Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The early stage of the state in which coagulation or fibrinolytic pathway is activated has been difficult to estimate. It has become possible to detect disseminated intravascular coagulation (DIC) at an early stage due to the development of highly sensitive methods which quantitate so called "molecular markers". Herein, to evaluate the clinical usefulness of plasmin-alpha 2-plasmin inhibitor complex (PIC) and tissue factor activity in plasma were examined. The first time, monitoring the plasma levels of PIC might be useful for the diagnosis of a pre-DIC condition and for effective control of therapy. We believed that combination assay for both PIC and D dimer will be adequate to differentiate whether the hemostatic abnormalities are induced mainly by DIC or hepatic insufficiency. Recently, new clinical usefulness of PIC has been reported. The PIC/thrombin-antithrombin III complex ratio was lower in patients with poor prognosis than in those with good prognosis, and it was also lower in those with organ failure than in those without it. The tissue factor is a major activator of the coagulation cascade and may play a role in initiating thrombosis. A simple chromogenic substrate assay for the quantitation of tissue factor activity in plasma samples was developed. Abnormally high levels were found in 80% of the patients with DIC, predominantly in patients with non-hematological solid tumors and acute leukemia. Serial determinations of plasma tissue factor demonstrated that plasma tissue factor changes immediately with the course of DIC. Plasma tissue factor did not correlate with hemostatic markers of DIC such as thrombin-antithrombin III complex, PIC, FDP D-dimer. Tissue factor activity correlated well with membrane anchoring region of tissue factor protein levels. Tissue factor activity correlate with tumor necrosis factor alpha levels in patients with non-hematological solid tumors without hepatocellular carcinoma. These findings suggest that the plasma tissue factor is potentially valuable for monitoring the progress of DIC in a limited population of patients.
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PMID:[Clinical usefulness of the measurements of plasmin-alpha 2-plasmin inhibitor complex and plasma tissue factor activity in patients with disseminated intravascular coagulation]. 881 61

An 84-year-old man was referred to our hospital on December 3, 1993, because of excessive bleeding after tooth extraction. Coagulation studies revealed thrombocytopenia (2.2 x 10(4)/microliter), increased serum levels of FDP-E (3172 ng/ml) and D dimer (42.6 micrograms/ml), and increased plasma levels of thrombin-atithrombin III complex (48.0 ng/ml) and plasmin-alpha 2-plasmin inhibitor complex (6.8 micrograms/ml). Computed tomography showed bilateral common iliac artery aneurysms. A diagnosis of DIC due to bilateral common iliac artery aneurysms was made. Heparin (10,000 U/day) administered to treat DIC resulted in good control, and operative repair of the aneurysms was successful. This is the second reported case of isolated iliac artery aneurysms associated with DIC.
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PMID:[Isolated iliac artery aneurysms associated with disseminated intravascular coagulation (DIC)]. 886 44

During activation of the fibrinolytic system plasminogen is converted to plasmin by tissue plasminogen activator (t-PA) or urokinase-type plasminogen activator (u-PA). t-PA is predominantly released from endothelial cells, u-PA primarily by renal parenchymal cells. The activation of plasminogen is regulated by plasminogen activator inhibitor-1 (PAI-1), plasmin is controlled by alpha 2-plasmin inhibitor. The fibrinolytic system is not only involved in the intravascular dissolution of fibrin (thrombi), it also plays a vital role in normal physiologic reproduction, wound repair, angiogenesis, and tissue remodeling. Fibrinolysis is also a vital component in the pathogenesis of neoplastic disease. It is essential in releasing cells from their primary site of origin, providing nutrition for neoplastic cell growth and promoting cell mobility and motility. In neoplastic cells the degradation of the extracellular matrix proteins is facilitated by excessive expression of u-PA, t-PA, and u-PAR. In many forms of carcinoma increased expression of u-PAR and u-PA is associated with significantly shorter survival. Greater expression of u-PA in breast cancer cells, for example, is associated with shorter survival and increased relapse rate. Progressively aggressive neoplastic cells evidence high expression of u-PA and u-PAR activities, variable expression of t-PA, and enhanced PAI-1 and PAI-2 activities. In acute nonlymphocytic leukemias, poor outcome correlates with high t-PA levels. In acute progranulocytic leukemia there is a high incidence of DIC. Neoplastic prostatic tissue also expresses high u-PA activity and the more aggressive the cell line, the greater the number of u-PAR and the higher the u-PA activity. In gynecologic malignancies, a greater expression of u-PA in combination with cathepsin D is associated with widespread disease and poor prognosis. High u-PA values were also seen in patients with brain, gastric, and hepatic malignancies. It is evident that the plasminogen-plasmin system is a vital component in the biology of neoplastic disease and that it is, in theses conditions, in no way beneficial to the host.
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PMID:The fibrinolytic system in neoplasia. 912 11

