Hypercoagulable Disorders
Overview | Activation Problems | Regulation Problems | Breakdown Problems | Other Factors | Laboratory Tests | Treatment | Related Pages
Problems with clot breakdown (fibrinolysis)
Inherited:
- Congenital plasminogen deficiency -- rare factor deficiency; plasminogen is activated to form plasmin. Plasmin helps break apart the clot's crosslinked fibrin net. Most of these patients have eye problems, not thrombotic complications.
- Dysfibrinogenemia -- abnormal fibrinogen; it leads to fibrin that does not break down normally. Most patients with dysfibrinogenemia have laboratory results within normal limits, but some have bleeding symptoms, and a small number have been reported to have thrombotic complications.
Acquired:
- Plasminogen deficiency -- plasminogen is the precursor to plasmin, which helps to break down clots; may also be an acquired deficiency (see above)
- Decreased plasminogen activator
