深圳市龙华区中小学生肥胖人群发生OSAHS的相关危险因素分析

目的探讨深圳市龙华区中小学生肥胖人群发生阻塞性睡眠呼吸暂停低通气综合征(OSAHS)的相关危险因素。方法选择深圳市龙华区中小学生肥胖人群共410例为研究对象。根据患者呼吸暂停低通气指数(AHI)结果将其分为OSAHS组(195例)和非OSAHS组(215例),记录所有患者体质发育情况、血压、血脂、肝功能指标、血糖、PSG睡眠监测等指标。对OSAHS组患者按严重程度区分,分析不同严重度OSAHS患者临床资料特点及相关高危因素。结果 OSAHS组患者颈围、DBP、FPG、2h PG、HbA1c、谷丙转氨酶(ALT)、谷草转氨酶(AST)及三酰甘油(TAG)值均明显高于非OSAHS组,差异有统计学意义(P0.05)。不同程度OSAHS患者年龄、BMI、颈围、腰围、SBP、DBP、FPG及HbA1c值不同,且随着程度加重而增加,差异有统计学意义(P0.05)。多元回归分析显示,校正年龄、性别的影响后,BMI、颈围、DBP和FPG是本研究人群的OSAHS发生的高危因素(OR值1,P0.05)。结论导致深圳市龙华区中小学生肥胖人群发生OSAHS的代谢相关高危因素是BMI、颈围的增加,DBP和FPG的升高,应早期采取有效干预措施,预防或延缓OSAHS额发展。     

阻塞性睡眠呼吸暂停低通气综合征与颈围的相关性研究

目的　研究颈围与阻塞性睡眠呼吸暂停低通气综合征(OSAHS)的相关性。方法　测量92 0例被临床怀疑为OSAHS患者的身体参数(包括颈围、身高和体重) ,并进行夜间睡眠监测。符合OSAHS诊断的有71 9例,为OSAHS组;2 0 1例不符合OSAHS ,为鼾症组,对其颈围、BMI和体重与睡眠呼吸紊乱指数(AHI)进行统计学分析。结果　OSAHS组患者的年龄明显大于鼾症组(P <0 .0 0 1 ) ;两组患者的颈围与BMI、体重均高度相关(P <0 .0 0 1 ) ;除中度OSHAS患者的AHI与体重、BMI和颈围有相关性外,其余OS HAS患者的颈围与AHI无相关关系(P >0 .0 5)。结论　颈围是反映肥胖程度的一项有效指标;颈围粗是OSAHS发病的相关因素;但使用颈围值预测OSAHS患者夜间睡眠呼吸紊乱的严重程度不具有临床意义。OSAHS的影响因素是多方面的,不同程度的OS AHS ,影响因素不同。     

高血压合并阻塞性睡眠呼吸暂停患者的血压变异性

目的探讨高血压合并阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者的血压变异性特点。方法纳入疑似OSAHS的高血压患者217例,根据睡眠呼吸暂停低通气指数(AHI)分为4组:非OSAHS组(33例),轻度OSAHS组(57例),中度OSAHS组(68例),重度OSAHS组(59例),比较各组患者血生化指标、血压及血压变异性,分析AHI与血压变异性的关系。结果 4组患者的体质量指数(BMI)和血压变异性明显不同,随睡眠呼吸暂停的严重程度增加而增大(P<0.05)。以BMI进行分层后,超重及肥胖高血压患者的夜间血压变异性随睡眠呼吸暂停严重程度的增加而增大(P<0.05)。偏相关分析显示控制年龄、BMI、血压后,AHI与24h收缩压变异性、24h舒张压变异性、白昼收缩压变异性、白昼舒张压变异性、夜间收缩压变异性及夜间舒张压变异性呈正相关(分别r=0.346,0.414,0.263,0.324,0.445,0.570,均P<0.05)。结论 AHI与血压变异性相关,睡眠呼吸暂停对夜间血压变异性影响更为明显。     

