12-01-2011, 08:04 PM
Disseminated Intravascular Coagulopathy in Acute Promyelocytic Leukemia:
http://www.medscape.com/viewarticle/583101
* DIC results from the activation of the virtually unregulated coagulation cascade, characterized by the generation of thrombin with fibrin deposition within the micro- and macrovascular systems (i.e., multiple thrombi), combined with a hemorrhagic diathesis. The counteraction by the fibrinolytic cascade is variable and is characterized by the conversion of plasminogen to plasmin, the latter functioning as a potent proteolytic enzyme, capable of degrading fibrinogen, fibrin, and several clotting factors. The kinin and complement cascades also partake in the promotion of DIC. In addition, antithrombin (AT), proteins C and S, antiplasmin, and plasminogen activator inhibitor 1, play a functional role in curtailing the activation of the coagulation and fibrinolytic mechanisms, but they too may be affected by the DIC process, particularly because a marked decrease in AT takes place in severe cases.
* lab findings of DIC include elevation of D-dimer (a product of lysed fibrin), fibrinogen degradation products (FDP), as well as prolongation of prothrombin time (PT), partial thromboplastin time (PTT), and thrombin time, accompanied by thrombocytopenia and hypofibrinogenemia (noted mostly in obstetrical cases). Because some of these assays are not specific for the diagnosis of DIC, we propose the use of a new, simple, and cost effective panel: D-dimer, FDP, and AT. Elevations in FDP and D-dimer are sensitive for the diagnosis of DIC and a marked drop in AT establishes a poor prognosis.
http://www.medscape.com/viewarticle/583101
* DIC results from the activation of the virtually unregulated coagulation cascade, characterized by the generation of thrombin with fibrin deposition within the micro- and macrovascular systems (i.e., multiple thrombi), combined with a hemorrhagic diathesis. The counteraction by the fibrinolytic cascade is variable and is characterized by the conversion of plasminogen to plasmin, the latter functioning as a potent proteolytic enzyme, capable of degrading fibrinogen, fibrin, and several clotting factors. The kinin and complement cascades also partake in the promotion of DIC. In addition, antithrombin (AT), proteins C and S, antiplasmin, and plasminogen activator inhibitor 1, play a functional role in curtailing the activation of the coagulation and fibrinolytic mechanisms, but they too may be affected by the DIC process, particularly because a marked decrease in AT takes place in severe cases.
* lab findings of DIC include elevation of D-dimer (a product of lysed fibrin), fibrinogen degradation products (FDP), as well as prolongation of prothrombin time (PT), partial thromboplastin time (PTT), and thrombin time, accompanied by thrombocytopenia and hypofibrinogenemia (noted mostly in obstetrical cases). Because some of these assays are not specific for the diagnosis of DIC, we propose the use of a new, simple, and cost effective panel: D-dimer, FDP, and AT. Elevations in FDP and D-dimer are sensitive for the diagnosis of DIC and a marked drop in AT establishes a poor prognosis.