Anti-Factor X | Activity

General Information

Coagulation factor X deficiency may be congenital or acquired.
Coagulation factor X is a vitamin K-dependent serine protease (a protein with enzymatic activity) that is synthesized in the liver. Its biological half-life is 24 to 48 hours. Factor X participates in both the intrinsic and extrinsic cascades of coagulation, where it acts as an enzyme (factor Xa) in the prothrombinase complex.

Congenital deficiency of factor X is rare. Acquired deficiency is usually associated with liver disease, warfarin therapy, vitamin K deficiency, systemic amyloidosis, and inhibitors. Factor X deficiency results in increased prothrombin time and activated partial thromboplastin time.

Factor X activity is determined by a clotting time assay based on aPTT (activated partial thromboplastin time).

Referral norms:

Adults: 70-150%
Newborns with normal development time and also premature babies may have a decrease in the concentration of coagulation factor X levels (> or =15-20%)

Interpretation

A decrease in the activity of coagulation factor X characterizes such pathologies as:
• Amyloidosis – a rare condition when pathological protein-amyloid accumulates in the cells of organs and causes damage to the function and structure of the organ.
• Congenital deficiency of factor 10 as a result of F10-gene mutation
• Disseminated intravascular coagulation syndrome – a condition when the entire blood mass clots and blocks the lumen of blood vessels. This disrupts the blood supply to the tissues.
• Decreased ability to absorb fat - because factor 10 is a protein related to vitamin K, and vitamin K is fat-soluble.
• Heparin therapy – for the treatment or prevention of increased blood clotting
• Liver diseases
• Vitamin K deficiency

An increase in the activity of coagulation factor 10 is observed during pregnancy, when taking oral contraceptives. Increasing its activity increases the risk of thrombosis.