2型糖尿病合并阻塞性睡眠呼吸暂停综合征

阻塞性睡眠呼吸暂停综合征（OSAS）是一种日渐受到重视的与多系统学科相关联的疾病。OSAS可引发呼吸、心血管及内分泌等多个系统疾病,危害人体健康,影响生活质量。近年来研究发现,2型糖尿病患者中存在OSAS的高患病率,OSAS患者又常合并2型糖尿病,且二者都极易诱发心血管疾病。本文就OSAS的概况、2型糖尿病合并OSAS的流行病学、发生机理及危害的干预治疗作一综述。     

阻塞性睡眠呼吸暂停综合征的治疗及体会

阻塞性睡眠呼吸暂停综合征（OSAS）是由于某些原因而致上呼吸道阻塞，睡眠时有呼吸暂停，伴有缺氧、鼾声、白天嗜睡等症状的一种较复杂的疾病。好发于肥胖、老年人。上呼吸道任何一个部位的阻塞性病变都可致OSAS。笔者临床治疗36例，报告如下。     

2型糖尿病患者阻塞性睡眠呼吸暂停综合征患病状况及相关因素分析

目的调查2型糖尿病患者阻塞性睡眠呼吸暂停综合征(OSAS)患病情况,并分析其相关特点。方法选择2型糖尿病患者213例,使用便携式睡眠呼吸监测仪调查睡眠呼吸情况。分析OSAS患病状况、严重程度,并分析其相关因素。最终完成睡眠呼吸监测共145例。根据诊断分为OSAS组114例和非OSAS组31例。结果与非OSAS组比较,OSAS组患者体重指数、腰围、糖化血红蛋白、高血压及冠心病患病率明显升高(P<0.01)。糖化血红蛋白与OSAS患病风险独立相关(OR=6.24,95%CI:2.21～9.23,P<0.01)。糖化血红蛋白、体重指数、高血压、年龄、糖尿病病程与呼吸暂停低通气指数独立相关,糖化血红蛋白是主要的独立危险因素。结论 2型糖尿病患者OSAS患病率较高,血糖控制差者OSAS发病风险高,且病情更为严重,肥胖、年龄大、病程长或合并高血压者OSAS较为严重。     

肥胖伴阻塞性睡眠呼吸暂停综合征患者术后SICU管理

阻塞性睡眠呼吸暂停综合征（OSAS ）是成年患者中常见的疾病,其在中年男性和女性中的发病率分别高达4%和2%,其中60%～90%的患者合并肥胖.悬雍垂腭咽成形术（UPPP）是重度阻塞性睡眠呼吸暂停综合征手术治疗的主要方法 .虽然阻塞性睡眠呼吸暂停综合征的外科治疗有了很大进展,但由于OSAS患者咽部的病理生理变化的特点,以及肥胖患者呼吸、循环的病理生理改变,加之手术、麻醉药物的使用等诸多方面的因素影响,使这些患者在手术后可以产生严重的合并症,如低氧血症、高血压、心律失常、气道梗阻甚至死亡,致患者术后苏醒期的处理更加困难.我院对肥胖OSAS患者术后多采用保留气管插管,转入SICU病房,进行监护、治疗,待患者恢复,基本生命体征平稳并顺利拔除气管插管后,安全返回病房.本文就我院12例肥胖伴OSAS患者术后SICU管理积累的一些经验,现报道如下。     

阻塞性睡眠呼吸暂停综合征与高血压

阻塞性睡眠呼吸暂停综合征（OSAS）是指睡眠时上气道塌陷阻塞引起的以睡眠过程中反复出现呼吸暂停和或低通气,导致反复低氧血症和高碳酸血症,伴打鼾、睡眠结构紊乱、白天嗜睡为特征的睡眠呼吸紊乱性疾病。长期暴露于这种疾病,可引起高血压、脑卒中、冠心病、心律失常、糖耐量异常、认知功能障碍等,OSAS多与肥胖、脂质代谢紊乱、高血压等并存,     

阻塞性睡眠呼吸暂停综合征合并高血压的发病机制

阻塞性睡眠呼吸暂停综合征(obstructive sleepapnea syndrom,OSAS)是一种睡眠呼吸障碍性疾病,主要表现为睡眠时打鼾并伴有呼吸暂停和呼吸表浅,夜间反复发生低氧血症、高碳酸血症和睡眠结构紊乱,导致白天嗜睡、心脑肺血管并发症乃至多脏器损害,严重影响患者的生活质量和寿命[1]。目前研究认为OSAS与高血压密切相关,至少50%~60%的OSAS患者合并有高血压,50%的高血压患者伴有OSAS[2]。调查显示OSAS是独立于年龄、性别、肥胖、吸烟、酗酒、生活压力以及心脏、肾脏疾病以外的高血压发病的一个独立危险因素[3]。近年来国内外学者对OSAS合…     

