阻塞性睡眠呼吸暂停低通气综合征与胰岛素抵抗研究进展

阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnoea-hypopnoea syndrome,OSAHS)有较高的代谢性疾病并发症.胰岛素抵抗(insulin resistance,IR)与十余种代谢疾病有关,也是导致这些疾病的主要因素.两者在临床上有较高的并存率.以下就OSAHS与IR相关性作一综述.     

阻塞性睡眠呼吸暂停低通气综合征与胰岛素抵抗的临床研究

目的 探讨阻塞性睡眠呼吸暂停低通气综合征（0SAHS）与胰岛素抵抗（IR）的相关性及其可能的发病机制。方法 82例打鼾者根据多导睡眠图检查结果分为：OSAHS组42例，均为中、重度患者（AHI〉20）；对照组40例，两组年龄、性别、血压相匹配。比较两组一般资料（年龄、性别、体质量指数、呼吸紊乱指数、最低血氧饱和度）、血清指标[空腹血糖、空腹胰岛素、胰岛素敏感指数、甘油三脂、胆固醇、脂蛋白a（LPa）、尿酸]，并作统计学分析。结果 一般资料比较：体质量指数、呼吸紊乱指数、最低血氧饱和度组间差异有统计学意义；血清指标比较：除LPa外，其余各项组间差异均有统计学意义。卡方检验显示两组糖尿病的发病率差异有统计学意义。相关分析显示OSAHS组呼吸紊乱指数与胰岛素敏感指数呈显著负相关（r=-0．415，P=0．006），与空腹胰岛素呈显著正相关（r=0．402，P=0．008）。在控制多个变量的影响后，逐步回归分析显示呼吸紊乱指数与体重指数对胰岛素敏感指数具有显著性影响。结论 中、重度OSAHS患者胰岛素敏感性下降，存在IR，两者呈独立相关关系。OSAHS与肥胖、糖耐量低减、高血压、高甘油三脂共同为IR的重要致病因素。     

阻塞性睡眠呼吸暂停低通气综合征与胰岛素抵抗关系探讨

阻塞性睡眠呼吸暂停低通气综合征（0SAHS）患者中普遍存在胰岛素抵抗状态,并且与其病情的严重程度呈正相关。导致OSAHS患者产生胰岛素抵抗的机制是多方面的,包括反复间断低氧引起交感兴奋、激素和炎症因子的分泌紊乱、脂肪组织内分泌功能紊乱、以及脂蛋白受体的异常等。瘦素、脂联素、抵抗素都是脂肪组织的产物,在OSAHS致胰岛素抵抗中发挥着重要作用。此外TNF-α、IL-6也参与了OSAHS致胰岛素抵抗的机制。持续正压通气治疗可以改善OSAHS患者的胰岛素敏感性。OSAHS是胰岛素抵抗的独立危险因素。     

阻塞性睡眠呼吸暂停低通气综合征与胰岛素抵抗的关系

目的探讨阻塞性睡眠呼吸暂停低通气综合征（OSAHS）与胰岛素抵抗（IR）的关系。方法选男性肥胖OSAHS患者60例（肥胖OSAHS组）、非OSAHS肥胖男性60例（肥胖非OSAHS组）、体重正常非OSAHS男性60例（正常体重非OSAHS组）,计算3组受试者的腰臀比和体重指数（BMI）;观察脉搏血氧饱和度（SpO2）;测空腹血糖,用高度特异的单克隆抗体夹心放大酶联免疫分析法测真胰岛素（TI）,IR的体内稳定状态模式评估方法（HOMA-IR）评估IR;行多导睡眠图（PSG）监测,计算呼吸暂停低通气指数（AHI）。结果同样是肥胖者,肥胖OSAHS组TI、HOMA—IR高于肥胖非OSAHS组,而最低SpO2低于肥胖非OSAHS组;在非OSAHS者中,肥胖非OSAHS组TI、HOMA-IR高于正常体重非OSAHS组,而最低SpO2低于正常体重非OSAHS组。协方差分析校正年龄、BMI、腰臀比的影响后,肥胖OSAHS组的TI、HOMA-IR仍明显高于肥胖非OSAHS组和正常体重非OSAHS组,肥胖非OSAHS组的TI、HOMA—IR明显高于正常体重非OSAHS组。多元线性回归分析显示MTU、HOMA—IR均与年龄和最低SpO2呈负相关,与BMI、腰臀比、AHI呈正相关;当以TU作因变量时,腰臀比是影响肥胖OSAHS组IR的主要因素,AHI与最低SpO2是TI的独立影响因素;当以HOMA—IR作因变量时,腰臀比是其主要影响因素,AHI与最低SpO2是其独立影响因素。结论OSAHS与IR独立相关,OSAHS可能经IR这一中间途径导致心血管疾病。     

