Portal vein thrombosis in cirrhosis: Why a well-known complication is still matter of debate

Table 1 Reassessment between anti- and pro-hemostatic drivers in liver cirrhosis

Hemostasis phase	Anti-hemostatic drivers	Pro-hemostatic drivers
Primary hemostasis (vasoconstriction and platelet plug formation)	Thrombocytopenia	Platelet hyperactivity High molecular weight multimers von Willebrand factor levels Low ADAM TS 13 levels and activity
Secondary hemostasis (coagulation cascades)	Low anticoagulant factors levels: AT, protein C and S High procoagulant factor levels: factor VIII	Low procoagulant factors levels: fibrinogen, factor II, V, VII, IX, X, XI
Tertiary hemostasis (fibrinolysis)	Low plasminogen and high PAI levels	High t-PA levels Low TAFI and plasmin inhibitor levels

AT: Antithrombin; ADAM TS 13: A disintegrin-like and metalloproteinase with thrombospondin type 1 motif 13; PAI: Plasminogen activator inhibitor; t-PA: Tissue plasminogen activator; TAFI: Thrombin-activatable fibrinolysis inhibitor[18].