肥胖对阻塞性睡眠呼吸暂停综合征及血压的影响

目的探讨肥胖对阻塞性睡眠呼吸暂停综合征（OSAS）及血压的影响。方法测量261例OSAS患者的血压、腰围、腹内脂肪等指标，分析肥胖与睡眠监测相关指标及血压的关系，探讨OSAS者腹内脂肪在其中的作用。结果肥胖的OSAS的患者者高血压检出率明显高于正常体重OSAS患者；腹内脂肪面积≥85cm。组与〈82组比较，患者的收缩压较高，睡眠监测相关指标也有显著差异（P〈0．01）。结论肥胖及腹内脂肪堆积对OSAS及血压有显著影响。     

阻塞性睡眠呼吸暂停综合征与高同型半胱氨酸血症

阻塞性睡眠呼吸暂停综合征（OSAS）与高同型半胱氨酸血症是心脑血管疾病的独立危险因素,两者合并存在时会加速动脉粥样硬化的进展。具有中心性肥胖的OSAS患者咽部脂肪组织增厚,气道狭窄,睡眠时不断产生呼吸暂停或低通气而导致严重低氧血症。缺氧是诱发胰岛素抵抗的主要原因。胰岛素对同型半胱氨酸代谢具有重要的调节作用,2型糖尿病的高胰岛素血症可以通过抑制肝脏胱硫醚β-合成酶活性而影响血同型半胱氨酸的分解代谢。采取有效地治疗OSAS的方法可增加胰岛素敏感性,改善胰岛素抵抗,同时也会降低同型半胱氨酸浓度。     

阻塞型睡眠呼吸暂停综合征的内科治疗

阻塞型睡眠呼吸暂停综合征(OSAS)又称阻塞型睡眠呼吸暂停低通气综合征(OSAHS),临床表现为打鼾并反复发作呼吸暂停和低通气,致低氧血症、高碳酸血症和睡眠结构紊乱,是多种疾病的独立危险因素.OSAS的内科治疗包括一般治疗、药物治疗、气道正压通气治疗和口腔矫治器治疗等.目前OSAS仍首选内科治疗.     

睡眠呼吸暂停低通气综合征致脑卒中的研究进展

睡眠呼吸暂停低通气综合征（sleepapneahy．popneasyndrome,SAHS）也称为呼吸暂停综合征（sleepapneasyndrome,SAS）,是指以呼吸结构异常伴低通气为特征的一类疾病。它按发生原因不同主要分为阻塞型睡眠呼吸暂停低通气综合征（obstruc．tivesleepapneasyndrome,OSAS）、中枢型睡眠呼吸暂停低通气综合征（centralsleepapneasyndrome,CSAS）以及混合型睡眠呼吸暂停低通气综合征（mixedsleepapneasyndrome,MSAS）,其中以OSAS最为多见。     

Obstructive sleep apnea syndrome, endothelial dysfunction and coronary atherosclerosis

In obstructive sleep apnea syndrome (OSAS), repetitive episodes of apnea cause increased sympathetic nerve activity, increased surges in arterial blood pressure, swings in intrathoracic pressure, oxidative stres, hypoxia and hypercapnia. The association of OSAS with some diseases, having endothelial dysfunction in their physiopathology, such as hypertension, diabetes mellitus, obesity, coronary artery diseases, stroke and heart failure is common. Increased sympathetic nerve activity and also endothelial dysfunction which are the results of hypoxia, have important roles in vascular complications of OSAS. When compared with healthy population, an important endothelial dysfunction in OSAS patients and relationship between OSAS severity and endothelial dysfunction have been shown. In this review, the relationship between OSAS and endothelial dysfunction was overviewed.     

A case of obstructive sleep apnea syndrome remarkably improved by gastric restriction surgery

A 23-year-man with morbid obesity and obstructive sleep apnea syndrome (OSAS) was admitted. He was 170 cm in height and 170 kg in weight. He underwent dietary treatment several times, but his weight returned to its original level, or even higher, within a short period. A diagnosis of OSAS was made by nocturnal polysomnography. In this morbidly obese patient with OSAS a nocturnal sleep apnea study was performed before and after weight reduction surgery (gastric restriction). The postoperative findings revealed a dramatic body weight reduction. At the same time, the results of apnea and oxygen desaturation were remarkably improved too. These results indicate that weight reduction surgery is a definitely effective treatment for morbid obesity associated with OSAS.     

Obesity, metabolic syndrome and sleep apnoea: all pro-inflammatory states

Obesity is associated with significant morbidity and mortality and is increasing in prevalence worldwide. Associated conditions include insulin resistance (IR), diabetes, hypertension and dyslipidaemia; a clustering of these has recently been termed as metabolic syndrome. Weight gain is a major predictor of the metabolic syndrome with waist circumference being a more sensitive indicator than body mass index as it reflects both abdominal subcutaneous adipose tissue and visceral adipose tissue (VAT). VAT has more metabolic activity and secretes a number of hormones and pro-inflammatory cytokines which are linked with the metabolic abnormalities listed above. Central obesity also increases the risk of obstructive sleep apnoea syndrome (OSAS), where the sleep disordered breathing may also independently lead to/or exacerbate IR, diabetes and cardiovascular risk. The contribution of OSAS to the metabolic syndrome has been under-recognized. The putative mechanisms by which OSAS causes or exacerbates these other abnormalities are discussed. We propose that activation of nuclear factor kappa B by stress hypoxia and/or by increased adipokines and free fatty acids released by excess adipose tissue is the final common inflammatory pathway linking obesity, OSAS and the metabolic syndrome both individually and, in many cases, synergistically.     