阻塞性睡眠呼吸暂停低通气综合征与胰岛素抵抗的临床研究

阻塞性睡眠呼吸暂停低通气综合征（OSAHS）常常与代谢综合征大家族中的多种疾病，如高血压、肥胖、糖尿病等伴发或先后出现，其最终结果导致心血管事件发生和死亡的危险性增加。业已证明代谢综合征的核心是胰岛素抵抗（IR）。IR在多种疾病的发病中起重要作用，特别是动脉粥样硬化及冠状动脉疾病。我们试图初步探讨：（1）OSAHS与IR的相互关系；（2）OSAHS发生IR的可能发病机制。     

阻塞性睡眠呼吸暂停低通气综合征与胰岛素抵抗的关系研究进展

目前很多研究发现阻塞性睡眠呼吸暂停低通气综合征（OSAHS）与胰岛素抵抗（IR）关系密切,OS-AHS可以通过多种机制导致IR。OSAHS的间歇低氧可引起交感神经兴奋、神经内分泌功能改变、并增加炎症因子的水平,也引起了脂肪因子的改变,从而导致IR的发生。本文就OSAHS导致IR的各种机制进行论述。     

阻塞性睡眠呼吸暂停低通气综合征与胰岛素抵抗关系的研究进展

有研究表明,中心性肥胖是阻塞性睡眠呼吸暂停低通气综合征(OSAHS)的主要危险因素,可导致胰岛素抵抗.OSAHS患者存在胰岛素抵抗,中心性肥胖可能是联系OSAHS和胰岛素抵抗的中间环节.早期开展经鼻持续气道正压通气治疗OSAHS,可提高组织对胰岛素的敏感性,促进组织对葡萄糖摄取利用,从而减轻或避免产生胰岛素抵抗.     

脂联素、胰岛素抵抗与阻塞性睡眠呼吸暂停低通气综合征

脂联素是一种具有增强胰岛素敏感性的脂肪因子。近年来研究发现阻塞性睡眠呼吸暂停低通气综合征患者血清脂联素水平明显降低,且胰岛素抵抗是阻塞性睡眠呼吸暂停低通气综合征及其并发症的典型特征。因此,脂联素水平的下降可能在阻塞性睡眠呼吸暂停低通气综合征及其并发症的发生、发展中具有重要作用。     

阻塞性睡眠呼吸暂停低通气综合征患者胰岛素抵抗与骨密度的关系

目的观察不同程度阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea hypopnea syndrome,OSAHS)患者骨密度变化及其与胰岛素抵抗的关系。方法根据呼吸暂停低通气指数(apnea hypopnea index,AHI)将OSAHS患者分为:轻度(AHI 5~20次/h)、中度(AHI 21~40次/h)、重度(AHI40次/h),测定以上3组及正常对照组的骨密度、骨代谢多个参数,血脂、空腹血糖、胰岛素水平及计算胰岛素抵抗指数(homeostasis model assessment for insulin resistance,HOMA-IR),并进行组间比较及与AHI的相关性。结果重度OSAHS患者骨密度(BMD L1-4:0.79±0.07 g/cm~2,BMD neck:0.78±0.09 g/cm~2)明显低于轻度OSAHS患者(BMD L1-4:0.95±0.12 g/cm~2,BMD neck:0.90±0.08 g/cm~2)及正常对照组(BMD L1-4:0.98±0.10 g/cm~2,BMD neck:0.91±0.11 g/cm~2),差异有统计学意义(P0.05);但轻度OSAHS患者骨密度与正常对照组比较,差异无统计学意义(P0.05)。OSAHS患者与正常对照(2.14±0.32)相比,及OSAHS不同程度3组(轻度、中度和重度OSAHS分别为2.53±0.29、3.34±0.35、3.98±0.31)间比较,HOMA-IR差异均有统计学意义(P0.05);对于OSAHS患者,其胰岛素抵抗指数(HOMA-IR)与AHI呈正相关(r=0.398,P=0.000)。结论 OSAHS患者骨密度降低,易发生骨质疏松,且与缺氧程度及胰岛素抵抗密切相关。     

