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Query: UMLS:C0012739 (disseminated intravascular coagulation)
8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute systemic blood changes were measured in New Zealand white rabbits after severe and mild frostbite injury to the foot. There were observed after 72 hr, in the severely frostbitten rabbits, a decrease in erythrocytes, hematocrit, lymphocytes, and albumin, and an increase in total leukocytes, neutrophils, platelets, fibrinogen, and antithrombin III. Mildly frostbitten rabbits showed similar changes except for no changes in the platelets, albumin, and antithrombin III. In severely frostbitten rabbits, after 72 hr, the changes in the plasma coagulation tests were a prolonged partial thromboplastin time, an accelerated prothrombin time, and increased activities of Factors VII, IX, X, and XI. In mildly frostbitten rabbits there were a prolonged partial thromboplastin time and an increased activity of Factor VII. No changes in fibrinolysis were seen in either group of rabbits. Platelet aggregation, studied only in the severely frostbitten rabbits, showed a change only by an increase in the slope of the collagen-induced platelet aggregation. The blood changes observed in the rabbit model are different than those reported in human frostbite cases. No disseminated intravascular coagulation was apparent in the rabbit model after frostbite injury.
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PMID:Acute systemic changes in blood cells, proteins, coagulation, fibrinolysis, and platelet aggregation after frostbite injury in the rabbit. 673 44

The clinical value of a new in vitro test of hemostasis, which we have called Filter Bleeding Time (FBT), was determined in 59 patients referred because of a suspected bleeding disorder. FBT is based on the progressive slowing of the drop rate of citrated blood through a filter of woven Dacron under constant pressure as platelet aggregates occlude the filter. The value for FBT is defined as the time when the blood drop interval has reached 1 minute. The Mayo modification of the Ivy bleeding time (IBT) was performed in all patients; platelet response to ADP, collagen, epinephrine and arachidonate was performed in 24 patients. In 30 normal volunteers FBT measured 1-3 hr after venipuncture was 2.8 +/- 1.5 (means +/- 1SD) min. The FBT was prolonged in 3 of 3 patients with Glanzmann's thrombasthenia, 2 with disseminated intravascular coagulation, 1 with chronic lymphocytic leukemia, 1 with myelofibrosis, and 1 who had taken aspirin. In 6 patients FBT was prolonged while IBT was normal: 4 after taking aspirin, 2 with polycythemia vera. All 6 had reduced platelet aggregation (PA) to ADP (5 microM), collagen (2 mg/ml), epinephrine (5 microM) and/or arachidonate (1.7 mM). In 3 patients FBT was normal while IBT was abnormal: 1 with disseminated intravascular coagulation, 2 undiagnosed; 1 of these 3 had abnormal PA. Of 6 patients with von Willebrand's disease, FBT was prolonged in 5 and borderline in 1; IBT was prolonged in 3, normal in 1, and not done in 2 infants.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical evaluation of a new test of hemostasis: the Filter Bleeding Time. 674 May 68

A term newborn suffered disseminated herpes simplex virus (HSV) type II infection five days after cesarean section delivery for fetal distress. The mother had no history or evidence of herpetic lesions; the father had a history of genital herpetic lesions. The infant's terminal course was dominated by disseminated intravascular coagulation (DIC) with hepatic and renal failure. Microscopic examination revealed a necrotizing vasculitis of small and medium-sized lung and peripancreatic arteries. Nuclear inclusions characteristic of HSV were found in these arteries, as well as in the adrenal parenchyma, spleen, and lymph node; electron microscopy confirmed replication of virus within the arterial endothelial cells. The mechanism of arterial damage in severe herpetic infection contrasts with the immune-complex mechanism postulated for other viral vasculitides. Direct, virally induced arterial damage resulting in exposure of collagen may set the stage of DiC, a commonly fatal complication of this disease.
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PMID:Necrotizing vasculitis in a case of disseminated neonatal herpes simplex infection. 689 28

