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Approximately 2 million people in the United States die each year from an arterial or venous thrombosis. Effective prophylaxis and treatment for venous thrombosis are available, but are often not administered because testing for hypercoagulable disorders is not routinely performed and risk factors are not fully understood. Known acquired and hereditary thrombotic risk factors are summarized below. Acquired thrombotic risk factors
According to the "second hit" theory for initiation of thrombosis, the presence of more than one risk factor is needed to manifest thrombosis in most patients. For example, 1 hereditary risk factor plus 1 acquired risk factor results in thrombosis. A patient with the factor V Leiden mutation (1st hit) who uses oral contraceptives (2nd hit) greatly increases their risk of thrombosis by combining the 2 risk factors. The clinical relevance of the various inherited and acquired prothrombotic risk factors and the strength of their interactions are only partially understood. In some instances it is not known whether patients with inherited thrombophilia should be treated differently from those without these disorders, particularly with regard to duration of oral anticoagulant therapy following a thrombotic episode. In general, patients with a history of VTE may be stratified into three risk categories for recurrent thrombosis. 1. Low-risk category: Patients with a single episode of VTE that occurred in the presence of one or more transient risk factors (such as surgery, immobilization, pregnancy, the puerperium, oral contraceptive or hormone replacement therapy). In general, these patients receive relatively short-term anticoagulation (3-6 months). 2. High-risk category:
3. Intermediate category
The laboratory investigation of hypercoagulable disorders is a rapidly expanding field. Indications for laboratory testing include: 1. A history of venous or arterial thrombosis with one or more of the following features:
Testing should be avoided when it is likely that an acquired deficiency may exist, since this makes interpretation of results difficult. An acquired decrease in antithrombin, protein C and protein S may be seen in acute thrombosis, DIC, and liver disease. An acquired decrease in protein C and protein S may be associated with any acute phase reaction. During pregnancy there is a significant acquired decrease in protein S levels (total and free). If there has been a recent acute event (including thrombosis), it is advisable to defer testing for 4 to 6 weeks. Protein C and S assays should not be run while a patient is taking Coumadin, because it produces a decrease in protein C and protein S levels and results cannot be reliably interpreted. If Coumadin therapy cannot be stopped, it can be temporarily discontinued for 10 days prior to testing, while the patient is covered with heparin. Heparin may cause a mild acquired decrease in antithrombin. In general, if a deficiency of antithrombin, protein C or protein S is observed, it is recommended that testing be repeated after an interval to confirm persistent deficiency. As a rough guide, the level of antithrombin in hereditary antithrombin deficiency is usually < 65%, and the level of free protein S antigen in hereditary protein S deficiency is usually < 50%. For both protein C and total protein S assays there is considerable overlap in values between normal individuals and those with the genetic deficiency. Family studies may be helpful. Reference ranges are:
Specimen requirement is 4 blue top and 1 red top tubes of blood. |
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