Non-neoplastic portal vein thrombosis in HCV cirrhosis: the weight of inflammation on a fragile hemostatic balance
The historical paradigm of spontaneous bleeding tendency of cirrhosis as consequence of an intrinsic coagulopathy has faded in the last years (1). This theory has been first challenged by milestones studies of Tripodi et al. demonstrating normal thrombin generation by plasma from cirrhotic patients and, consequently, the need of more comprehensive coagulation tests to evaluate hemostatic changes in advanced chronic liver disease (2). This is coherent with the clinical observation of thrombotic events occurring among cirrhotic patients, despite altered prothrombin- and partial thromboplastin-time, which are inadequate to evaluate the profound changes in balance between pro- and anti-coagulant factors alongside the disruption of liver function (3,4). Moreover, plasma from patients with cirrhosis shows a pro-coagulant imbalance alongside disease severity, as expressed by the resistance to the action of thrombomodulin, a strong anti-coagulant factor (5).