Hypercoagulable States

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Abstract
In the last few years it has become apparent that certain alterations in the coagulation system predispose to thromboembolic diseases. Increased clotting or decreased fibrinolysis can be associated with such hypercoagulable states. Increased clotting is found in patients with major deficiencies in the regulators of the system. Antithrombin III, protein C, protein S, and heparin cofactor 11 abnormalities are associated with increased intravascular fibrin formation. These disorders may be congenital and are usually autosomal dominant. In most cases thrombosis is triggered by an outside event, such as trauma, surgery, or childbirth. Decreased fibrinolysis predisposing to thromboembolism is encountered in patients with plasminogen abnormalities, decreased tissue plasminogen activator release, or increased tissue plasminogen activator inhibitor levels. Some patients with factor XII or prekallikrein deficiencies also present with thrombosis. Both factors activate plasminogen intrinsically. The presence of a lupus anticoagulant or an anticardiolipin antibody also predisposes to thrombosis. These are acquired IgG or IgM antibodies directed against phospholipid moieties essential for the formation of clotting complexes. The mechanism by which they predispose to thrombosis is as yet uncertain.

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