阻塞性睡眠呼吸暂停低通气综合征与胰岛素抵抗、血脂及C反应蛋白的关系研究

目的探讨阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea hypopnea syndrome,OSAHS)对患者的胰岛素抵抗、血脂及炎症反应的影响。方法根据多导睡眠图(PSG)检测结果将60例符合OSAHS诊断的受试对象分为轻中度OSAHS组、重度OSAHS组,同时选取40例作为正常对照组。测量每位受试对象的身高、体质量,计算体质量指数(BMI),比较3组受试对象的睡眠状况及睡眠中末梢血氧变化,抽取患者的空腹血行生化指标检查及空腹胰岛素、血糖及C反应蛋白检测并进行比较。结果 OSAHS组睡眠中末梢平均血氧及最低血氧均较对照组下降(P0.01),呼吸暂停低通气指数(AHI)较对照组升高(P0.01),且与OSAHS严重程度相关。OSAHS组三酰甘油、低密度脂蛋白胆固醇、载脂蛋白B、BMI、胰岛素抵抗指数均较对照组明显升高(P0.05),且与OSAHS严重程度相关。相反,OSAHS组高密度脂蛋白胆固醇、载脂蛋白A较对照组下降,且重度OSAHS组下降显著(P0.05)。OSAHS组外周血CRP较对照组升高(P0.05),且与OSAHS严重程度相关(P0.05)。结论OSAHS影响机体的胰岛素抵抗、血脂代谢,炎症反应参与其中。     

阻塞性睡眠呼吸暂停低通气综合征患者应激事件和下丘脑-垂体-肾上腺轴相互作用的研究进展

下丘脑-垂体-肾上腺(HPA)轴的活性改变是机体对应激反应的主要表现,阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者的呼吸暂停/低通气和氧去饱和被看作睡眠呼吸紊乱相关疾病应激反应的指示器,影响HPA轴的活性,睡眠片断为OSAHS患者又一应激反应也影响HPA轴的活性,激活的HPA轴加重OSAHS患者的病情。经鼻持续正压气道通气治疗能有效治疗OSAHS,可能改善HPA轴的活性。     

OSAHS患者呼吸障碍的差异及SaO2检测的诊断价值

目的探索连续血氧饱和度(SaO2)检测是否对阻塞性睡眠呼吸暂停低通气综合症(OSAHS)有诊断价值,以及不同程度OSAHS患者之间的呼吸障碍的差异。方法对104例鼾症患者进行多导睡眠图(PSG)的检测,分为单纯鼾症、轻、中、重度OSAHS共4组,收集资料并分析。结果1各OSAHS组SaO2的基础值和最低值均小于单纯鼾症组(P均<0.05);2所有患者的SaO2的基础值和最低值均与睡眠呼吸暂停低通气指数(AHI)呈显著负相关(R=-0.478,-0.507;P均<0.05);3OSAHS患者的SaO2的基础值和最低值均与AHI呈显著负相关(R=-0.315,-0.334;P均<0.05);4所有患者的SaO2的基础值和最低值均与体重指数(BMI)呈显著负相关(R=-0.579,-0.601;P均<0.05);5若以SaO2基础值<95%和SaO2<85%作为诊断OSAHS的标准,敏感性分别是78.5%和73.8%;特异性均是100%;6各OSAHS组睡眠呼吸障碍在不同睡眠期的分布不同。结论OSAHS患者存在睡眠时SaO2下降,并与疾病的严重程度有关;连续检测SaO2是在鼾症患者中鉴别出OSAHS的一个有效的简易方法;各OSAHS组睡眠呼吸障碍在不同睡眠期的分布不同。     

