4.6 Article

The portal vein in patients with cirrhosis is not an excessively inflammatory or hypercoagulable vascular bed, a prospective cohort study

Journal

JOURNAL OF THROMBOSIS AND HAEMOSTASIS
Volume 20, Issue 9, Pages 2075-2082

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1111/jth.15797

Keywords

cirrhosis; coagulation; inflammation; portal vein thrombosis

Funding

  1. Instituto de Salud Carlos III [PI20/00569, PI21/00131]
  2. Ministerio de Educacion y Ciencia [SAF PID2019-105/48RB-100]
  3. Trombosestichting Nederland [2018-02]

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This study aimed to determine whether the portal vein (PV) has specific proinflammatory/hypercoagulable characteristics by comparing plasma sampled in the PV, hepatic vein (HV), and the systemic circulation. The results showed that although there were slightly higher levels of inflammatory markers in the PV, there was no clear proinflammatory or prothrombotic environment in the PV of cirrhotic patients. Multiple markers were found to be lower in the HV compared to the PV and systemic circulation, indicating that the liver plays a role in the clearance of these markers.
Background 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. Aim To determine whether the PV has particular proinflammatory/hypercoagulable characteristics by comparing plasma sampled in the PV, hepatic vein (HV), and the systemic circulation. Methods 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-alpha, 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. Results 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. Conclusion 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.

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