|Molecular mass||55 000 D|
|Half life||30 - 60 hours|
|Plasma concentration||10 mg/l|
|Normal range||70 - 120% or 0.7 - 1.2 U/ml|
The vitamin K-dependent factor X is a central enzyme of the coagulation cascade. It can be activated by the intrinsic pathway through the tenase complex consisting of factor IXa, factor VIIIa, phospholipids and calcium ions or by the complex of tissue factor and factor VIIa of the extrinsic pathway. Factor Xa is a serine protease and forms together with factor Va, phospholipids and calcium ions the prothrombinase complex, by which prothrombin (factor II) is activated to thrombin (factor IIa). Factor Va acts as a cofactor, which amplifies this activation step a thousandfold.
The rare hereditary form of factor X deficiency is autosomal recessively inherited. As with all vitamin K-dependent factors an acquired deficiency results from vitamin K-deficiency or coumarin therapy. Hepatic disorders, L-asparaginase therapy and DIC lead to reduced FX levels. The symptoms of a factor X deficiency extend from articular and mucosal bleedings to postoperative and cerebral bleedings. Increased factor X activities are observed during vitamin K-administration and in hyperlipidaemia.
- of anticoagulant diagnosis of a to date unknown hereditary bleeding disorder
- Reason for pathological INR values
- Adjustment of INR in patients with pathological Quick values due to inhibitors
- Monitoring of plasma levels during anticoagulant therapy with heparin or coumarin derivatives (during the transition phase) and during a fibrinolytic therapy
- Monitoring of plasma levels during anticoagulant therapy with thrombin inhibitors
- Differential diagnosis between synthesis disorder and increased consumption
- Monitoring therapy in patients with phospholipid antibody syndrome
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