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Factor V Leiden (rs6025 or F5 p.R506Q [1]) is a variant (mutated form) of human factor V (one of several substances that helps blood clot), which causes an increase in blood clotting (hypercoagulability).
14067 Ensembl ENSG00000198734 ENSMUSG00000026579 UniProt P12259 O88783 RefSeq (mRNA) NM_000130 NM_007976 RefSeq (protein) NP_000121 NP_032002 Location (UCSC) Chr 1: 169.51 – 169.59 Mb Chr 1: 163.98 – 164.05 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Coagulation factor V (Factor V), also less commonly known as proaccelerin or labile factor, is a protein involved in ...
APC resistance is the inability of protein C to cleave Factor Va and/or Factor VIIIa, which allows for longer duration of thrombin generation and may lead to a hypercoagulable state. This may be hereditary or acquired. [4] The best known and most common hereditary form is Factor V Leiden, which is responsible for more than 95% of cases. [5]
[1] [5] This ratio is inversely related to the degree of APC resistance. [7] The ETP-based APC resistance test involves the addition of APC to a thrombin generation assay (TGA). [5] This results in an inhibition of thrombin generation as measured by reduction of the endogenous thrombin potential (ETP; area under the thrombin generation curve). [5]
There have also been cases in patients with other deficiency, including protein S deficiency, [6] [7] activated protein C resistance (Factor V Leiden) [8] and antithrombin III deficiency. [ 9 ] Although the above hypothesis is the most commonly accepted, others believe that it is a hypersensitivity reaction or a direct toxic effect.
The exact prevalence of protein S deficiency in the population is unknown; it is found 1.3–5% of people with thrombosis. [14] The minor ("type 2") thrombophilias are much more common. Factor V Leiden is present in 5% of the population of Northern European descent, but much rarer in those of Asian or African extraction.
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Congenital factor X deficiency is also extremely rare, affecting an estimated 1 in 1,000,000. [23] A point mutation in the gene encoding factor V can lead to a hypercoagulability disorder called factor V Leiden. In factor V Leiden, a G1691A nucleotide replacement results in an R506Q amino acid mutation.