Surgical Research Laboratory and Section of Hepatobiliary Surgery and Liver Transplantation, Department of Surgery, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Barcelona Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clínic, Institut de Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain.
J Thromb Haemost. 2022 Sep;20(9):2075-2082. doi: 10.1111/jth.15797. Epub 2022 Jul 11.
A hypercoagulable state is not associated with development of portal vein thrombosis in cirrhosis, as we previously demonstrated. However, some groups demonstrated elevated levels of inflammatory markers and activation of hemostasis in the portal vein (PV) compared to posthepatic veins, but because the liver is involved in clearance of these markers, we hypothesize that interpretation of these data is not straightforward.
To determine whether the PV has particular proinflammatory/hypercoagulable characteristics by comparing plasma sampled in the PV, hepatic vein (HV), and the systemic circulation.
Plasma samples from 51 cirrhotic patients with portal hypertension undergoing transjugular intrahepatic portosystemic shunt placement, were taken from the PV, HV, and jugular vein (JV). Markers of inflammation (lipopolysaccharide, tumor necrosis factor-α, interleukin-6, thiobarbituric acid-reactive substances), neutrophil-extracellular-traps (cfDNA, MPO-DNA), endothelial damage (von Willebrand factor [VWF]), and hemostasis were determined and compared among the three vascular beds.
Markers of inflammation were slightly, but significantly higher in the PV than in the HV and systemic circulation. VWF and markers of hemostasis were modestly elevated in the PV. Levels of multiple markers were lower in the HV compared with the PV and systemic circulation. Higher model for end-stage liver disease score was associated with a more prothrombotic state in all three sample sites.
In contrast to published studies, we did not detect a clear proinflammatory or prothrombotic environment in the PV of cirrhotic patients. Many markers are lowest in the HV, indicating that the low levels of these markers in the HV, at least in part, reflect clearance of those markers in the liver.
我们之前已经证明，高凝状态与肝硬化门静脉血栓形成无关。然而，一些研究小组发现门静脉（PV）中的炎症标志物和止血系统的活性水平高于肝后静脉，但由于肝脏参与这些标志物的清除，我们假设这些数据的解释并不简单。
通过比较在 PV、肝静脉（HV）和体循环中取样的血浆，确定 PV 是否具有特殊的促炎/高凝特征。
对 51 例接受经颈静脉肝内门体分流术的门静脉高压症肝硬化患者进行研究，从 PV、HV 和颈静脉（JV）采集血浆样本。测定炎症标志物（内毒素、肿瘤坏死因子-α、白细胞介素-6、硫代巴比妥酸反应物质）、中性粒细胞细胞外陷阱（cfDNA、MPO-DNA）、内皮损伤（血管性血友病因子 [VWF]）和止血，并比较三个血管床之间的差异。
PV 中的炎症标志物略高于 HV 和体循环，但差异具有统计学意义。PV 中的 VWF 和止血标志物略有升高。HV 中的多种标志物水平低于 PV 和体循环。更高的终末期肝病模型评分与三个采样部位的血栓形成状态更为相关。
与已发表的研究不同，我们未在肝硬化患者的 PV 中检测到明确的促炎或促血栓形成环境。许多标志物在 HV 中水平最低，表明 HV 中这些标志物的低水平至少部分反映了肝脏对这些标志物的清除。