体质量指数对病情分级相同的阻塞性睡眠呼吸暂停低通气综合征患者的影响

目的 探讨体质量指数(BMI)对病情分级相同的阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea-hypopnea syndrome,OSAHS)患者的影响.方法 选取267例已行多导睡眠监测的OSAHS患者,按国内通用BMI标准分两组,BMI≥24者为肥胖组(206例),BMI＜24者为正常组(61名).按AHI及夜间最低SaO2将患者病情分为轻、中、重三级,分别比较相同病情分级的正常与肥胖两组患者睡眠结构、呼吸紊乱、临床症状及合并症的情况.结果 病情分级相同的OSAHS患者因BMI不同,睡眠结构、呼吸紊乱程度及合并症差异有统计学意义(P＜0.05),肥胖组病情严重程度重于正常组,合并症比例高于正常组,在重度分级中差异显著.结论 肥胖使OSAHS患者的病情严重程度加重,随着OSAHS病情分级的加重,肥胖对于OSAHS的影响也更加明显.     

阻塞性睡眠呼吸暂停低通气综合症与高血压关系的分析

目的 探索伴有高血压的阻塞性睡眠呼吸暂停低通气综合症(OSAHS)的睡眠呼吸障碍特点,并分析两者间的关系.方法 对已诊断为OSAHS的患者中90例高血压和65例非高血压者进行相关指标的分析.结果 高血压组睡眠呼吸暂停低通气指数(AHI)高于非高血压组,体重指数(BMI)是引起两组间AHI差异的显著因素(F=23.92,P＜0.01).在引入年龄和BMI、AHI作为协变量后,两组间夜间平均SaO2和最低SaO2比较差异无显著性(P＞0.05);AHI是引起夜间缺氧的显著因素(P＜0.05).在不同的睡眠期,高血压组的阻塞性呼吸暂停指数(OAI)均显著高于非高血压组;引入相关协变量后,仍然存在显著性差异(P＜0.05);而两组间的低通气指数(HI)比较差异无显著性.OSAHS患者中高血压的危险因素是AHI、年龄、BMI.结论 伴有OSAHS的高血压患者的睡眠呼吸障碍程度更重,夜间低氧血症与高血压无关,而与睡眠呼吸障碍的严重度有关.在不同的睡眠期,高血压组的阻塞性呼吸暂停程度更严重.年龄、肥胖和睡眠呼吸障碍的严重程度是OSAHS患者中高血压的危险因素.     

动态心电图对阻塞性睡眠呼吸暂停综合征严重程度的预测价值

目的 评价动态心电图(Hoher)预测阻塞性睡眠呼吸暂停综合征(OSAHS)严重程度的价值.方法 选择2008年1月至2009年7月在我院老年科就诊经多导睡眠分析仪(PSG)检查确诊为OSAHS患者76例,并于1个月内行Hoher检查.其中,28例呼吸暂停低通气指数(AHI)≤20诊断为轻度OSAHS,48例AHI>20诊断为中、重度OSAHS.根据Hoher心率变异性分析对13项睡眠窒息危险指标进行评分,总和为睡眠窒息危险总分.将体质指数(BMI)及13项睡眠窒息危险指标各项得分进行logistic二元回归分析,评估Holler预测OSAHS严重程度的价值.结果 轻度OSAHS和中、重度OSAHS患者的性别、年龄,合并高血压、冠心病、糖尿病、高脂血症及服用B受体阻滞剂的临床特征无显著性差异.严重程度不同的OSAHS患者Hoher睡眠窒息危险评分总分差异无统计学意义(分别为5.64±2.33和6.42±2.22,P>0.05).极低频/总功率百分比>70%和△白天/夜晚低频功率差异<-70以及BMI与中、重度OSAHS相关,OR值分别为3.98(1.087～14.596),3.69(1.106～12.285)和1.28(1.062～1.544)(P<0.05).结论 应用Hoher心率变异性分析指标中的极低频/总功率百分比和△白天/夜晚低频功率差异以及BMI有助于早期识别中、重度OSAHS患者.     