阻塞性睡眠呼吸暂停低通气综合征与慢性咳嗽

阻塞性睡眠呼吸暂停低通气综合征是慢性咳嗽的病因之一.胃食管反流、鼻后滴流、气道炎症可能是阻塞性睡眠呼吸暂停低通气综合征诱发慢性咳嗽的机制.持续气道正压通气是有效治疗阻塞性睡眠呼吸暂停低通气综合征所致慢性咳嗽的首选治疗方案.     

阻塞性睡眠呼吸暂停低通气综合征与急性呼吸衰竭

阻塞性睡眠呼吸暂停低通气综合征(obstructivesleep apnea hypopnea syndrome,OSAHS)可导致昏迷、猝死,除严重心律失常外,急性呼吸衰竭也是其     

阻塞性睡眠呼吸暂停低通气综合征与胰岛β细胞功能障碍

阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea-hypopnea syndrome,OSAHS)是一种氧化应激性疾病,其特征性低氧方式-慢性间歇低氧诱导了机体氧化应激的产生,是累积多系统、多器官损害的病理生理基础.胰岛β细胞是最易受到氧化损伤和极易凋亡的细胞,氧化应激引起胰岛β细胞损伤是...     

老年阻塞性睡眠呼吸暂停综合征与高血压及胰岛素抵抗的相关性研究

目的探讨阻塞性睡眠呼吸暂停综合征(OSAS)与高血压及胰岛素抵抗(IR)的关系。方法随机选择符合OSAS患者48例作为OSAS组,并分为高血压组(28例)和正常血压组(20例)2个亚组,同期选择无OSAS的高血压患者30例作为单纯高血压组,健康体检者26例作为正常对照组,均进行整夜睡眠呼吸监测(7 h),并记录睡眠呼吸暂停低通气指数(AHI)等;空腹血糖(FPG)及空腹胰岛素(FINS)测定,对患者进行24 h的动态血压监测并进行相关分析。结果与单纯高血压组比较,高血压组患者非杓形血压比例和脉压均明显升高,差异有统计学意义(P0.05,P0.01)。OSAS组患者的FPG、FINS水平及胰岛素抵抗指数(HOMA-IR)均明显高于正常对照组,差异有统计学意义(P0.05);OSAS患者的AHI与FINS和HOMA-IR均呈正相关。结论 OSAS与IR存在独立的相关性,可能通过IR导致并进一步加重心血管疾病的发生和发展。     

睡眠呼吸障碍应成为呼吸功能衰竭的原因之一

近年来越来越多的研究结果提示OSAHS与胰岛素抵抗(IR)、高胰岛素血症、2型糖尿病以及代谢综合征密切相关,其中IR是将OSAHS与这些代谢紊乱相联系的重要纽带[1-2].Ip等[3]报道在平衡了肥胖和其他重要的引起IR的因素后,OSAHS患者的呼吸暂停低通气指数(AHI)和最低SaO2仍与空腹胰岛素水平和反映IR的体内稳态模式评估(OMA)指数明显相关,即AHI每增加一个单位,IR的程度增加0.5%,而且即使是在非肥胖患者中,OSAHS与IR仍相关联.     

Obstructive sleep apnoea syndrome, plasma adiponectin levels, and insulin resistance

