Bitto Niccolò, Ghigliazza Gabriele, Lavorato Stanislao, Caputo Camilla, La Mura Vincenzo
Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Angelo Bianchi Bonomi Hemophilia and Thrombosis Center, 20122 Milan, Italy.
Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Division of Sub-Intensive Care Medicine, 20122 Milan, Italy.
J Clin Med. 2023 Jan 25;12(3):934. doi: 10.3390/jcm12030934.
Portal hypertension is the consequence of cirrhosis and results from increased sinusoidal vascular resistance and hepatic blood inflow. Etiological therapies represent the first intervention to prevent a significant increase in portal pressure due to chronic liver damage. However, other superimposed pathophysiological drivers may worsen liver disease, including inflammation, bacterial translocation, endothelial dysfunction, and hyperactivation of hemostasis. These mechanisms can be targeted by a specific class of drugs already used in clinical practice. Albumin, rifaximin, statins, aspirin, and anticoagulants have been tested in cirrhosis and were a topic of discussion in the last Baveno consensus as non-etiological therapies. Based on the pathogenesis of portal hypertension in cirrhosis, our review summarizes the main mechanisms targeted by these drugs as well as the clinical evidence that considers them a valid complementary option to manage patients with cirrhosis and portal hypertension.
门静脉高压是肝硬化的后果,由肝血窦血管阻力增加和肝血流增多所致。病因治疗是预防慢性肝损伤导致门静脉压力显著升高的首要干预措施。然而,其他叠加的病理生理驱动因素可能会使肝病恶化,包括炎症、细菌移位、内皮功能障碍和止血系统的过度激活。这些机制可以通过临床实践中已使用的一类特定药物来靶向作用。白蛋白、利福昔明、他汀类药物、阿司匹林和抗凝剂已在肝硬化患者中进行了试验,并且在最近的巴韦诺共识会议上作为非病因治疗方法进行了讨论。基于肝硬化门静脉高压的发病机制,我们的综述总结了这些药物所靶向的主要机制,以及将它们视为管理肝硬化和门静脉高压患者的有效补充方案的临床证据。