阻塞性睡眠呼吸暂停综合征患者胰岛素敏感性的变化

目的 研究阻寒性睡眠呼吸暂停低通气综合征(OSAHS)患者胰岛素敏感性(IS)的变化.方法 55例男性鼾症患者行整夜睡眠呼吸监测,放免法测定FIns,C-P水平,计算ISI和QUICKI观察患者IS变化. 结果 随呼吸紊乱指数(AHI)增加,OSAHS患者胰岛素抵抗(IR)和肥胖的程度越来越明显.多元逐步线性回归分析结果提示BMI、最低血氧饱和度和AHI是IS下降的独立危险因素.OS-AHS患者持续气道正压通气治疗1个月后IS无明显变化. 结论 严重呼吸紊乱常与肥胖、IR合并存在.睡眠呼吸紊乱可能足IR的独立危险因素.     

Underdiagnosis of Sleep Apnea Syndrome in U.S. Communities

We hypothesize that clinical recognition rates for obstructive sleep apnea-hypoapnea syndrome (OSAHS) are influenced by comorbidity and demographic factors. Data on medical disorders, symptoms of sleep disorders, and cardiovascular risk factors gathered from 15,699 individuals in the Sleep Heart Health Study were compared. Participants were classified into three groups: those with a self-reported physician diagnosis of OSAHS, those with self-reported physician-diagnosed and -treated OSAHS, and those reporting both frequent snoring and daytime sleepiness (two-symptom group). Among all participants, 4.1% reported two symptoms (range across sites: 1.55 to 7.23%), whereas 1.6% reported a physician diagnosis of OSAHS (range: 0.66 to 2.88%) and 0.6% reported physician diagnosis and treatment (range: 0.11 to 0.88%). Recognized OSAHS groups were similar to the two-symptom group in age, having a sleeping partner, measured blood pressure, total cholesterol, and race. In a logistic model that included age along with characteristics found to vary significantly among the three groups (gender, body mass index [BMI], high-density lipoprotein cholesterol levels, hypertension), only male gender and BMI were increased in those with physician-diagnosed and -treated OSAHS. We conclude that disparities (especially in women and in those with lower BMI) exist between current recognition rates for OSAHS and the estimated prevalence by symptom report across the United States.     

Sleep oxygen desaturation and circulating leptin in obstructive sleep apnea-hypopnea syndrome

BACKGROUND: Obstructive sleep apnea-hypopnea syndrome (OSAHS) is characterized by repeated oxygen desaturation. Obesity and visceral fat accumulation (VFA) are risk factors for the development of OSAHS. Circulating leptin increases in accordance with body mass index (BMI), and under experimental conditions intermittent hypoxia stimulates leptin production. METHODS: The primary objective of this study was to investigate whether hypoxemia during sleep influences the levels of circulating leptin and whether the location of body fat deposits, ie, the distribution of VFA and subcutaneous fat accumulation (SFA), affects circulating leptin levels in patients with OSAHA who are not obese. We assessed VFA and SFA by abdominal CT scan and measured circulating levels of leptin in 96 male patients with OSAHS and 52 male patients without OSAHS matched for BMI. To be matched for BMI in the two groups, patients whose BMIs were < 27 were selected for the OSAHS group. RESULTS: In the whole study group, circulating leptin levels correlated with BMI (r = 0.30), VFA (r = 0.44), SFA (r = 0.28), apnea-hypopnea index (AHI) [r = 0.48], sleep mean arterial oxygen saturation (Sao(2)) [r = 0.59], and sleep lowest Sao(2) (r = 0.37). Multiple regression analysis showed that average Sao(2) (p < 0.01) and lowest Sao(2) (p = 0.03) were explanatory variables for serum leptin values, but AHI (p = 0.054), BMI (p = 0.33), VFA (p = 0.11), and SFA (p = 0.36) were not. CONCLUSIONS: These results suggest that sleep hypoxemia may be the main determinant of circulating leptin levels, although the location of body fat deposits could contribute to the elevated circulating leptin levels in patients with OSAHS who are not obese.     

Effects of obstructive sleep apnea syndrome on hepatic steatosis and nonalcoholic steatohepatitis.