High-altitude hypoxia causes polycythaemia and a hypercoagulable state in humans and animals. This study examines the effects of a hypobaric, hypoxic environment (HHE) on the blood coagulation system in rats. A total of 170 male Wistar rats were housed in a chamber at the equivalent of 5500 m in altitude for 1-12 weeks. After 2 weeks of exposure to HHE, platelet counts decreased significantly; after 4 weeks, the prothrombin and activated partial thromboplastin times were significantly prolonged, compared with those of control rats. In addition, individual coagulation factors (VII, IX, X, XI, and XII) were significantly decreased at 8 weeks (P < 0.05). Levels of anti-thrombin III and alpha 2-plasmin inhibitor also decreased (between 4 and 8 weeks). After 4-12 weeks of exposure to HHE, 30 of 56 rats (54 per cent) developed (i) non-bacterial thrombotic endocarditis (NBTE) or (ii) infarction of the myocardium or kidney, or both (i) and (ii). The incidence of NBTE increased from 33 per cent (5/15 rats) at 4 weeks to 100 per cent (7/7 rats) at 12 weeks. Electron microscopy showed detached endothelial cells in the mitral valves at 1 week; platelets adhered to the subendocardial matrix and platelet aggregation with thrombus formation was seen at 2 weeks of exposure. The results suggest that exposure to HHE induces a hypercoagulable state and causes an NBTE in rats that may result in consumption coagulopathy.
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PMID:Hypercoagulable state in a hypobaric, hypoxic environment causes non-bacterial thrombotic endocarditis in rats. 915 22

The alterations of the haemostatic system (platelet count, activated partial thromboplastin time [APTT], thromboplastin time [standard test, modified test], thrombin time, fibrinogen concentration, activity of the coagulation factors II, V, VII, X, VIII:C, IX, XI, XII, of prekallikrein, high molecular weight kininogen, antithrombin III, protein C, plasminogen and alpha 2-plasmin inhibitor, concentration of soluble fibrin and fibrin(ogen) degradation products [FDP], resonance thrombogram) were described in seven dogs with haemorrhagic diathesis in consequence of an infiltrative, growing mammary carcinoma with multifocal invasion of lymphatic and blood vessels. In most of the cases metastases in different organs could be demonstrated. In every case a serious stage of disseminated intravascular coagulation and hyperfibrinolysis was existent. This was indicated by the distinctly increased concentration (p < 0.0001) of soluble fibrin (27.7 [16.0-79.2] micrograms/ml, median [minimum-maximum], reference range [RR.]: < 9.4 micrograms/ml) and FDP (340 [50-860] micrograms/ml, RR.: < 18 micrograms/ml) as well as a diminished plasma level of nearly all components of the coagulation and fibrinolytic system concerning especially the concentration of fibrinogen (0.16 [0.01-0.46] g/l, RR.: 1.17-3.09 g/l), the activity of factors V (30 [21-40]%, RR.: 75-158%) and VIII:C (9 [4-16]%, RR.: 72-136%) as well as the activity of protein C (8 [3-13]%, RR.: 68-139%) (each: p < 0.0001).
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PMID:[Disseminated intravascular coagulation and hyperfibrinolysis in dogs with metastasizing mammary carcinoma]. 986 56


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