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Factor V Leiden is an autosomal dominant genetic condition that exhibits incomplete penetrance, i.e. not every person who has the mutation develops the disease. The condition results in a factor V variant that cannot be as easily degraded by activated protein C. The gene that codes the protein is referred to as F5.
Coagulation factor V (Factor V), also less commonly known as proaccelerin or labile factor, is a protein involved in coagulation, encoded, in humans, by F5 gene. [5] In contrast to most other coagulation factors, it is not enzymatically active but functions as a cofactor . [ 5 ]
Discontinuation of heparin is critical in a case of heparin-induced thrombocytopenia (HIT). Beyond that, however, clinicians generally treat to avoid thrombosis. [32] Treatment may include a direct thrombin inhibitor, such as lepirudin or argatroban. Other "blood thinners" sometimes used in this setting include bivalirudin and fondaparinux.
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Factor V Leiden is responsible for 8% of cases. [2] Other less common inherited disorders leading to the condition include factor II mutation (3%), protein C deficiency (5%), protein S deficiency (4%), and antithrombin III deficiency(1%). [2] [16] Budd–Chiari syndrome may be the presenting sign of these hypercoagulable disorders.
Up to 8% of patients receiving heparin are at risk to develop HIT antibodies, but only 1–5% on heparin will progress to develop HIT with thrombocytopenia and subsequently one-third of them may develop arterial or venous thrombosis. [1] After vascular surgery, 34% of patients receiving heparin developed HIT antibodies without clinical symptoms ...
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]
Human Chr 3. In terms of the cause of protein S deficiency it can be in inherited via autosomal dominance.A mutation in the PROS1 gene triggers the condition. The cytogenetic location of the gene in question is chromosome 3, specifically 3q11.1 [6] [7] Protein S deficiency can also be acquired due to vitamin K deficiency, treatment with warfarin, liver disease, kidney disease, chemotherapy ...