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Hypercoagulable Disorders

What is it? | Activation problems | Regulation problems | Breakdown problems | Other factors | Laboratory tests | Treatments | 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 cross-linked fibrin net. Most of these patients have eye problems, not thrombotic complications.
  • Dysfibrinogenaemia - abnormal fibrinogen; it leads to fibrin that does not break down normally. Most patients with dysfibrinogenaemia 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 

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