factor v leiden造句

• While only 1 percent of people with factor V Leiden have two copies of the defective gene, these homozygous individuals have a more severe clinical condition.
• The risk of developing a clot in a blood vessel depends on whether a person inherits one or two copies of the factor V Leiden mutation.
• There have also been cases in patients with other deficiency, including protein S deficiency, activated protein C resistance ( Factor V Leiden ) and antithrombin III deficiency.
• The most common one of these, factor V Leiden, is due to the replacement of an arginine residue with glutamine at amino acid position 506 ( R506Q ).
• People with factor V Leiden are at a relatively low risk of thrombosis, but may develop thrombosis in the presence of an additional risk factor, such as immobilization.
• The first major form of thrombophilia, antithrombin deficiency, was identified in 1965, while the most common abnormalities ( including factor V Leiden ) were described in the 1990s.
• Heterozygous carriers who take combined birth control pills are at a 15-fold increased risk of VTE, while carriers also heterozygous with factor V Leiden have an approximate 20-fold higher risk.
• All prothrombotic factor V mutations ( factor V Leiden, factor V Cambridge, factor V Hong Kong ) make it resistant to cleavage by activated protein C ( " APC resistance " ).
• The previously reported relationship of inflammatory bowel disease ( i . e ., Crohn's disease or ulcerative colitis ) and prothrombin G20210A or factor V Leiden mutation have been contradicted by research.
• Hypercoagulability states as a pre-existing condition in pregnancy include both acquired ones, such as antiphospholipid antibodies, and congenital ones, including factor V Leiden, prothrombin mutation, proteins C and S deficiencies, and antithrombin III deficiency.
• Factor V Leiden is a variant ( mutated form ) of human factor V ( one of several substances that helps blood clot ) that causes an increase in blood clotting ( hypercoagulability ).
• The most common mutation leading to activated protein C resistance among Caucasians is at the cleavage site in Factor V for APC . There, Arg 506 is replaced with Gln, producing Factor V Leiden.
• Women with factor V Leiden have a substantially increased risk of clotting in pregnancy ( and on estrogen-containing birth control pills or hormone replacement ) in the form of deep vein thrombosis and pulmonary embolism.
• Most cases of venous thrombosis are due to acquired states ( older age, surgery, cancer, immobility ) or inherited thrombophilias ( e . g ., antiphospholipid syndrome, factor V Leiden, and various other genetic deficiencies or variants ).
• Roughly 8 percent of white Americans, or about 18 million people, are carriers of one of the two mutations _ Factor V Leiden and prothrombin, the two most common causes of inherited thrombophilia, a tendency to develop blood clots.
• The presence of acquired risk factors for venous thrombosis including smoking, use of estrogen-containing ( combined ) forms of hormonal contraception, and recent surgery further increase the chance that an individual with the factor V Leiden mutation will develop DVT.
• Examples of genetic tendencies include protein C deficiency, protein S deficiency, the Factor V Leiden mutation, hereditary anti-thrombin deficiency and prothrombin mutation G20210A . An important non-genetic risk factor is the use of estrogen-containing ( combined ) forms of hormonal contraception.
• Recurrent miscarriage is an indication for thrombophilia screening, particularly antiphospholipid antibodies ( anti-cardiolipin IgG and IgM, as well as lupus anticoagulant ), factor V Leiden and prothrombin mutation, activated protein C resistance and a general assessment of coagulation through an investigation known as thromboelastography.
• The Factor V Leiden mutation at Arg 506 renders Factor Va resistant to inactivation by activated protein C . As a result of this resistance, the half-life of Factor Va in plasma is increased, resulting in increased thrombin production and increased risk of thrombosis.
• Fracture itself is known to do the same through another independent mechanism unknown to me, and several genetic traits can increase one's risk of making a blood clot even if they have been silent for a lifetime ( factor V leiden, prothrombin 20210, etc ).