Hepatic steatosis occasionally progresses to nonalcoholic steatohepatitis. This study was designed to examine whether non-obese patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) were prone to develop hepatic steatosis and whether repeated hypoxemia contributed to the progression of steatohepatitis. This study included 83 OSAHS patients and 41 age-, body mass index (BMI)- and gender-matched non-OSAHS patients diagnosed by polysomnography. Hepatic steatosis was defined by a liver/spleen ratio <0.9 on abdominal computerized tomography, and latent steatohepatitis was evaluated based on serum levels of type III procollagen (P-III-P). Visceral fat (V-fat) accumulated much more in OSAHS patients. Liver/spleen ratios in OSAHS patients correlated negatively with BMI and, especially, with the amount of visceral fat. Serum levels of P-III-P in OSAHS patients correlated negatively with the average of oxygen saturation during sleep, and positively with BMI, the apnea-hypopnea index (AHI) and the amount of V-fat. Multiple regression analysis showed that average SaO(2) was the only explanatory variable for P-III-P values, but AHI, BMI and V-fat was not. These observations confirmed that non-obese patients with OSAHS are at a risk for visceral obesity, and suggested that oxygen desaturation during sleep is a risk for developing latent steatohepatitis, especially in patients with substantial hepatic steatosis.     

Obstructive sleep apnea and hypopnea syndrome (OSAHS): association with obesity, gender and age

Obstructive sleep apnea and hypopnea syndrome (OSAHS) has been the focus of extensive research because of its association with neurocognitive and cardiovascular complications. The aim of this study was to evaluate the frequency and association between OSAHS and the class of obesity, gender and age in outpatients referred to a sleep laboratory. We selected 1,595 patients, 71.7% male. Mean +/- SD age was 46.7 +/- 11.7 years, BMI was 28.1 +/- 5.1 kg/m2 and AIH was 13.9 +/- 15.5 events/ hour of sleep. The patients were considered apneic when the apnea-hypopnea index (AHI) was > 5 events/hour of sleep; OSAHS was present in: (1) 71.1% of men and 50.3% of women (p < 0.001); (2) in 45.3% of patients with normal BMI, in 64.3% of those overweighed and in 80% of obese (p < 0.001). According to age, 61.2% with age < 55 were apneic, as well as 78% of those with age > 55 years old (p < 0.001). We concluded that OSAHS was directly and strongly associated to the male gender, obesity class and to aging.     

新疆维汉民族OSAHS患者与血清脂联素研究

目的探讨新疆维汉民族阻塞性睡眠呼吸暂停低通气综合征(OSAHS)与血清脂联素相互关系。方法随机选择OSAHS维族及汉族患者各60例,采用酶联免疫法(ELISA)测定两组血清脂联素水平。结果在OSAHS患者中维族与汉族比较年龄、BMI、睡眠呼吸暂停低通气指数(AHI)、颈围、腰围、腹围、最低血氧饱合度(LSaO2)、最长呼吸暂停时间(Tmax)、脂联素,发现维族患者BMI高于汉族,脂联素水平低于汉族(P<0.05),其余均无统计学意义。在维族与汉族OSAHS患者中比较超重与肥胖所占比例,维族肥胖人数大于汉族(P<0.05)。结论除去年龄、性别的影响,维族OSAHS患者血清脂联素水平低于汉族。     

Fat accumulation, leptin, and hypercapnia in obstructive sleep apnea-hypopnea syndrome