A women with congenital cavernous hemangiomas and a bleeding diathesis since childhood was found to have a qualitative platelet defect characterized by the absence of a second-phase aggregation induced by epinephrine, adenosine diphosphate (ADP), and collagen, accompanied by decreased levels of adenosine triphosphate (ATP) and ADP, with a high ATP-ADP ratio consistent with the diagnosis of "storage pool disease" of the platelets. There was no evidence of disseminated intravascular coagulation or circulating antiplatelet antibodies. The bleeding tendency responded to platelet transfusion.
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PMID:'Storage pool disease' of platelets. Association with multiple congenital cavernous hemangiomas. 738 76

An 82-year-old man with a one-year history of spontaneous ecchymoses and posttraumatic bleeding was found on physical examination to have a pulsatile abdominal mass. Ultrasonography revealed a large abdominal aortic aneurysm with a freely moving 1.5--2-cm intraluminal thrombus. Laboratory data disclosed intravascular hemolysis, disseminated intravascular coagulation, and a prolonged bleeding time. Further investigation of platelet function demonstrated decreased glass bead retention (0-15%), and reduced or delayed aggregation responses to adenosine diphosphate, epinephrine, and collagen. Studies of platelet factor 3 availability, antiplatelet antibodies, and aggregation response to ristocetin were normal. Transfusion of ten units of normal platelets failed to shorten the patient's bleeding time, despite a marked rise in platelet count. Glass bead retention studies on normal and patient blood were not altered by mixture with patient and normal platelet-poor plasma, respectively. Platelet dysfunction in the presence of arterial aneurysm does not appear to have been reported previously.
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PMID:Platelet dysfunction associated with abdominal aortic aneurysm. 744 78

Tick anticoagulant peptide (TAP) is a potent and selective inhibitor of factor Xa. TAP has shown good antithrombotic efficacy in experimental animal models of disseminated intravascular coagulation and venous and arterial thrombogenesis. In the present study we evaluated the effect of recombinant TAP (rTAP) on acute thrombus formation in human nonanticoagulated blood triggered either by tissue factor (TF) or by collagen at arterial shear conditions. The main goal was to establish the role of factor Xa in thrombus formation by use of an optimal inhibitory concentration of rTAP. Blood was drawn directly from an antecubital vein by a pump over the respective thrombogenic surfaces, which were positioned in a parallel-plate perfusion chamber. rTAP was mixed homogeneously into the flowing blood by a heparin-coated device positioned proximal to the perfusion chamber. The passage of blood through this device caused minor activation of coagulation but little activation of platelets. Fibrinopeptide A and beta-thromboglobulin levels after 5 minutes of blood perfusion were, on average, 14 ng/mL and 45 IU/mL, respectively. rTAP at a plasma concentration of 0.90 mumol/L completely inhibited TF/factor VIIa-dependent thrombus formation at wall shear rates of 650 and 2600 s-1. These shear conditions are comparable to those in medium-sized arteries and in moderately stenosed small arteries, respectively. In contrast to the TF-coated surface, rTAP was less efficient in reducing collagen-induced thrombus formation. While a significant reduction of 53% was observed at 650 s-1, thrombus formation at 2600 s-1 was not affected by rTAP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of selective factor Xa inhibition on arterial thrombus formation triggered by tissue factor/factor VIIa or collagen in an ex vivo model of shear-dependent human thrombogenesis. 748 41

Concentrations of thrombomodulin in blood plasma were measured by a one-step sandwich enzyme immunoassay (EIA). The concentrations in normal healthy subjects were 9.9 +/- 2.9 ng/ml. The concentrations were found to be significantly higher in patients with SLE, RA and other collagen diseases in their active stages than at their non-active stages. The concentrations increased in patients with DIC, and significantly higher levels were observed when DIC was complicated by multiple organ failure. These findings indicate that plasma concentrations of thrombomodulin may be a useful parameter for vascular injuries caused by inflammatory processes or coagulation/fibrinolysis reactions.
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PMID:[Blood concentrations of thrombomodulin in patients with various diseases]. 786 93

