dysfibrinogenemia

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dys·fi·brin·o·ge·ne·mi·a

(dis'fī-brin'ō-jĕ-nē'mē-ă), [MIM*134820]
An autosomal dominant disorder of qualitatively abnormal fibrinogens of various types; each type is named for the city in which the abnormal fibrinogen was discovered. Examples include: 1) Amsterdam, Bethesda II, Cleveland, Los Angeles, Saint Louis, Zurich I and II: major defect, aggregation of fibrin monomers; thrombin time prolonged; inhibitory effect on normal clotting; asymptomatic; 2) Bethesda I and Detroit: major defect, fibrinopeptide release; thrombin time prolonged; inhibitory effect on normal clotting; abnormal bleeding; 3) Baltimore: major defect, fibrinopeptide release; thrombin time prolonged; no inhibitory effect on normal clotting; bleeding and thrombosis; 4) Leuven: major defect, questionable aggregation of fibrin monomers; thrombin time prolonged; slight inhibitory effect on normal clotting; abnormal bleeding; 5) Metz: major defect unreported; thrombin time infinite; effect on normal clotting unreported; abnormal bleeding; 6) Nancy: major defect, aggregation of fibrin monomers; thrombin time prolonged; slight inhibitory effect on normal clotting; asymptomatic; 7) Oklahoma: major defect unreported; thrombin time normal; no effect on normal clotting; abnormal bleeding; 8) Oslo: major defect unreported; thrombin time shortened; effect on normal clotting unreported; abnormal thrombosis; 9) Parma: major defect unreported; thrombin time infinite; no inhibitory effect on normal clotting; abnormal bleeding; 10) Paris I: major defect unreported; thrombin time infinite; inhibitory effect on normal clotting; asymptomatic; 11) Paris II: major defect unreported; thrombin time prolonged; inhibitory effect on normal clotting; asymptomatic; 12) Troyes: major defect unreported; thrombin time prolonged; effect on normal clotting unreported; asymptomatic; 13) Vancouver: major defect unreported; thrombin time prolonged; no effect on normal clotting; abnormal bleeding; 14) Wiesbaden: major defect, aggregation of fibrin monomers; thrombin time prolonged; inhibitory effect on normal clotting; bleeding and thrombosis.

dysfibrinogenemia

/dys·fi·brin·o·ge·ne·mia/ (dis-fi-brin″o-jĕ-ne´me-ah) the presence in the blood of abnormal fibrinogen.

dysfibrinogenemia

A group of qualitative, usually AD, fibrinogen defects ranging in severity from innocuous to hemorrhagic diathesis; most are asymptomatic and detected by presurgical screens, given the abnormalities in coagulation parameters; these subjects suffer frequent spontaneous abortion, bleeding, poor wound healing, and thrombosis Lab Normal fibrinogen and clotting times; ↑ PT, ↑ thrombin time, ↑ reptilase time. See Fibrinogen.

dys·fi·brin·o·ge·ne·mi·a

(dis'fī-brin'ō-jĕ-nē'mē-ă)
An autosomal dominant disorder of qualitatively abnormal fibrinogens of various types, resulting in abnormalities of coagulation tests (bleeding time, clotting time, thrombin time); symptoms vary from none to abnormal bleeding and excessive clotting.
Synonym(s): dysfibrinogenaemia.

dysfibrinogenemia

the presence of abnormal fibrinogens in the body. An inherited dysfibrinogenemia occurs in humans and has been reported in a collie dog.
References in periodicals archive ?
Dysfibrinogenaemias are qualitative defects that may be associated with bleeding or thrombosis, depending on the site of mutation.
The test therefore only detects disturbances in the final stages of coagulation, especially dysfibrinogenaemia or the presence of thrombin inhibitors (Koch and Biber, 2007).