|Values are valid only on day of printing.|
Diagnosing congenital deficiency of coagulation factor VII
Evaluating acquired deficiencies associated with liver disease, oral anticoagulant therapy, and vitamin K deficiency
Determining degree of anticoagulation with warfarin to correlate with level of protein C
Investigation of a prolonged prothrombin time
Factor VII is a vitamin K-dependent serine protease synthesized in the liver. It is a component of the extrinsic coagulation scheme, measured by the prothrombin time. Plasma biological half-life is about 3 to 6 hours. Deficiency may result in a bleeding diathesis.
Normal, full-term newborn infants or healthy premature infants may have decreased levels (> or =20%) which increase within the first postnatal week but may not reach adult levels for > or =180 days postnatal.*
*See Pediatric Hemostasis References in Coagulation Studies in Special Instructions.
Liver disease, vitamin K deficiency, or warfarin anticoagulation can cause decreased factor VII activity.
Heterozygotes generally have levels of < or =50%.
Homozygotes have levels usually <20%.
Newborn infants usually have levels > or =25%.
Factor VII is the first vitamin K-dependent coagulation factor to decrease after starting warfarin therapy and 1 of the first to return to normal when anticoagulation is discontinued.
1. Girolami A, Scandellari R, Scapin M, Vettore S: Congenital bleeding disorders of the vitamin K-dependent clotting factors. Vitam Horm 2008;78:281-374
2. Brenner B, Kuperman AA, Watzka M, Oldenburg J: Vitamin K-dependent coagulation factors deficiency. Semin Thromb Hemost 2009 Jun;35(4):439-446
3. Mariani G, Bernardi F: Factor VII deficiency. Semin Thromb Hemost 2009 Jun;35(4):400-406