Plasma visfatin levels in severe obstructive sleep apnea—hypopnea syndrome

Background  

Obstructive sleep apnea syndrome (OSAS) is associated with obesity and insulin resistance. Visfatin is an insulin-mimicking adipokine, which is considered a link between obesity and insulin resistance. Aim of this study was to evaluate levels of plasma visfatin in patients with severe OSAS and examine their potential correlation with sleep characteristics and several biochemical parameters.     

Inflammation accelerates atherosclerotic processes in obstructive sleep apnea syndrome (OSAS)

Obstructive sleep apnea syndrome (OSAS) is an often underestimated sleep disorder that has been associated with cardiovascular disease. OSAS is characterized by cycles of apnea and/or hypopnea during sleep caused by the collapse of the upper airways. Intermittent hypoxia deriving from the cycles of apnea/arousals (to retrieve the ventilation) plays a pivotal role in the pathogenesis of the disease. Obesity is the most frequent predisposing condition of OSAS. Recent evidence suggests that OSAS could be considered as a pro-atherosclerotic disease, independently of visceral fat amount. Oxidative stress, cardiovascular inflammation, endothelial dysfunction, and metabolic abnormalities in OSAS could accelerate atherogenesis. The present review is focused on the possible pathophysiological mediators which could favor atherosclerosis in OSAS.     

Women and the obstructive sleep apnea syndrome

Twenty-seven women referred to a sleep disorders clinic for symptoms of obstructive sleep apnea syndrome (OSAS) during one year were systematically analyzed after polygraphic monitoring of sleep and cephalometric x-ray examination. Our subjects, one-third of whom were premenopausal, comprised approximately 12 percent of the total OSAS population seen. Women with OSAS were compared with 110 OSAS men and with a group of 16 women without OSAS but referred to orthodontists for mild dental malocclusion. Women with OSAS were massively obese, much more so than their male counterparts. There was no significant difference between pre- and postmenopausal women, with the exception of the respiratory disturbance index (RDI), which was lower in the postmenopausal group despite similar morbid obesity (seemingly better tolerated by women with OSAS than by men with the same syndrome) and long mandibular plane-hyoid bone distance. The significantly higher RDI noted in premenopausal women, despite equally massive obesity and upper airway abnormalities, is thought to be related to hormonal status and better arousal response. Chronic obstructive lung disease (COLD) seen in a subgroup of women with OSAS did not differentiate this subgroup from the other OSAS patients when oxygen saturation during sleep, frequency of abnormal respiratory events and sleep variables were considered. Massive obesity is the dominant factor for the appearance of OSAS in women.     

Exposure to intermittent hypoxia inhibits allergic airway inflammation in a murine model of asthma

Sleep and Breathing - Obesity increases the severity of asthma, and patients with severe asthma are often complicated with obstructive sleep apnea syndrome (OSAS), a concomitant disease of obesity....     

Cortisol circadian rhythm and 24-hour Holter arterial pressure in OSAS patients

Obstructive sleep apnea syndrome (OSAS) is a syndrome in which the principal symptom is apnea during sleep. Hypoxia in OSAS is a stress condition, which when prolonged in time, could alter hypothalamo-hypophysial-suprarenal control and the cortisol cicadian rhythm. We studied 28 patients with OSAS (30-60 years old), 20 female and 8 male. We calculated the OSAS class according to the Simmons classification. Twenty of the 28 patients maintained unmodified cortisol circadian rhythms, while 8 had cortisol levels more elevated in late and nocturnal hours. Holter monitoring showed arterial hypertension in 8 of the 28 patients (the same patients with cortisol circadian rhythm alteration). Our data seem to indicate that when the OSAS patients lack cortisol circadian rhythm they are having arterial hypertension.     

阻塞性睡眠呼吸暂停综合征患者消化系统损害与氧化应激相关性的研究进展

阻塞性睡眠呼吸暂停综合征(obstructive sleep apnea syndrome,OSAS)是一种常见的睡眠呼吸紊乱疾病,慢性间歇低氧是引起其损害的核心机制。随着 OSAS研究的深入,有学者研究发现氧化应激在 OSAS造成的系统性损害中发挥一定的作用,那么氧化应激在 OSAS并发的消化系统损害中如何发挥作用呢？本文就氧化应激在 OSAS并发消化系统相关疾病发病机制中可能发挥的作用进行综述,从而为防治 OSAS患者消化系统损害开辟一条新的思路。