Coagulation factor VIII testing is used to diagnose hemophilia A, to diagnose von Willebrand disease (along with von Willebrand factor measurement), to diagnose factor deficiencies, and to investigate prolonged activated partial thromboplastin time.
Factor VIII is synthesized in the liver, circulates bound to the von Willebrand factor, and is part of the intrinsic coagulation pathway. Its biological half-life is 9 to 18 hours. Congenital deficiency of factor VIII is the cause of hemophilia A, which is inherited in a sex-linked recessive manner. Severe factor VIII deficiency is characterized by hemarthrosis, excessive bleeding on injury, and ecchymoses. Factor VIII may be reduced in von Willebrand disease and certain acquired conditions. The presence of antibodies specific to factor VIII is the most common inhibitor of coagulation factors and can cause severe bleeding disorders (acquired hemophilia).
More information
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: Coronary artery disease, Cushing's syndrome, hyperthyroidism, hypoglycemia, inflammation, advanced pregnancy, macroglobulinemia, myeloma, postoperative period, progesterone use, rebound effect after sudden discontinuation of warfarin, thromboembolic conditions
- Decrease: Autoimmune disease, congenital deficiency, disseminated intravascular coagulation, fibrinolysis, hemophilia A, von Willebrand disease
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.
