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Management of Patients with Hereditary Hypercoagulable Disorders

Management of Patients with Hereditary Hypercoagulable Disorders ▪ Abstract The inherited hypercoagulable states can be divided into those that are common and associated with a modest risk of thrombosis (i.e. factor V Leiden and G20210A prothrombin gene) and those that are uncommon but asssociated with a high risk of thrombosis. There is no convincing evidence that, independent of other clinical factors, the presence of factor V Leiden or the prothrombin gene mutation should influence the use of primary prophylaxis or the duration of anticoagulant therapy following an episode of thrombosis. Indrect evidence sugests that the presence of antithrombin, protein C deficiency, or protein S deficiency justifies avoiding additional risk factors for thrombosis, such as estrogen therapy, and justifies use of more aggressive primary prophylaxis when additional risk factors cannot readily be avoided (e.g. pregnancy). The presence of one of these three abnormalities also favors more prolonged anticoagulant therapy following venous thrombosis. However, their presence or absence appears to have less influence on the risk of recurrent venous thromboembolism than whether thrombosis was provoked by a major reversible risk factor, such as surgery. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annual Review of Medicine Annual Reviews

Management of Patients with Hereditary Hypercoagulable Disorders

Kearon, C.; Crowther, M.; Hirsh, J.
Annual Review of Medicine , Volume 51 (1) – Feb 1, 2000
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Publisher
Annual Reviews
Copyright
Copyright © 2000 by Annual Reviews. All rights reserved
Subject
Review Articles
ISSN
0066-4219
eISSN
1545-326X
DOI
10.1146/annurev.med.51.1.169
pmid
10774459
Publisher site
See Article on Publisher Site

Abstract

▪ Abstract The inherited hypercoagulable states can be divided into those that are common and associated with a modest risk of thrombosis (i.e. factor V Leiden and G20210A prothrombin gene) and those that are uncommon but asssociated with a high risk of thrombosis. There is no convincing evidence that, independent of other clinical factors, the presence of factor V Leiden or the prothrombin gene mutation should influence the use of primary prophylaxis or the duration of anticoagulant therapy following an episode of thrombosis. Indrect evidence sugests that the presence of antithrombin, protein C deficiency, or protein S deficiency justifies avoiding additional risk factors for thrombosis, such as estrogen therapy, and justifies use of more aggressive primary prophylaxis when additional risk factors cannot readily be avoided (e.g. pregnancy). The presence of one of these three abnormalities also favors more prolonged anticoagulant therapy following venous thrombosis. However, their presence or absence appears to have less influence on the risk of recurrent venous thromboembolism than whether thrombosis was provoked by a major reversible risk factor, such as surgery.

Journal

Annual Review of Medicine – Annual Reviews

Published: Feb 1, 2000

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