Acquired hypercoagulable states

Bauer KA. Inherited and acquired hypercoagulable states. In LoscalzoJ, Schafer Al, eds. Thrombosis and Hemorrhage, 2nd ed. Baltimore, MD Williams Wilkins, 1998. 

Estrogens have a dose-related effect in the development of venous thromboembolism (VTE) and pulmonary embolism. This is especially true in women with underlying hypercoagulable states or who have acquired conditions (e.g., obesity, pregnancy, immobility, trauma, surgery, and certain malignancies.)... 

The hypercoagulable states can be inherited or acquired. One inherited hypercoagulable state is antithrombin (AT) deficiency. AT deficiency is an autosomal dominant condition. The type I antithrombin deficiency is characterized by reduced synthesis of normal protease inhibitor molecules. The antigenic and functional activities of antithrombin are reduced due to small deletions or insertions or single base substitutions. Type II antithrombin deficiency is due to defects within the protease inhibitor. While the immunologic activity levels are normal, the plasma levels of antithrombin are reduced. About 42% of afflicted individuals develop clinical manifestations spontaneously. Manifestations related to pregnancy, parturition, oral contraceptives, or trauma occur in 58% of AT deficient individuals (190). 

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