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)

Hematological studied were carried out serially in the rats transplanted subcutaneously with Yoshida ascites hepatoma AH-109A. Significant changes were observed in fibrinogen level, fibrinogen degradation products, recalcification time, platelet count, and fragmentation of red blood cells. Formation of thrombi was revealed in the vessels of tumor tissue morphologically from early stage when the tumor grew to a palpable size. Thrombi were formed also in the arterioles of the lungs in the terminal stage. Bleeding tendency was noted in some cases at death. These findings suggested the experimental induction of a type of disseminated intravascular coagulation. The systemic changes of the blood occurring in the terminal stage were preceded by localized intravascular coagulation and fibrinolysis in the tumor in early stage of tumor growth.
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PMID:Hematological alterations in tumor-bearing rats, with reference to pathogenesis of chronic type of disseminated intravascular coagulation syndrome. 20 34

In a 44-year-old female acute promyelocytic leukemia (APL) presented with abrupt onset of right hemiplegia and aphasia due to occlusion of the left carotid artery at bifurcatio. There was laboratory evidence of disseminated intravascular coagulation (DIC). Thrombotic complications are unusual in APL, even in cases with evidence of DIC. This report aims at underlying the important implication of a correct timely diagnosis in young patients presenting with stroke.
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PMID:Occlusion of the carotid artery as presenting symptom of acute promyelocytic leukemia. 171 25

Two unrelated families are described, of which four adult members were found to be suffering from severe protein C deficiency (less than or equal to 5% of normal plasma level). Newborn deaths were reported in the first family but the second family had no history of neonatal purpura fulminans and infant death. Thrombotic symptoms developed mainly in their early twenties, consisting chiefly of recurrent superficial and deep iliofemoral vein thromboses and pulmonary emboli. Other clinical features included generalized peritonitis due to massive mesenteric vein thrombosis, thrombosis of the cavernus sinus, renal vein thrombosis and priapism. In the second family, five members (all aged approximately 40 years) died of intravascular abdominal thrombosis. Massive thromboembolic episodes were associated with a compensated disseminated intravascular coagulation syndrome as evidenced by high concentrations of D-dimer (mean levels 5000 ng/ml plasma) and by a moderate reduction in platelet count and fibrinogen concentrations. D-dimer levels in noncrisis periods were also raised above normal (mean levels 400 ng/ml). The thrombotic problems of these patients were controlled satisfactorily by long-term administration of low molecular weight heparin alone or in combination with low dose warfarin.
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PMID:Congenital severe protein C deficiency in adults. 254 23

We collected 23 autopsied cases of thrombotic thrombocytopenic purpura (TTP) and examined them immunohistochemically and electronmicroscopically to elucidate the nature of thrombi and subendothelial deposits. The findings were compared with those of 10 cases of disseminated intravascular coagulation (DIC) and 3 cases of polyarteritis nodosa (PN). Intravascular thrombi and subendothelial hyaline deposits in TTP stained weakly for fibrinogen/fibrin by the PAP technique, while they stained strongly for factor VIII related antigen (FVIIIR: Ag). Electronmicroscopically, thrombi in TTP were composed of numerous, variably degranulated and altered platelets, and a small amount of amorphous materials. Thrombi in DIC were strongly positive for fibrinogen/fibrin, while they were weakly positive for FVIIIR:Ag. Electronmicroscopically they were composed of polymerized fibrin. Fibrinoid necrotic lesions in PN were strongly positive for fibrinogen/fibrin but negative for FVIII R:Ag. Based on these findings, we concluded that thrombi in TTP are essentially platelet thrombi and that subendothelial hyaline deposits may not be a result of increased vascular permeability but may be platelet thrombi incorporated into the arterial wall and covered with newly formed endothelial cells.
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PMID:Immunohistochemistry of vascular lesion in thrombotic thrombocytopenic purpura, with special reference to factor VIII related antigen. 286 71

Two cases of complete sagittal sinus occlusion with multiple brain hemorrhages, elevated intracranial pressure, and disseminated intravascular coagulation are described. These patients were successfully managed using pentobarbital-induced coma to ameliorate intracranial pressure elevation. This therapy was combined with monitoring of intracranial pressure and intermittent drainage of cerebrospinal fluid to further control intracranial pressure elevations. Thrombus and coagulopathy resolved with pentobarbital alone in one patient and after pentobarbital plus heparin therapy in the second patient. It is suggested that cases of severe distal sagittal sinus thrombosis with brain hemorrhage and intracranial hypertension may benefit from combined pentobarbital coma and intraventricular drainage. This allows for stabilization of bleeding tendencies before instituting heparin therapy when necessary. Management of sagittal sinus thrombosis with barbiturates or ventricular drainage is best performed in an intensive care unit environment with continuous monitoring of intracranial pressure and substantial electrophysiologic and neuroradiologic support.
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PMID:Treatment of sagittal sinus thrombosis associated with cerebral hemorrhage and intracranial hypertension. 338 62

