Accel

Definition & Etymology

Accel, an archaic term for Factor V, also known as proaccelerin or labile factor, is a protein essential for hemostasis and a key component of the coagulation cascade. (from Latin accelerare, ‘to hasten’). Synthesized primarily in the liver, this single-chain glycoprotein circulates in the plasma in an inactive form. Its name is derived from its function of accelerating the rate of blood clot formation. It is not an enzyme itself but functions as a crucial cofactor.

Clinical Significance

In the common pathway of the coagulation cascade, Factor V plays a vital role in amplifying thrombin generation. It is activated by thrombin (Factor IIa) or Factor Xa into its active form, Factor Va. Factor Va then serves as a non-enzymatic cofactor, binding to Factor Xa on the surface of activated platelets to form the prothrombinase complex. This complex significantly increases the catalytic efficiency of Factor Xa, accelerating the conversion of prothrombin (Factor II) into thrombin. This rapid burst of thrombin is critical for converting soluble fibrinogen into insoluble fibrin strands, forming a stable blood clot.

Related Conditions

Disorders of Factor V can lead to either bleeding or thrombosis. A congenital deficiency of Factor V, known as parahemophilia or Owren’s disease, is a rare autosomal recessive disorder that results in a mild to severe bleeding tendency. More commonly, a specific point mutation in the Factor V gene results in Factor V Leiden, the most prevalent inherited thrombophilia. This mutation makes Factor V resistant to inactivation by Activated Protein C (APC), leading to a hypercoagulable state and an increased risk of venous thromboembolism (VTE), including deep vein thrombosis (DVT) and pulmonary embolism (PE).

Key Takeaways

• Accel is an older name for Factor V (proaccelerin), a pivotal protein cofactor synthesized in the liver for blood coagulation.
• Its primary function is to form the prothrombinase complex with Factor Xa, dramatically accelerating the conversion of prothrombin to thrombin.
• Deficiency leads to bleeding disorders, while the Factor V Leiden mutation causes resistance to inactivation and is a major genetic risk factor for thrombosis.

Note: This content is for informational purposes only and does not substitute for professional medical advice. Always consult your doctor for diagnosis and treatment.