肥胖相关睡眠呼吸障碍中的体重管理：机制、临床管理与新兴疗法。
Weight Management in Obesity-Associated Sleep-Disordered Breathing: Mechanisms, Clinical Management, and Emerging Therapies.
文献信息
| PMID | 42855133 |
|---|---|
| 原文 | 在 PubMed 查看原文 ↗ |
| 发表日期 | 2026 |
| 作者 | Ron T Varghese |
| 作者单位 | Assistant Professor, Sleep - Endocrinology Clinic, Bascom Palmer, University of Miami Miller School of Medicine, Miami, Florida, USA; Assistant Professor, Division of Endocrinology, Department of Internal Medicine, University of Miami Miller School of Medicine, Miami, Florida, USA; Department of Internal Medicine, Jackson Memorial Hospital, Miami, FL, United States. Electronic address: rxv492@miami.edu. |
| 期刊 | Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists |
| SCI 分区 | Q2 |
| IF | 4.4 |
| 研究类型 | 综述 Meta · 临床 |
| 所属专科 | 鼻科 |
中文摘要
目的： 综述肥胖与睡眠呼吸障碍（SDB）之间的机制联系，并总结针对体重、针对睡眠以及基于表型的实用管理方法。
方法： 我们对通过PubMed/MEDLINE、Embase和Google Scholar检索到的临床试验、系统综述、荟萃分析、指南和机制研究进行了聚焦的叙述性综述。检索词包括肥胖、阻塞性睡眠呼吸暂停、肥胖低通气综合征、体重减轻、气道正压、减重手术、基于肠促胰岛素的药物治疗、内型以及昼夜节律紊乱。
结果： 肥胖通过上气道机械负荷、肺容积减少、炎症、通气控制改变和睡眠行为途径促进睡眠呼吸障碍。气道正压仍是许多阻塞性睡眠呼吸暂停和肥胖低通气综合征患者的核心治疗。持续体重减轻可提供互补的疾病修饰作用。生活方式干预、代谢与减重手术以及基于肠促胰岛素的药物治疗可以改善阻塞性睡眠呼吸暂停，尽管残余疾病常见。替尔泊肽在肥胖合并中度至重度阻塞性睡眠呼吸暂停的成人中显示出呼吸暂停低通气指数的临床意义降低，主要与体重减轻相关。在肥胖低通气综合征中，稳定的门诊患者通常需要气道正压。可能需要约25%至30%的持久体重减轻才能解决低通气。针对内型的疗法和基于设备的选项可能有助于选定患者，但它们仍为辅助性、研究性或由专科医生指导。
结论： 肥胖相关睡眠呼吸障碍最好作为一种异质性心脏代谢和睡眠呼吸状况进行管理。治疗应将气道正压或其他睡眠特异性治疗与个体化体重管理相结合。需要持续重新评估残余疾病、肥胖低通气综合征和非典型表型。
英文摘要
OBJECTIVE: To review the mechanistic links between obesity and sleep-disordered breathing (SDB) and summarize practical approaches to weight-directed, sleep-directed, and phenotype-informed management.
METHODS: We conducted a focused narrative review of clinical trials, systematic reviews, meta-analyses, guidelines, and mechanistic studies identified through PubMed/MEDLINE, Embase, and Google Scholar. Search terms included obesity, obstructive sleep apnea, obesity hypoventilation syndrome, weight loss, positive airway pressure, bariatric surgery, incretin-based pharmacotherapy, endotypes, and circadian disruption.
RESULTS: Obesity promotes sleep-disordered breathing through upper airway mechanical loading, reduced lung volumes, inflammation, altered ventilatory control, and sleep behavior pathways. Positive airway pressure remains a core therapy for many patients with obstructive sleep apnea and obesity hypoventilation syndrome. Sustained weight loss provides complementary disease modification. Lifestyle intervention, metabolic and bariatric surgery, and incretin based pharmacotherapy can improve obstructive sleep apnea, although residual disease is common. Tirzepatide has shown clinically meaningful reductions in apnea-hypopnea index in adults with obesity and moderate to severe obstructive sleep apnea, largely in association with weight reduction. In obesity hypoventilation syndrome, stable ambulatory patients generally require positive airway pressure. Durable weight loss of approximately 25% to 30% may be needed to resolve hypoventilation. Therapies targeting endotypes and device based options may help selected patients, but they remain adjunctive, investigational, or directed by specialists.
CONCLUSION: Obesity associated sleep-disordered breathing is best managed as a heterogeneous cardiometabolic and sleep breathing condition. Treatment should integrate positive airway pressure or other sleep specific therapy with individualized weight management. Ongoing reassessment is needed for residual disease, obesity hypoventilation syndrome, and atypical phenotypes.