代谢功能障碍相关脂肪性肝病合并原发性胆汁性胆管炎的中西医临床研究进展

Clinical Research Progress on Metabolic Dysfunction-Associated Steatotic Liver Disease Combined with Primary Biliary Cholangitis: Insights from Western and Traditional Chinese Medicine

摘要: 代谢功能障碍相关脂肪性肝病(metabolic dysfunction-associated steatotic liver disease, MASLD)是全球范围内发病率最高的慢性肝病之一，其病理过程与肥胖、胰岛素抵抗及代谢综合征密切相关。原发性胆汁性胆管炎(primary biliary cholangitis, PBC)是一种以小胆管破坏和胆汁淤积为特征的自身免疫性肝病，近年来合并MASLD的病例逐渐增多，提示两者在病理机制上可能存在交叉与耦合。二者共病不仅加速肝纤维化进展，还显著增加肝硬化与终末期肝病风险，严重威胁患者健康。现代医学研究认为，该类复合病理状态主要涉及代谢异常、免疫炎症反应、肠–肝轴失衡及昼夜节律与表观遗传学改变等多因素协同作用；中医学则从肝、脾、肾功能失调出发，提出肝郁脾虚证、肝胆湿热证及肝肾阴虚证等核心病机，揭示了痰湿、湿热与阴虚贯穿疾病始终的演变规律。本文将从中西医两个角度对MASLD合并PBC的病因病机进行综述，为进一步开展临床与基础研究提供理论依据。

Abstract: Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disease worldwide, and its development is closely linked to obesity, insulin resistance, and metabolic syndrome. Primary biliary cholangitis (PBC), an autoimmune liver disease characterized by progressive bile duct injury and cholestasis, has increasingly been reported in patients with MASLD, suggesting shared and interacting mechanisms. The coexistence of these conditions accelerates hepatic fibrosis and markedly increases the risk of cirrhosis and end-stage liver disease, thereby threatening patient health. Modern medical research indicates that this combined pathophysiology involves metabolic disturbances, immune-inflammatory activation, gut-liver axis imbalance, and alterations in circadian rhythm and epigenetic regulation. From the perspective of traditional Chinese medicine (TCM), dysfunction of the liver, spleen, and kidney constitutes the fundamental pathogenesis, with core syndromes including liver qi stagnation with spleen deficiency, damp-heat accumulation in the liver and gallbladder, and liver-kidney yin deficiency. These patterns underscore the continuous involvement of phlegm-dampness, damp-heat, and yin deficiency in disease progression. This review synthesizes recent evidence from both Western medicine and TCM to elucidate the mechanisms of MASLD complicated by PBC, providing a theoretical basis for further clinical and experimental studies.