Abdallah Heba M, Elbassal Fathia, Saber Eman M, Sabry Aliaa, Hendy Olfat M, Nassar Mervat R, Al-Morshedy Suzan M
Department of Clinical Pathology, National Liver Institute, Menoufia University, Shebin EL-Kom, Menoufia, Egypt.
Department of Clinical Pathology, Faculty of Medicine, Menoufia University, Shebin EL-Kom, Menoufia, Egypt.
Clin Exp Hepatol. 2025 Jun;11(2):179-189. doi: 10.5114/ceh.2025.151827. Epub 2025 Jun 12.
Portal vein thrombosis (PVT) is frequently observed in liver cirrhosis patients and correlates with the severity of the underlying liver disease. Thrombocytopenia and thrombocytopathy are signs of liver cirrhosis. A disruption in platelet function may have an impact on the development of thrombosis, considering that platelets are essential in the formation of thrombosis. Previous studies on platelet function in liver disease have not been conclusive; therefore, this study aimed to evaluate platelet function to identify its possible role in the development of PVT in cirrhosis.
The study included 100 subjects (30 cirrhotic patients with PVT, 40 cirrhotic without PVT, and 30 healthy individuals as a control group). Platelet function was evaluated using light transmission aggregometry (LTA) in addition to serum von Willebrand factor antigen (vWF-Ag) to assess the platelet activation and adhesion function.
Platelet aggregation was decreased in response to aggregating agonists (ADP and ristocetin) in cirrhotic patients with and without PVT compared to healthy controls. Notably, among cirrhotic patients, platelet aggregation was higher in those with PVT compared to those without. Univariate analysis identified six PVT-associated factors: Child-Pugh classification ( = 0.004), D-dimer ( = 0.011), platelet count ( = 0.001), platelet aggregation following stimulation with ADP and ristocetin ( < 0.001, = 0.023, respectively) and vWF-Ag concentration ( = 0.001). After adjusting multiple confounding variables, multivariate analysis revealed that only vWF-Ag level was an independent risk factor for PVT pathogenesis in cirrhosis.
Platelet aggregation is significantly higher in cirrhotic PVT patients compared to non-PVT patients. Additionally, elevated vWF-Ag level is an independent risk factor for PVT development in cirrhotic patients. These findings suggest the role of platelet activation in the pathogenesis of PVT and could enhance critical care strategies in patient management and prevention of PVT.
门静脉血栓形成（PVT）在肝硬化患者中较为常见，且与潜在肝脏疾病的严重程度相关。血小板减少和血小板病是肝硬化的体征。考虑到血小板在血栓形成中至关重要，血小板功能的破坏可能会对血栓形成的发展产生影响。先前关于肝病中血小板功能的研究尚无定论；因此，本研究旨在评估血小板功能，以确定其在肝硬化患者PVT发生发展中的可能作用。
该研究纳入了100名受试者（30例患有PVT的肝硬化患者、40例无PVT的肝硬化患者以及30名健康个体作为对照组）。除了使用血清血管性血友病因子抗原（vWF-Ag）评估血小板激活和黏附功能外，还采用光透射聚集法（LTA）评估血小板功能。
与健康对照组相比，患有和未患有PVT的肝硬化患者对聚集激动剂（ADP和瑞斯托霉素）的血小板聚集反应均降低。值得注意的是，在肝硬化患者中，患有PVT的患者血小板聚集率高于未患PVT的患者。单因素分析确定了六个与PVT相关的因素：Child-Pugh分级（P = 0.004）、D-二聚体（P = 0.011）、血小板计数（P = 0.001）、ADP和瑞斯托霉素刺激后的血小板聚集率（分别为P < 0.001、P = 0.023）以及vWF-Ag浓度（P = 0.001）。在调整多个混杂变量后，多因素分析显示，只有vWF-Ag水平是肝硬化患者PVT发病机制的独立危险因素。
与无PVT的肝硬化患者相比，患有PVT的肝硬化患者血小板聚集率显著更高。此外，vWF-Ag水平升高是肝硬化患者PVT发生的独立危险因素。这些发现提示血小板激活在PVT发病机制中的作用，并可能加强患者管理和预防PVT的重症护理策略。
