Coagulation factor X testing is used to diagnose congenital or acquired factor deficiency, assess hemostatic function in liver disease, and investigate prolonged prothrombin or activated partial thromboplastin time.
Factor X is a vitamin K-dependent serine protease synthesized in the liver. Its biological half-life is 24 to 48 hours. Factor X participates in the intrinsic and extrinsic coagulation pathways (final common pathway) by serving as an enzyme (factor Xa) in the prothrombinase complex. Congenital factor X deficiency is rare. Acquired deficiency is associated with liver disease, warfarin therapy, vitamin K deficiency, systemic amyloidosis, and rarely with the presence of inhibitors. Deficiency can cause prolonged prothrombin time and activated partial thromboplastin time.
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Platelets accumulate in the area of injury whenever there is tissue damage or blood vessel injury. They release factors that initiate the coagulation process (hemostasis). The initial type of injury dictates which pathway the process will proceed through.
The endogenous pathway is involved when blood is damaged or exposed to the collagen of the walls of injured blood vessels. It requires the sequential activation of several coagulation factors: factor XII (Hageman factor), factor XI, factor IX (Christmas factor), and factor VIII.
The extrinsic pathway begins when tissues or the vascular wall are damaged. In this pathway, coagulation is triggered by the release of tissue thromboplastin (factor III) from the damaged vessel or tissue cells. When this substance meets factor VII, the extrinsic pathway is stimulated.
Both pathways eventually lead to the activation of coagulation factor X. This leads to the next step, in which prothrombin (factor II) is converted to thrombin (factor IIa [activated]). Thrombin then stimulates the formation of fibrin (factor Ia) by fibrinogen (factor I). This fibrin, by adding the fibrin stabilizing factor (XIII), forms a fixed fibrin clot at the injury site. When the fibrin clot is no longer needed, fibrinolytic agents, such as plasmin, dissolve it, producing fibrin degradation products. Any of the above coagulation factors remaining after hemostasis are inactivated by fibrin inhibitors, such as antiplasmin, antithrombin III, and protein C.
The action of the coagulation factors determines whether each factor has a congenital or acquired deficiency. These tests help diagnose hemophilia and coagulation disorders.
Possible Interpretations of Pathological Values
- Increase: Pregnancy
- Decrease: Congenital insufficiency, diffuse intravascular coagulation, liver disease, vitamin K deficiency
Important Note
Laboratory test results are the most critical parameter for diagnosing and monitoring all pathological conditions. Between 70 to 80% of diagnostic decisions are based on laboratory tests. Correctly interpreting laboratory results allows a doctor to distinguish "healthy" from "diseased."
Laboratory test results should not be interpreted from the numerical result of a single analysis. Test results should be analyzed based on each case and family history, clinical findings, and the results of other laboratory tests and information. Your physician should explain the importance of your test results.
At Diagnostiki Athinon, we answer any questions you may have about the test you perform in our laboratory and contact your doctor to ensure you receive the best possible medical care.