OBJECTIVE: To investigate whether sleep-disordered breathing and/or plasma adiponectin levels are associated with insulin resistance independent of obesity or fat distribution in obstructive sleep apnoea syndrome (OSAS). DESIGN: Cross-sectional clinical study. PATIENTS: Two-hundred and thirteen Japanese patients with OSAS aged 27-80 years were divided into three groups: 30 with mild OSAS [apnoea-hypopnoea index (AHI) = 10.3 +/- 0.9 episodes/h, minimum oxygen saturation (min SpO2) = 87.3 +/- 0.9%], 98 with moderate OSAS (AHI = 28.9 +/- 0.6 episodes/h, min SpO2 = 82.1 +/- 0.7%), and 85 with severe OSAS (AHI = 68.1 +/- 2.8 episodes/h, min SpO2 = 72.3 +/- 1.6%). Twenty-one patients undergoing diabetic treatments (two mild, nine moderate and 10 severe) were excluded from the assessment of insulin resistance and plasma adiponectin measurements. MEASUREMENTS: Fat distribution [evaluated according to visceral (V) and subcutaneous (S) fat areas using computed tomography scanning at the umbilical level], blood pressure, metabolic parameters and hormones including insulin and adiponectin were measured. After full polysomnography, venous blood was collected between 0600 and 0700 h. RESULTS: Severe OSAS patients were more hypertensive than mild and moderate OSAS. Fasting plasma glucose (FPG) and fasting plasma insulin and homeostasis model assessment of insulin resistance (HOMA-IR) levels were all higher in severe OSAS than mild and moderate OSAS patients. HOMA-IR was correlated not only with obesity [body mass index (BMI), V and S areas] but also with apnoea (AHI, min SpO2 and desaturation time). Additionally, HOMA-IR was correlated positively with haemoglobin (Hb)A1c, systolic (SBP) and diastolic blood pressure (DBP), triglycerides and free fatty acids (FFA), and negatively with high density lipoprotein (HDL)-cholesterol, suggesting that insulin resistance is a key component of the metabolic syndrome in OSAS. Plasma adiponectin levels were not different between mild, moderate and severe OSAS groups. Plasma adiponectin levels were correlated with HOMA-IR and V area, but not AHI or min SpO2. Stepwise multiple regression analysis, however, revealed that BMI, AHI and plasma adiponectin were independently associated with HOMA-IR. CONCLUSION: Sleep-disordered breathing was associated with insulin resistance independent of obesity. Although plasma adiponectin was also an independent determinant of HOMA-IR in OSAS patients, plasma adiponectin was more closely related to obesity than to sleep apnoea. Although treatment of sleep-disordered breathing with nasal continuous positive airway pressure reportedly improves insulin sensitivity, our findings suggest that treatment of obesity is also essential in ameliorating insulin resistance at least through increased plasma adiponectin levels in OSAS.     

Obstructive sleep apnea syndrome is associated with metabolic syndrome rather than insulin resistance

The aim of this study was to investigate cross-sectionally the prevalence and covariates of obstructive sleep apnea syndrome (OSAS) and its relationship to metabolic syndrome (MS), insulin resistance (IR), and coronary heart disease (CHD) in a population sample of 1,946 men and women representative of Turkish adults. OSAS was identified when habitual snoring and episodes of apnea were combined with another relevant symptom. MS was diagnosed based on modified criteria of the Adult Treatment Panel III and IR by homeostatic model assessment (HOMA). OSAS was identified in 61 men (6.4%) and 58 women (5.8%), at a similar prevalence, after adjusting for covariates. Among individuals with OSAS, significantly higher odds ratios (ORs), adjusted for age, body mass index (BMI), and waist girth, were observed for MS, hypertension, and prevalent CHD, but not for HOMA or menopause. Significantly higher C-reactive protein existed only in women with OSAS who were also more frequent smokers. In logistic regression models, waist circumference, but not BMI nor hypertension, was significantly associated with OSAS among men. In women, by contrast, current cigarette smoking and hypertension were the significant independent covariates. Regression models controlling for sex, age, and smoking revealed that MS (and not IR per se) was associated significantly with OSAS (OR 1.94) in nondiabetic individuals. To conclude, abdominal rather than overall obesity in men and smoking among women are significant independent determinants of OSAS in Turkish adults. OSAS is associated with MS rather than IR per se. Relatively high prevalence of OSAS is observed in Turkish women in whom it is significantly associated with CHD.     

阻塞性睡眠呼吸暂停低通气综合征在心血管疾病中的误诊误治

病例1:男,41岁。5年前查体发现血压升高,达160/100mmHg(1mmHg=0.133kPa),无高血压病的症状,无高血压家族史,诊断为原发性高血压。给予雷米普利、氨氯地平及氢氯噻嗪合用亦不能有效控制血压。8个月前去上级医院就诊,追问病史,有打鼾史9年,加重并被发现有夜间呼吸暂停现象5年,白天明显嗜睡、乏力、驾驶时曾出现入睡现象及发现性功能减退5年。查体:问诊时患者难以保持清醒状态,体重89kg、身高168cm,口咽部明显狭窄,双侧扁桃体2度大,纤维鼻咽喉镜下见鼻中隔偏曲,舌扁桃体肥