Platelet aggregation as a thrombotic marker in cirrhotic patients with portal vein thrombosis.

Abstract

Aim of the study: 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 in vitro platelet function to identify its possible role in the development of PVT in cirrhosis.

Material and methods: 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.

Results: 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 (p = 0.004), D-dimer (p = 0.011), platelet count (p = 0.001), platelet aggregation following stimulation with ADP and ristocetin (p < 0.001, p = 0.023, respectively) and vWF-Ag concentration (p = 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.

Conclusions: 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.