TAFI Quick Facts
- IUB denotation: EC 18.104.22.168
- Molecular mass: 60 000 D
- Synthesis: Liver
- Plasma concentration: approx. 2.5μg/ml
Biochemistry of TAFI
TAFI (Plasma Procarboxy Peptidase B, Plasma Procarboxy Peptidase U) is synthesized in the liver and circulates in plasma as a proenzyme, to a certain extent in complex with plasminogen. Its main path of activation to TAFIa is mediated by the thrombin/thrombomodulin-complex, but activation by thrombin alone or plasmin is also possible. TAFIa inhibits fibrinolysis by cleaving off C-terminal lysin residues from fibrin. This prevents t-PA and plasminogen to bind to fibrin, subsequently leading to a delayed clot lysis.
Clinical significance of TAFI
An increased level of TAFI leads to a state of hyperfibrinolysis, causing such subjects to have an elevated risk of thrombosis. Additionally, another patophysiologic function of TAFI is also debated: Activated TAFI inhibits a premature lysis of a thrombus. Subjects with factor VIII or factor IX deficiency (hemophilia A or B) suffer from a premature lysis of the fibrin clot due to the low prothrombin activation, which in turn, leads to a deficiency of activated TAFI. Discussions are ongoing whether the bleeding complications in subjects with hemophilia A or B could be a result of a defect in stabilization rather than the missing formation of a thrombus.
Clinical or Research use of of TAFI
- Differential diagnosis in hemorrhagic diathesis
- Idiopathic thromboembolism