Pathophysiological role of prostanoids in coagulation of the portal venous system in liver cirrhosis

Background Prostanoids are important regulators of platelet aggregation and thrombotic arterial diseases. Their involvement in the development of portal vein thrombosis, frequent in decompensated liver cirrhosis, is still not investigated. Methods Therefore, we used pro-thrombotic venous milieu generation by bare metal stent transjugular intrahepatic portosystemic shunt insertion, to study the role of prostanoids in decompensated liver cirrhosis. Here, 89 patients receiving transjugular intrahepatic portosystemic shunt insertion were included in the study, and baseline levels of thromboxane B-2, prostaglandin D-2 and prostaglandin E-2 were measured in the portal and the hepatic vein. Results While the hepatic vein contained higher levels of thromboxane B-2 than the portal vein, levels of prostaglandin E-2 and D-2 were higher in the portal vein (all P<0.0001). Baseline concentrations of thromboxane B-2 in the portal vein were independently associated with an increase of portal hepatic venous pressure gradient during short term follow-up, as an indirect sign of thrombogenic potential (multivariable P = 0.004). Moreover, severity of liver disease was inversely correlated with portal as well as hepatic vein levels of prostaglandin D-2 and E-2 (all P<0.0001). Conclusions Elevated portal venous thromboxane B-2 concentrations are possibly associated with the extent of thrombogenic potential in patients with decompensated liver cirrhosis.