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

Authors
Alexander Queck, Dominique Thomas, Christian Jansen, Yannick Schreiber, Sabrina Rüschenbaum, Michael Praktiknjo, Katharina Maria Schwarzkopf, Marcus Maximilian Mücke, Robert Schierwagen, Frank Erhard Uschner, Carsten Meyer, Joan Clària, Stefan Zeuzem, Gerd Geisslinger, Jonel Trebicka, Christian Markus Lange

Abstract
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 B2, prostaglandin D2 and prostaglandin E2 were measured in the portal and the hepatic vein.

Results
While the hepatic vein contained higher levels of thromboxane B2 than the portal vein, levels of prostaglandin E2 and D2 were higher in the portal vein (all P<0.0001). Baseline concentrations of thromboxane B2 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 D2 and E2 (all P<0.0001).

Conclusions
Elevated portal venous thromboxane B2 concentrations are possibly associated with the extent of thrombogenic potential in patients with decompensated liver cirrhosis.

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