Driever Ellen G, Lisman Ton
Surgical Research Laboratory, Department of Surgery, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Res Pract Thromb Haemost. 2023 Jan 20;7(1):100055. doi: 10.1016/j.rpth.2023.100055. eCollection 2023 Jan.
Patients with cirrhosis frequently acquire profound hemostatic alterations, which may affect thrombus quality and composition-factors that determine the susceptibility to embolization and fibrinolysis. In this narrative review, we describe studies on fibrin clot formation and quantitative and qualitative changes in fibrinogen in patients with cirrhosis, and describe recent findings on the composition of portal vein thrombi in patients with cirrhosis. Patients with mild cirrhosis have increased thrombin generation capacity and plasma fibrinogen levels, which may be balanced by delayed fibrin polymerization and decreased factor XIII levels. With progressing illness, plasma fibrinogen levels decrease, but thrombin generation capacity remains elevated. Fibrinogen is susceptible to posttranslational protein modifications and is, for example, hypersialylated and carbonylated in patients with cirrhosis. Despite changes in thrombin generation, factor XIII levels and the fibrinogen molecule, fibrin fiber thickness, and density are normal in patients with cirrhosis. Paradoxically, fibrin clot permeability in patients with cirrhosis is decreased, possibly because of posttranslational protein modifications. Most patients have normal fibrinolytic potential. We have recently demonstrated that portal vein thrombosis is likely a misnomer as the material that may obstruct the cirrhotic portal vein frequently consists of a thickened portal vein wall, rather than a true thrombus. Patients with cirrhosis often have thrombocytopenia and anemia, which may also affect clot stability and composition, but the role of cellular components in clot quality in cirrhosis has not been extensively studied. Finally, we summarize abstracts on fibrin formation and clot quality that were presented at the ISTH 2022 meeting in London.
肝硬化患者常常会出现严重的止血功能改变，这可能会影响血栓的质量和组成，而这些因素决定了对栓塞和纤维蛋白溶解的易感性。在这篇叙述性综述中，我们描述了关于肝硬化患者纤维蛋白凝块形成以及纤维蛋白原定量和定性变化的研究，并阐述了肝硬化患者门静脉血栓组成的最新研究结果。轻度肝硬化患者的凝血酶生成能力和血浆纤维蛋白原水平升高，不过这可能会被延迟的纤维蛋白聚合和降低的因子 XIII 水平所平衡。随着病情进展，血浆纤维蛋白原水平降低，但凝血酶生成能力仍保持升高。纤维蛋白原易受翻译后蛋白质修饰的影响，例如，肝硬化患者的纤维蛋白原会出现高度唾液酸化和羰基化。尽管凝血酶生成、因子 XIII 水平以及纤维蛋白原分子发生了变化，但肝硬化患者的纤维蛋白纤维厚度和密度仍属正常。矛盾的是，肝硬化患者的纤维蛋白凝块通透性降低，这可能是由于翻译后蛋白质修饰所致。大多数患者的纤维蛋白溶解潜能正常。我们最近证实，门静脉血栓形成可能是一个误称，因为阻塞肝硬化门静脉的物质通常由增厚的门静脉壁组成，而非真正的血栓。肝硬化患者常伴有血小板减少症和贫血，这也可能影响凝块的稳定性和组成，但细胞成分在肝硬化凝块质量中的作用尚未得到广泛研究。最后，我们总结了在伦敦举行的 2022 年国际血栓与止血学会会议上发表的关于纤维蛋白形成和凝块质量的摘要。
