炎症性肠病与阻塞性睡眠呼吸暂停之间的机制性相互作用。

文献信息

中文摘要

炎症性肠病（IBD），包括克罗恩病（CD）和溃疡性结肠炎（UC），日益被认为与阻塞性睡眠呼吸暂停（OSA）相关。近期队列研究和荟萃分析将IBD确定为OSA的独立危险因素，支持对IBD患者进行OSA筛查并管理可改变的危险因素。然而，这些关联主要来自观察性研究，几乎没有验证性机制研究。此外，关于OSA与IBD之间关联的现有临床和实验证据高度异质，且来自多学科来源，提示这种关联可能反映多种共享的生物学机制，而非简单的疾病共存。IBD相关炎症、上皮屏障功能障碍、免疫失调、肠道菌群失调，以及OSA相关的间歇性缺氧、氧化应激、免疫激活、肠道屏障功能障碍和肠道菌群失调，似乎是建立连接肠道与呼吸病理生理学的自我强化循环的关键相互过程。本理论综述综合了临床、实验和机制研究中的多学科异质性证据，以提出假设生成性的肠道屏障-微生物群-免疫-缺氧（GBMIH）框架。这一假设生成性的系统理论强调肠道屏障破坏、菌群失调、免疫激活和间歇性缺氧是可能介导这种双向关系的相互关联的生物学节点，并定义了未来的生物标志物和治疗开发方向。

英文摘要

Inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), is increasingly recognized as being associated with obstructive sleep apnea (OSA). Recent cohort studies and meta-analyses identify IBD as an independent risk factor for OSA, supporting the need for OSA screening in patients with IBD and management of modifiable risk factors. However, these associations come primarily from observational studies with virtually no confirmatory mechanistic studies. Further, the available clinical and experimental evidence of an association between OSA and IBD is highly heterogeneous and comes from multidisciplinary sources, suggesting that the association may reflect multiple shared biological mechanisms rather than simple disease coexistence. IBD-associated inflammation, epithelial barrier dysfunction, immune dysregulation, gut dysbiosis, and OSA-associated intermittent hypoxia, oxidative stress, immune activation, gut barrier dysfunction, and gut dysbiosis appear to be the key reciprocal processes establishing a self-reinforcing cycle that links intestinal and respiratory pathophysiology. This theoretical review synthesizes multidisciplinary heterogeneous evidence across clinical, experimental, and mechanistic studies to develop the hypothesis-generating Gut Barrier-Microbiota-Immune-Hypoxia (GBMIH) framework. This hypothesis-generating systems theory highlights intestinal barrier disruption, dysbiosis, immune activation, and intermittent hypoxia as interconnected biological nodes that may mediate this bidirectional relationship and define future biomarker and therapeutic development.