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Factor VII is the first coagulation protein to decrease when there is a hepatocyte damage, probably because of its short half-life (2-4h) [28,29].
The disease is caused by deficient or defective blood coagulation proteins, known as factor VIII or IX.
Thrombin, factors Xa and VIIa, in addition to their roles in activating coagulation protein zymogens, can interact with specific cell receptors and activate intracellular signaling pathways that mediate inflammatory responses.
Drugs (see Table 4) Wiskott-Aldrich syndrome, May-Hegglin anomaly Systemic illness (liver disease, myeloproliferative disorder, infection) Platelet dysfunction Drugs Myeloproliferative disorder Von Willebrand disease Thrombocytopenia Absent Radius (TAR) syndrome Bernard-Soulier Glanzmann thrombasthenia Storage disease Renal disease Coagulation protein disorders Hemophilia (factor VIII, IX, XI deficiency) Von Willebrand disease Dysfibrinogenemia Factor XIII Plasmin or plasminogen deficiency or inhibitor Circulating anticoagulant or inhibitor Vitamin K deficiency, warfarin therapy Systemic illnesses (liver disease, amyloidosis) Table 2.
Recombinant factor VIII and factor IX products, designed for hemophilia patients with deficiencies of these respective circulating coagulation proteins, are not derived from human plasma.