BACKGROUND: Obesity and visceral fat accumulation (VFA) are risk factors for the development of obstructive sleep apnea-hypopnea syndrome (OSAHS), and a subgroup of OSAHS patients acquire hypoventilation. Circulating leptin, an adipocyte-derived signaling factor, increases in accordance with body mass index (BMI); under experimental conditions, leptin selectively decreases visceral adiposity and it is also a respiratory stimulant. OBJECTIVE: To investigate whether the location of body fat deposits, ie, the distribution of VFA and subcutaneous fat accumulation (SFA), contributes to hypoventilation and whether circulating levels of leptin are involved in the pathogenesis of hypoventilation, which is often observed in OSAHS. METHODS: We assessed VFA and SFA by abdominal CT scan, and measured lung function and circulating levels of leptin in 106 eucapnic and 79 hypercapnic male patients with OSAHS. RESULTS: In the whole study group, circulating leptin levels correlated with BMI (r = 0.56), VFA (r = 0.24), and SFA (r = 0.47), but not with Po(2) or sleep mean arterial oxygen saturation (Sao(2)). BMI, percentage of predicted vital capacity, FEV(1)/FVC ratio, apnea-hypopnea index, sleep mean Sao(2), VFA, and SFA were not significantly different between two groups. Circulating leptin levels were higher in the hypercapnic group than in the eucapnic group. Logistic regression analysis indicated that serum leptin was the only predictor for the presence of hypercapnia (beta = 0.21, p < 0.01). CONCLUSIONS: These results suggest that the location of body fat deposits may not contribute to the pathogenesis of hypoventilation, and circulating leptin may fail to maintain alveolar ventilation in hypercapnic patients with OSAHS.     

阻塞性睡眠呼吸暂停低通气综合征患者睡眠时咽部CT与体质量的关系研究

目的 探讨睡眠状态下阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea hypopneasyndrome,OSAHS)患者咽部CT测量与体质量的关系.方法 在于天津医科大学总医院行多导睡眠监测被确诊为OSAHS的患者中随机选取40例可以配合的患者进行睡眠状态下螺旋CT扫描,依体质量指数(body mass index,BMI)将其分为BMI<25组和BMI≥25组,比较两组一般资料[平均年龄、颈围、最低血氧饱和度、睡眠呼吸暂停低通气指数(apnea hypopnea index,AHI)、吸烟情况、醒时血氧饱和度]及咽腔形态学(包括鼻咽和口咽的最小面积,舌体长度、厚度和面积,软腭长度、厚度和横截面积,悬雍垂直径等)的差异.结果 睡眠状态下,BMI≥25的患者颈围、AHI明显高于BMI<25的患者(P<0.01),而最低血氧饱和度明显低于后者(P<0.001),同时BMI≥25患者的舌体长度、舌体面积较BMI<25患者明显增加(P<0.001),软腭后区最小横截面积减小(P<0.05),而舌后区最小横截面积、舌体厚度、软腭长度、软腭厚度、软腭横截面积及悬雍垂直径随着BMI的增大有增加趋势,但两组间差别无统计学意义.相关分析结果也显示AHI与BMI呈正相关(r=0.608,P<0.001).结论 睡眠状态下不同BMI的OSAHS患者之间气道结构存在一定的差异,同时BMI与AHI有相关性,提示BMI可反映OSAHS患者上气道阻塞程度.     

Plasma orexin-A levels in obstructive sleep apnea-hypopnea syndrome

STUDY OBJECTIVES: Orexin and orexin receptors are present in the CNS. The effects of orexin peptides have been uniformly reported as excitatory, and the posterior hypothalamus containing orexin neurons has been implicated in arousal state control. Therefore, it is probable that the orexin system may have a neuromodulatory effect on arousal states. The aim of the present study was to investigate the relationship between plasma orexin-A levels and arousals from sleep in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS). DESIGN: An analysis was conducted in 30 male patients with OSAHS, which had been diagnosed by polysomnography by the presence of an apnea-hypopnea index (AHI) of > 5, and 20 male age-matched and body mass index (BMI)-matched control subjects. RESULTS: Plasma orexin-A levels were higher in patients with OSAHS compared with those in control subjects (p < 0.05). Plasma orexin-A levels correlated positively, but weakly, with the arousal index (r = 0.51; p < 0.05) and the AHI (r = 0.52; p < 0.05). However, plasma orexin-A levels did not relate to age, BMI, Epworth sleepiness scale, PaO(2), PaCO(2), minimum arterial oxygen saturation (SaO(2)) during sleep, or mean SaO(2) during sleep. Plasma orexin-A levels can be a measure of both AHI and arousal index. CONCLUSION: These results suggested that the orexin system may be involved in arousal mechanisms in patients with OSAHS.