1999
DOI: 10.1056/nejm199909093411104
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The Risk of Recurrent Deep Venous Thrombosis among Heterozygous Carriers of Both Factor V Leiden and the G20210A Prothrombin Mutation

Abstract: The risk of recurrent deep venous thrombosis is similar among carriers of factor V Leiden and patients without this mutation. Carriers of both factor V Leiden and the G20210A prothrombin mutation have an increased risk of recurrent deep venous thrombosis after a first episode and are candidates for lifelong anticoagulation.

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Cited by 450 publications
(280 citation statements)
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“…In a small subset of patients, thrombosis is associated with coinheritance of other prothrombotic gene mutations. [5][6][7][8] However, the potential contribution of additional genetic risk factors in most patients remains unknown. Mice homozygous for the murine FvL mutation exhibit spontaneous thrombosis that is variable depending on the background genetic strain, indicating the presence of strain-dependent genetic modifiers of thrombosis.…”
Section: Discussionmentioning
confidence: 99%
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“…In a small subset of patients, thrombosis is associated with coinheritance of other prothrombotic gene mutations. [5][6][7][8] However, the potential contribution of additional genetic risk factors in most patients remains unknown. Mice homozygous for the murine FvL mutation exhibit spontaneous thrombosis that is variable depending on the background genetic strain, indicating the presence of strain-dependent genetic modifiers of thrombosis.…”
Section: Discussionmentioning
confidence: 99%
“…Several reports have documented enhanced thrombosis risk associated with FVL and the cosegregation of other known prothrombotic genetic risk factors, such as mutations in protein C, 5 protein S, 6 antithrombin III, 7 and prothrombin. 8 Tissue factor, the primary initiator of blood coagulation, is regulated by tissue factor pathway inhibitor (TFPI). 9 TFPI is a Kunitz-type proteinase inhibitor that regulates extrinsic pathway initiation of coagulation by producing factor Xamediated feedback inhibition of the factor VIIa/tissue factor (TF) catalytic complex.…”
mentioning
confidence: 99%
“…4 -7 It is still a matter of debate whether inherited thrombophilia should be considered a persistent risk factor and whether it requires a longer course of OAT. 8,9 A higher incidence of recurrence has been shown in patients with an antithrombin, protein C, or protein S deficiency, 10 in patients with multiple thrombophilic defects, 11,12 and in patients with a homozygosity for factor V Leiden. [13][14][15] It is still debated whether carriers of heterozygous factor V Leiden or the G20210A prothrombin mutation, the two most common thrombophilic alterations, are at higher risk of recurrence.…”
mentioning
confidence: 99%
“…For the same reason, patients should also be screened for the prothrombin gene mutation, G20210A, perhaps the second most common cause of inherited thrombophilia and another risk factor for BCS. 13 In patients homozygous (and perhaps even heterozygous) for these mutations, discontinuation of anticoagulation after liver transplantation should be considered. Just as factor V Leiden can be corrected by liver transplantation, it can also be transmitted.…”
Section: Discussionmentioning
confidence: 99%