28 Jun The portal vein in patients with cirrhosis is not an excessively inflammatory or hypercoagulable vascular bed, a prospective cohort study
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 haemostasis in the portal vein (PV) compared to post-hepatic veins, but as 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.
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 (LPS, TNF-α, IL-6, TBARS), neutrophil-extracellular-traps (cfDNA, MPO-DNA), endothelial damage (VWF) and haemostasis were determined and compared between 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 haemostasis were modestly elevated in the PV. Levels of multiple markers were lower in the HV compared to the PV and systemic circulation. Higher MELD 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.