睡眠呼吸障碍与脂肪性肝病肝脏结局之间的关联：一项系统综述和荟萃分析。

文献信息

中文摘要

背景： 睡眠呼吸障碍（SDB），包括阻塞性睡眠呼吸暂停（OSA），已通过间歇性缺氧、氧化应激、炎症和代谢功能障碍等途径与脂肪性肝病患者的肝脏病理发展相关联。本系统综述和荟萃分析探讨了SDB与脂肪性肝病（代谢功能障碍相关脂肪性肝病（MASLD）和代谢功能障碍相关脂肪性肝炎（MASH））患者肝脏结局之间的关系。
方法： 综述按照PRISMA 2020指南进行。使用广泛的检索策略检索了PubMed/MEDLINE、Embase、Scopus、Web of Science核心合集、Cochrane CENTRAL、CINAHL数据库从建库至2026年5月15日的文献。偏倚评估和证据分级分别通过设计特异性标准和GRADE系统进行。本综述的方案已在PROSPERO注册（CRD420261384244）。
结果： 最终分析纳入了22篇文章。SDB患者中MASLD或肝脂肪变性的合并患病率为75.1%（95% CI 64.1-83.6%），但异质性为中等（I2 = 94.8%）。肝纤维化或纤维化风险的合并患病率为13.9%（95% CI 6.0-29.0%，I2 = 96.8%）。SDB的存在或OSA严重程度的增加与MASLD或脂肪变性的更高概率显著相关（OR 3.62，95% CI 1.59-8.25，I2 = 84.1%）。持续气道正压通气（CPAP）治疗显示丙氨酸氨基转移酶（平均差 -7.15 U/L，95% CI -9.50至-4.80；I2 = 35.9%）和天冬氨酸氨基转移酶（平均差 -3.38 U/L，95% CI -4.45至-2.30；I2 = 0.0%）水平降低。基于定性综合，夜间低氧血症指标与肝损伤的关联比呼吸暂停低通气指数（AHI）更强。同时，对照CPAP试验未能显示对肝脏结构（脂肪变性、纤维化、肝脏硬度及MASH相关参数）的一致效应。所有结局的证据确定性范围为低至极低。
结论： 睡眠呼吸障碍与大量肝脂肪变性病例及更高的MASLD几率相关，而纤维化结局的证据不一致。CPAP治疗显示生化肝损伤标志物改善，然而，由于研究设计、CPAP治疗依从性和随访时间的异质性，CPAP对肝脏结构的影响仍无定论。需要进一步的高质量前瞻性试验来评估SDB治疗对脂肪性肝病进展的影响。
系统综述注册： PROSPERO，CRD420261384244。

英文摘要

BACKGROUND: Sleep-disordered breathing (SDB) including obstructive sleep apnea (OSA) has been linked to liver pathology development in patients with steatotic liver disease via pathways of intermittent hypoxia, oxidative stress, inflammation, and metabolic dysfunction. This systematic review and meta-analysis examined the relationship between SDB and liver outcomes in patients with steatotic liver disease (metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH)).
METHODS: Review was performed according to PRISMA 2020 guidelines. The extensive search strategy was used for searching literature in databases PubMed/MEDLINE, Embase, Scopus, Web of Science Core Collection, Cochrane CENTRAL, CINAHL from inception to 15 May 2026. Bias assessment and grading of evidence were performed by design-specific criteria and using GRADE system correspondingly. The protocol for this review was registered in PROSPERO (CRD420261384244).
RESULTS: Twenty-two articles were included in the final analysis. Pooled prevalence of MASLD or hepatic steatosis among patients with SDB was 75.1% (95% CI 64.1-83.6%), however heterogeneity was moderate (I2 = 94.8%). The pooled prevalence of liver fibrosis or fibrosis risk was 13.9% (95% CI 6.0-29.0%, I2 = 96.8%). The presence of SDB or an increase in severity of OSA was significantly linked with higher probability of MASLD or steatosis (OR 3.62, 95% CI 1.59-8.25, I2 = 84.1%). The continuous positive airway pressure (CPAP) therapy showed reductions in alanine aminotransferase (mean difference -7.15 U/L, 95% CI -9.50 to -4.80; I2 = 35.9%) and aspartate aminotransferase (mean difference -3.38 U/L, 95% CI -4.45 to -2.30; I2 = 0.0%) levels. Based on qualitative synthesis, the measures of nocturnal hypoxemia were associated with liver damage stronger compared to apnea-hypopnea index (AHI). Meanwhile controlled CPAP trials failed to show consistent effects on structure of liver (steatosis, fibrosis, liver stiffness, and MASH-related parameters). Certainty of evidence ranged from low to very low for all outcomes.
CONCLUSION: Sleep-disordered breathing was linked to a significant number of liver steatosis cases and higher odds of MASLD, while evidence on fibrosis outcomes was inconsistent. CPAP therapy showed improvements in biochemical liver injury markers, however, effect of CPAP on structure of liver remained inconclusive due to heterogeneity in study design, adherence to CPAP treatment and duration of follow-up. Further high-quality prospective trials are required to assess influence of SDB treatment on steatotic liver disease progression.
SYSTEMATIC REVIEW REGISTRATION: PROSPERO, CRD420261384244.