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Updated: Jun 23, 2026
13:08
Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
Published on: September 9, 2012
Advances in understanding the bleeding diathesis in factor V deficiency
Connie Duckers1, Paolo Simioni, Jan Rosing
1Department of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.
British Journal of Haematology
|May 15, 2009
Summary
Severe coagulation factor V (FV) deficiency is rarely fatal in humans, unlike in mice. Platelets and reduced tissue factor pathway inhibitor contribute to this variable bleeding risk in FV deficiency.
Area of Science:
- Hematology
- Molecular Biology
- Genetics
Background:
- Coagulation factor V (FV) is essential for blood clotting, with FV knock-out mice exhibiting lethal bleeding.
- Severe FV deficiency in humans, however, often presents with mild or moderate bleeding, a paradox not fully understood.
Purpose of the Study:
- To review and integrate current findings on the variable clinical presentation of FV deficiency.
- To explore the roles of platelets and tissue factor pathway inhibitor (TFPI) in modulating bleeding risk in FV deficiency.
Main Methods:
- Literature review of studies on FV deficiency, platelet function, and TFPI levels.
- Analysis of clinical data correlating FV levels with bleeding severity.
Main Results:
- Platelets play a significant role in mitigating bleeding in FV-deficient individuals.
- Reduced plasma TFPI levels in FV deficiency lead to enhanced thrombin generation, particularly at very low FV levels (<2%).
Conclusions:
- The variable bleeding phenotype in human FV deficiency is influenced by platelet contribution and TFPI levels.
- Further research into these factors can elucidate the pathophysiology and improve management of FV deficiency.
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