The intravenous injection of colchicine (2 mg/kg body weight) into pregnant rats on the last 4 to 5 days of gestation induced disseminated intravascular coagulation, occluding glomerular capillaries with fibrin thrombi, typical of the generalized Shwartzman reaction. Thrombi did not form earlier than 9 hours after the injection of colchicine, whereas in the endotoxin-induced generalized Shwartzman reaction, thrombi were already observed 2(1/2) hours after the injection of endotoxin. The colchicine-induced generalized Shwartzman reaction could also be produced in hysterectomized "pregnant" rats. A single injection of colchicine into nonpregnant rats did not induce disseminated intravascular coagulation. If, however, fibrinolysis was inhibited with epsilon-aminocaproic acid, the colchicine-induced generalized Shwartzman reaction could also be elicited in nonpregnant rats. In this regard fibrinolysis inhibition represents one mechanism by which pregnancy prepares for the generalized Shwartzman reaction.
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PMID:Induction of the generalized Shwartzman reaction in pregnant and nonpregnant rats by colchicine. 456 95

Thrombus formation depends on adherence of blood-formed elements to the intimal surface through platelet-vessel surface interaction, platelet release phenomena and aggregation, formation of fibrin, and the enmeshing of blood cells. Arterial thrombi involve platelet aggregation, whereas venous thrombi found in low flow or during stasis have greater proportions of erythrocytes and fibrin. It is not known if or how abnormalities of flow resistance, platelet thrombus formation, or endothelial and dynamic parameters affect the microcirculation, largely due to the difficulty of obtaining comprehensive data from these systems. Increases of fibrinogen observed in many disorders may result in minor changes in blood viscosity without known physiologic consequence, but in most disorders in which thrombosis is observed, the pathophysiologic mechanisms are multifactorial and abnormal blood viscosity is presumed to be a significant but not limiting component. Therapeutic approaches in thrombotic disorders should recognize which elements of the thrombotic triad predominate. In arterial disorders focus should be on platelet activity, and the objectives of venous thrombosis treatment include prevention of morbidity and death from pulmonary embolism, reduction of morbidity resulting from the acute thrombotic episode, and prevention of the postphlebitic syndrome. Pathology, mechanism, and treatment for specific thrombogenic disorders are described. Treatments suggested for hyperviscosity involve giving antibiotics during crises. Also discussed are thalassemia, paroxysomal nocturnal hemoglobinuria, polycythemia, cryoglobulinemia, paraproteinemia, diabetes mellitus, and disseminated intravascular coagulation. Studies have established a relationship between thromboembolic disease and oral contraceptives (OCs). The risk is only increased while the patient is taking OCs but is compounded in women undergoing surgery or who have a disorder which predisposes to venous disease. The risk for myocardial infarction or stroke is significantly increased when OCs are taken over age 35 and when there is hypertension, smoking, type-II hyperlipoproteinemia, and diabetes mellitus. The risk appears to be a function of estrogen dosage, causing a 25% mean increase in calf venous volume and 30% decrease in vein velocity of venous blood compared to controls. Low flow rates may contribute to venous thromboembolism. OCs may alter precisely regulated systems of coagulation and fibrinolysis and recent studies confirm abnormalities in the hemostatic system attributed to OCs. 16% of women taking OCs have a 60% or greater reduction in antithrombin III activity. The multiple effects of OCs often result in low-grade activation of the hemostatic system, potentially lowering the threshold to precipitate thrombus formation and possibly explaining the increased incidence of thromboembolic disease. Heparin appears to reverse many of these problems.
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PMID:Blood viscosity and thrombosis: clinical considerations. 676 12

