梗塞,上呼吸道手术,III / IV级心力衰竭,妊娠,肢端肥大症,慢性肾功能衰竭或正在接受甲亢治疗,全身性类固醇治疗或激素替代治疗的患者被排除在研究范围之外。结果:将40名呼吸暂停肥胖受试者(AHI = 32.19,范围13-52.75)与40名非呼吸暂停肥胖对照组(AHI = 1.3,范围0-2.45)和40名正常体重对照受试者(AHI = 0.7,范围0-1)进行了比较)。空腹血糖,胰岛素抵抗(肥胖性呼吸暂停者61.9,肥胖对照者47.8,非肥胖对照者19.1),瘦素(肥胖症患者的肥胖症10.65 microg / L,肥胖者对照8.52 microg / L,非肥胖者)的水平没有显着差异与肥胖对照组相比,OSA组中的脂联素(2.83微克/升)或脂联素(肥胖呼吸暂停者4959.3 ng / ml,肥胖对照者5706 ng / ml,非肥胖对照者7412 ng / ml)。结论:OSA与脂质异常,胰岛素抵抗,血清瘦素和脂联素水平无独立关联。在多变量分析中,肥胖是该队列中代谢异常的主要决定因素。

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