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Primary fibrinogenolysis is a medical condition that appears with abnormal production of fibrinogen/fibrin degradation products (FDP), degradation of coagulation factors V, VIII, IX, XI and/or degradation of the fibrin present in any pre-existing localized thrombi and hemostatic clots.
Primary fibrinogenolysis is the pathological lysis of fibrinogen characterized with a low fibrinogen, high fibrin degradation products, prolonged prothrombin time and activated partial thromboplastin time, a normal platelet count and absence of microcirculatory thrombosis.
Fibrinolysis is a process that prevents blood clots from growing and becoming problematic. [1] Primary fibrinolysis is a normal body process, while secondary fibrinolysis is the breakdown of clots due to a medicine, a medical disorder, or some other cause. [2] In fibrinolysis, a fibrin clot, the product of coagulation, is broken down. [3]
Fibrinogen disorders are a set of hereditary or acquired abnormalities in the quantity and/or quality of circulating fibrinogens.The disorders may lead to pathological bleeding and/or blood clotting or the deposition of fibrinogen in the liver, kidneys, or other organs and tissues.
Coagulation activation markers are biomarkers of net activation of coagulation and fibrinolysis. [1] [2] Examples include prothrombin fragment 1+2 (F1+2), thrombin–antithrombin complex (TAT), fibrinopeptide A (FpA), fibrin monomers (FMs), plasmin-α 2-antiplasmin complex (PAP), activated protein C–protein C inhibitor (APC-PCI), and D-dimer (DD).
The fibrinolysis system is responsible for removing blood clots. Hyperfibrinolysis describes a situation with markedly enhanced fibrinolytic activity, resulting in increased, sometimes catastrophic bleeding. Hyperfibrinolysis can be caused by acquired or congenital reasons.
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Fibrinolysis syndrome is characterized by an acute hemorrhagic state brought about by inability of the blood to clot, with massive hemorrhages into the skin producing blackish, purplish swellings and sloughing.