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Prothrombin G20210A is a genotypic trait that provides a prompter coagulation response. It increases the risk of blood clots including from deep vein thrombosis , and of pulmonary embolism . [ 1 ] One copy of the mutation increases the risk of a blood clot from 1 in 1,000 per year to 2.5 in 1,000. [ 1 ]
Hyperprothrombinemia is a state of high of prothrombin levels in the blood [1] which leads to hypercoagulability. An example of a genetic cause includes the mutation prothrombin G20210A. [2] Hyperprothrombinemia is a risk factor for venous thromboembolism. [2]
Prothrombin G20210A is congenital. [21] Prothrombin G20210A is not usually accompanied by other factor mutations (i.e., the most common is factor V Leiden). The gene may be inherited heterozygous (1 pair), or much more rarely, homozygous (2 pairs), and is not related to gender or blood type. Homozygous mutations increase the risk of thrombosis ...
[14] [15] The most common ones are factor V Leiden (a mutation in the F5 gene at position 1691) and prothrombin G20210A, a mutation in prothrombin (at position 20210 in the 3' untranslated region of the gene). [1] [16] Compound heterozygotes and homozygotes, while rare, are at significant risk of thrombosis. [13]
[18] [19] In addition to the classic risk factors such as smoking, high blood pressure, and diabetes, genetic studies have shown that a common abnormality in the prothrombin gene (G20210A) increases the risk of cardiovascular events in people with FH. [20]
Other: TCT, bleeding time, mixing test (whether an abnormality corrects if the patient's plasma is mixed with normal plasma), coagulation factor assays, antiphospholipid antibodies, D-dimer, genetic tests (e.g. factor V Leiden, prothrombin mutation G20210A), dilute Russell's viper venom time (dRVVT), miscellaneous platelet function tests ...
The most common problem is the factor V Leiden and prothrombin G20210A mutation. [15] Some preliminary studies suggest that anticoagulant medication may improve the chances of carrying pregnancy to term but these studies need to be confirmed before they are adopted in clinical practice. [31]
Hypoprothrombinemia can be the result of a genetic defect, may be acquired as the result of another disease process, or may be an adverse effect of medication.For example, 5-10% of patients with systemic lupus erythematosus exhibit acquired hypoprothrombinemia due to the presence of autoantibodies which bind to prothrombin and remove it from the bloodstream (lupus anticoagulant ...