Thrombotic events have been reported in acute lymphoblastic leukaemia patients, especially during or after L-asparaginase administration. A so-called L-asparaginase associated coagulopathy has been well recognized, being characterized by a hypercoagulable state (decrease of antithrombin III, plasminogen, protein C, protein S and increase of prothrombin fragment F1 + 2, thrombin-antithrombin complexes and fibrinopeptide A). The aim of this study was to determine whether the supplementation of antithrombin III (AT-III) concentrates could improve the L-asparaginase associated coagulopathy, thereby blocking the activation of the haemostatic system. In 25 adult patients with acute lymphoblastic leukaemia (M 19, F6, mean age 34 years) antithrombin III (AT-III) concentrates were administered at daily doses of 50 U/kg for 10 consecutive days from the beginning of L-asparaginase therapy (6,000 U/m2/day s.c. for 7 days), given according to the GIMEMA ALL 0288 trial. A marked increase of antithrombin III was recorded on days IV-VIII-XI (P < 0.001). No changes in protein C, protein S, plasminogen, alpha 2-antiplasmin, factor VII and platelet count were observed and there was no increase in markers of hypercoagulability. There was no evidence of disseminated intravascular coagulation. In conclusion, AT-III concentrate supplementation during L-asparaginase therapy, by the achievement of high levels of antithrombin III, is associated with a lack of activation of the haemostatic system and appears to overcome the complex coagulopathy associated with L-asparaginase.
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PMID:Antithrombin III infusion suppresses the hypercoagulable state in adult acute lymphoblastic leukaemia patients treated with a low dose of Escherichia coli L-asparaginase. A GIMEMA study. 751 43

Thrombus formation and the sequential expression of tissue factor (TF), interleukin-1 beta (IL-1 beta) and interleukin-1 receptor antagonist (IL-1 ra) in several organs were examined immunohistochemically and morphometrically in a novel model of disseminated intravascular coagulation (DIC) developed by modifying the generalized Shwartzman reaction (GSR) in rabbits. The new model [carrageenan (CA)-lipopolysaccharide (LPS)] was induced by the administration of a priming dose of intraperitoneal CA, 10 mg/kg, followed 24 h later by a provocative dose of LPS 25 micrograms/kg, while GSR was induced by the intravenous injection of two doses of LPS 25 micrograms/kg. CA was detected predominantly within macrophages in the spleen and liver. Fibrin thrombi were formed as early as 1 h after the second LPS treatment in all examined organs reaching a peak at 3-9 h and their prevalence was higher in the CA-LPS group (p < 0.05). The sequential expressions of TF and IL-1 beta correlated well with each other in both groups reaching a peak at 3-9 h with the CA-LPS group showing a more pronounced expression than the GSR group. Macrophages in the liver, spleen and lungs, and Bowman's epithelial cells expressed both proteins, while IL-1 beta was also expressed by endothelial and epithelial cells. IL-1 ra was expressed by the same cells expressing IL-1 beta, however, its expression continued to increase gradually over 24 h. The mortality rate was lower (p < 0.05) and neutrophilic sequestration less prominent in the CA-LPS group than in the GSR group. These findings indicate that CA efficiently replaced the priming LPS treatment and the consequently enhanced production of IL-1 beta may have resulted in the upregulation of TF expression leading to the high level of thrombi in this new model which may provide a tool for further studies on the role of cytokines in DIC.
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PMID:Expression of tissue factor and interleukin-1 beta in a novel rabbit model of disseminated intravascular coagulation induced by carrageenan and lipopolysaccharide. 873 72

Laboratory evidence of disseminated intravascular coagulation (DIC) and/or fibrinolysis is present in the majority of patients with acute promyelocytic leukemia (APL). Historically, early hemorrhagic death (EHD) occurred in 10% to 30% of patients treated with chemotherapy. All-trans retinoic acid (ATRA), a differentiating agent, has a CR rate above 80% in patients, with ATRA-associated leukocytosis. We studied thrombotic events in this population and compared it to patients treated with chemotherapy alone. The results of studies using ATRA in patients with APL were reviewed. Patients received ATRA 45-50 mg/m(2) orally in two divided doses daily until complete remission. In newly diagnosed patients, Idarubicin 12 mg/m(2)/day was given intravenously for 4 to 5 days beginning on the fifth day of ATRA therapy or when the white blood cell count (WBC) was over 10x 10(3)/mu l. Thrombotic complications were noted in 3 of 31 patients during induction. Two died from thrombotic events during therapy with multiple thromboses documented at autopsy. ATRA syndrome was suspected in 2 of the patients with thromboses and only 1 of the patients without thrombosis. In previous studies, 1 of 25 APL patients treated with chemotherapy alone had thrombotic events during therapy. In conclusion, treatment of APL with ATRA may decrease the incidence of hemorrhagic complications, but does not eliminate thrombosis. While thrombotic events were not significantly increased in patients treated with ATRA, they were more common in patients suspected of having ATRA syndrome.
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PMID:Thrombosis in patients with acute promyelocytic leukemia treated with and without all-trans retinoic acid. 883 99


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