门静脉闭塞是胆汁性肝硬化门静脉高压症的诱因。

IF 5.6 2区医学 Q1 ONCOLOGY The Journal of Pathology Pub Date : 2024-03-29 DOI:10.1002/path.6273

Shan Shan, Xinyan Zhao, Michelle A Wood-Trageser, Doudou Hu, Liwei Liu, Beining Qi, Jianbo Jian, Ping Wang, Wenjuan Lv, Chunhong Hu

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引用次数: 0

摘要

人们对门静脉闭塞（OPV）在肝硬化门静脉高压症中的作用知之甚少。为了研究门静脉阻塞对胆汁性肝硬化门静脉高压症的影响及其内在机制，我们使用二维（2D）组织病理学评估了胆道闭锁（BA，63 例）、原发性胆汁性胆管炎（PBC，18 例）和乙型肝炎相关性肝硬化（Hep-B-cirrhosis，35 例）患者肝脏组织中的门静脉阻塞情况。然后，在胆管结扎（BDL）或四氯化碳（CCl4）给药后的两个平行模型中，通过 X 射线相位对比 CT 测量三维（3D）OPV，分别代表胆汁性肝硬化和坏死后肝硬化。同时还测量了两种模型的门静脉压力。最后，研究了胆管增生对 OPV 的影响。通过二维和三维定量分析，我们发现胆汁性肝硬化患者（包括 BA（78.57 ± 16.45%）和 PBC（60.00 ± 17.15%））的 OPV 发生率明显高于 Hep-B 型肝硬化患者（29.43 ± 14.94%，P 4）。BDL 模型的门静脉压力明显高于 CCl4 模型。随着胆管的增生，门静脉被压缩并不可逆地闭塞，导致胆汁性肝硬化的门静脉压力更早升高。OPV 作为窦前静脉成分，在胆汁性肝硬化门静脉高压的发病机制中起着关键作用。增生的胆管和胆囊逐渐占据了原本属于门静脉的 "领地"，并压迫门静脉，这可能会导致胆汁性肝硬化的 OPV。© 2024 大不列颠及爱尔兰病理学会。

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Obliteration of portal venules contributes to portal hypertension in biliary cirrhosis

The effects of the obliteration of portal venules (OPV) in cirrhotic portal hypertension are poorly understood. To investigate its contribution to portal hypertension in biliary cirrhosis and its underlying mechanism, we evaluated OPV using two-dimensional (2D) histopathology in liver explants from patients with biliary atresia (BA, n = 63), primary biliary cholangitis (PBC, n = 18), and hepatitis B-related cirrhosis (Hep-B-cirrhosis, n = 35). Then, three-dimensional (3D) OPV was measured by X-ray phase-contrast CT in two parallel models in rats following bile duct ligation (BDL) or carbon tetrachloride (CCl₄) administration, representing biliary cirrhosis and post-necrotic cirrhosis, respectively. The portal pressure was also measured in the two models. Finally, the effects of proliferative bile ducts on OPV were investigated. We found that OPV was significantly more frequent in patients with biliary cirrhosis, including BA (78.57 ± 16.45%) and PBC (60.00 ± 17.15%), than that in Hep-B-cirrhotic patients (29.43 ± 14.94%, p < 0.001). OPV occurred earlier, evidenced by the paired liver biopsy at a Kasai procedure (KP), and was irreversible even after a successful KP in the patients with BA. OPV was also significantly more frequent in the BDL models than in the CCl₄ models, as shown by 2D and 3D quantitative analysis. Portal pressure was significantly higher in the BDL model than that in the CCl₄ model. With the proliferation of bile ducts, portal venules were compressed and irreversibly occluded, contributing to the earlier and higher portal pressure in biliary cirrhosis. OPV, as a pre-sinusoidal component, plays a key role in the pathogenesis of portal hypertension in biliary cirrhosis. The proliferated bile ducts and ductules gradually take up the ‘territory’ originally attributed to portal venules and compress the portal venules, which may lead to OPV in biliary cirrhosis. © 2024 The Pathological Society of Great Britain and Ireland.

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来源期刊

The Journal of Pathology 医学-病理学

CiteScore

14.10

自引率

1.40%

发文量

144

审稿时长

3-8 weeks

期刊介绍： The Journal of Pathology aims to serve as a translational bridge between basic biomedical science and clinical medicine with particular emphasis on, but not restricted to, tissue based studies. The main interests of the Journal lie in publishing studies that further our understanding the pathophysiological and pathogenetic mechanisms of human disease. The Journal of Pathology welcomes investigative studies on human tissues, in vitro and in vivo experimental studies, and investigations based on animal models with a clear relevance to human disease, including transgenic systems. As well as original research papers, the Journal seeks to provide rapid publication in a variety of other formats, including editorials, review articles, commentaries and perspectives and other features, both contributed and solicited.