肝硬化中血管性血友病因子与凝血因子VIII的门体循环梯度：对门静脉血栓形成的影响
Von Willebrand and Factor VIII Portosystemic Circulation Gradient in Cirrhosis: Implications for Portal Vein Thrombosis.
作者信息
Praktiknjo Michael, Trebicka Jonel, Carnevale Roberto, Pastori Daniele, Queck Alexander, Ettorre Evaristo, Violi Francesco
机构信息
Department of Medicine I, University of Bonn, Bonn, Germany.
Department of Medicine I, University of Frankfurt, Frankfurt, Germany.
出版信息
Clin Transl Gastroenterol. 2020 Feb;11(2):e00123. doi: 10.14309/ctg.0000000000000123.
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.
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；关于内皮损伤的数据尚缺乏。
方法
对20例接受经颈静脉肝内门体分流术的肝硬化患者的门静脉和体循环中的血管性血友病因子（内皮损伤/扰动的标志物）、凝血因子VIII和脂多糖（LPS）进行了研究。
结果
与体循环相比，门静脉中的血管性血友病因子、凝血因子VIII和LPS水平更高，LPS与其他两个变量之间存在显著相关性。
讨论
肝硬化患者的门静脉系统中存在内皮损伤和高凝状态，两者都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。
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