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Hypercoagulable Disorders
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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
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Related Pages
 On This Site Tests: ACT, PTT, CBC, Coagulation factors, D-dimer, Fibrinogen, Homocysteine, Lupus Anticoagulant, Proteins C & S, PT, PT 20210 and Factor V Leiden
Conditions: Bleeding Disorders, Liver Disease, Lupus
In the News: How long to stay on anticoagulants: Study taps D-dimer test for answers
Elsewhere On The Web
This article last reviewed on May 23, 2007.
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