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炎症与阻塞性睡眠呼吸暂停综合征的发病机制:一个工作假说。

Inflammation and obstructive sleep apnea syndrome pathogenesis: a working hypothesis.

作者信息

Hatipoğlu Umur, Rubinstein Israel

机构信息

Section of Respiratory and Critical Care Medicine, Department of Medicine, University of Illinois at Chicago, Chicago, Ill. 60616-7323, USA.

出版信息

Respiration. 2003 Nov-Dec;70(6):665-71. doi: 10.1159/000075218.

DOI:10.1159/000075218
PMID:14732803
Abstract

Obstructive sleep apnea syndrome (OSAS) afflicts about 5% of adults in Western countries and is thought to play an important role in the pathogenesis of cardiovascular disorders and diabetes mellitus. Although the etiology of OSAS is uncertain, intense local and systemic inflammation are present in these patients. In the upper airway, this process may promote oropharyngeal inspiratory muscle dysfunction and amplify upper airway narrowing and collapsibility thereby worsening the frequency and duration of apneas during sleep. The presence of systemic inflammation, characterized by elevated levels of certain potent pro-inflammatory mediators, such as C-reactive protein, leptin, TNF-alpha, IL-1beta, IL-6, reactive oxygen species and adhesion molecules, may predispose to the development of cardiovascular complications observed in patients with OSAS. Treatment with nasal CPAP abrogates, in part, local and systemic inflammation in these patients. Whether therapeutic interventions aimed at abating inflammation could be a useful adjunct in the treatment of OSAS merits further investigation.

摘要

阻塞性睡眠呼吸暂停综合征(OSAS)困扰着西方国家约5%的成年人,被认为在心血管疾病和糖尿病的发病机制中起重要作用。尽管OSAS的病因尚不确定,但这些患者存在强烈的局部和全身炎症。在上呼吸道,这个过程可能会促进口咽吸气肌功能障碍,加剧上呼吸道狭窄和塌陷,从而加重睡眠期间呼吸暂停的频率和持续时间。以某些强效促炎介质水平升高为特征的全身炎症,如C反应蛋白、瘦素、肿瘤坏死因子-α、白细胞介素-1β、白细胞介素-6、活性氧和黏附分子,可能使OSAS患者易发生心血管并发症。鼻持续气道正压通气(CPAP)治疗可部分消除这些患者的局部和全身炎症。旨在减轻炎症的治疗干预措施是否可作为OSAS治疗的有用辅助手段值得进一步研究。

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