OBJECTIVES Portal vein thrombosis seems to be dependent on local hypercoagulation and venous stasis; data regarding endothelial damage are lacking. METHODS von Willebrad factor, a marker of endothelial damage/perturbation, factor VIII, and lipopolysaccharides (LPS) were studied in the portal and systemic circulation of 20 cirrhotic patients undergoing transjugular intrahepatic portosystemic procedure. RESULTS von Willebrad factor, factor VIII, and LPS were higher in the portal compared with systemic circulation, with a significant correlation between LPS and the other 2 variables. DISCUSSION Endothelial damage and hypercoagulation coexist in the portal tree of patients with cirrhosis, and both could contribute to portal vein thrombosis. LPS may be a potential trigger of endothelial damage.

中文翻译：

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Von Willebrand 和 VIII 因子门体循环梯度在肝硬化中：对门静脉血栓形成的影响。

目的 门静脉血栓形成似乎依赖于局部高凝状态和静脉淤滞；缺乏关于内皮损伤的数据。方法 在 20 名接受经颈静脉肝内门体手术的肝硬化患者的门静脉和体循环中研究血管性血友病因子、内皮损伤/扰动的标志物、因子 VIII 和脂多糖 (LPS)。结果 与体循环相比，门静脉中的 von Willebrad 因子、VIII 因子和 LPS 较高，LPS 与其他 2 个变量之间存在显着相关性。讨论 肝硬化患者门静脉树中内皮损伤和高凝状态并存，两者均可能导致门静脉血栓形成。LPS 可能是内皮损伤的潜在触发因素。