Venous Thromboembolism: Mechanisms, Treatment, and Public Awareness |
From the Division of Rheumatology, Allergy and Immunology, Department of Medicine, and Thurston Arthritis Research Center, The University of North Carolina at Chapel Hill.
Correspondence to Dr Robert Roubey, Division of Rheumatology, Allergy and Immunology, CB #7280, Rm. 3330 Thurston Bldg, UNC-CH, Chapel Hill, NC 27599-7280. E-mail roubey{at}med.unc.edu
The antiphospholipid syndrome is a relatively common acquired cause of venous thrombosis. Up to 20% of cases of deep vein thrombosis, with and without pulmonary embolism, may be associated with antiphospholipid antibodies. These antibodies are typically detected in lupus anticoagulant assays and tests for anticardiolipin antibodies. Most antiphospholipid antibodies are directed against several phospholipid-binding plasma proteins. The most common antigens are β2-glycoprotein I and prothrombin. Immunoassays using these purified antigens are now available. In addition to being markers for thrombotic risk, antiphospholipid antibodies have been shown to directly contribute to hypercoagulability in animal models and in various in vitro studies. Prevention of recurrent venous thrombosis in patients with the antiphospholipid syndrome requires long-term anticoagulation. The optimal intensity of warfarin therapy is an ongoing issue, but most clinicians currently favor a target INR in the 2.0 to 3.0 range. In certain patients, antiphospholipid antibodies may interfere with determination of the INR, requiring other approaches to monitor and adjust the warfarin dose. Low-dose aspirin is typically recommended for primary prevention of thrombosis in asymptomatic patients with moderate to high levels of antiphospholipid antibodies, although strong supporting data are lacking.
Key Words: antiphospholipid anticardiolipin lupus anticoagulant β2-glycoprotein I thrombosis
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