To investigate the clinical significance of determination of plasma tissue factor (TF) antigen, we have developed a highly sensitive enzyme-linked immunosorbent assay (ELISA) for plasma TF, using two different monoclonal antibodies against TF apoprotein, 6B4 (catching antibody) and 5G9 (detecting antibody), and tetramethyl benzidine/H2O2 as substrates. Titration curves of recombinant human TF in buffer containing Triton X-100 were linear within the range from 50 to 2000 pg/ml. The total assay time was 3 h. Ultracentrifugation and immunoblot analysis indicated that human plasma and urine contained 50,000 g sedimentable and non-sedimentable forms of TF, both of which were detected by our ELISA method. Plasma and urine concentrations of TF in healthy subjects and patients with various diseases were measured by the ELISA method. In healthy subjects, plasma and urinary TF levels were found to be 149 +/- 72 pg/ml (n = 30) and 175 +/- 60 pg TF/urine creatinine mg (n = 95), respectively. TF was increased in plasma of patients with disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura, vasculitis associated with collagen diseases, diabetic microangiopathy and chronic renal failure receiving haemodialysis, but not in the plasma of endotoxaemic patients without DIC. The plasma TF/serum creatinine ratio did not show a positive correlation. Measurement of TF antigen in plasma may be useful for evaluating the endothelial damage and cell destruction in TF-containing tissues.
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PMID:Determination of plasma tissue factor antigen and its clinical significance. 794 77

We investigated the intraglomerular distribution of thrombomodulin (TM) antigen in patients with various renal diseases. The subjects enrolled in this study were 28 patients with IgA nephropathy, 26 with collagen diseases, 10 with toxemia and 4 with DIC. Normal renal cortex used as a control was obtained from the normal pole of kidneys with a tumor of the opposite pole. Intraglomerular distribution of TM antigen was detected by an immunohistochemical method using a polyclonal antibody against human TM. The following results were obtained: 1) The staining intensity of TM on endothelial cells of glomerular tufts was higher in IgA nephropathy and collagen diseases than in the controls, but was the same in toxemia and DIC as in the controls. 2) The staining intensity of TM decreased with the progression of the glomerular lesion in IgA nephropathy and lupus nephritis. These findings suggest that the intraglomerular distribution of TM may be involved in the progression of glomerular lesions and in the acceleration of intraglomerular blood coagulation in various renal diseases.
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PMID:[Intraglomerular distribution of thrombomodulin in patients with various renal diseases]. 796 73

A case of pure red cell aplasia (PRCA) with various complications polyarthritis, angitis, acute renal failure and DIC was successfully treated with steroid pulse therapy was described. A 55-year-old woman was hospitalized with a 9-month of intermittent but progressive joint pain, morning stiffness, general fatigue, and fever. Her initial laboratory evaluation revealed a hemoglobin of 4.4 g/dl and absence of reticulocyte. Her bone marrow aspirate showed no erythroblast which was compatible with a diagnosis of PRCA. Marked leukocytosis and thrombocytosis, positive antinuclear antigen, elevation of gammaglobulin and C-reactive protein and the presence of polyarthritis and angitis which was confirmed by renal angiography, indicated an underlying autoimmune disorders. Steroid pulse therapy was administered at 500 mg/day for 3 days, resulting in the complete response in both red cell aplasia and above findings. PRCA is known to be associated with systemic lupus erythematosus and rheumatoid arthritis very rarely, but this case did not fulfill the criteria of known collagen diseases, and there is no previous report representing PRCA with various complications such as polyarthritis, angitis and acute renal failure. This case may help us to understand more about the relationship between PRCA and autoimmune disorders.
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PMID:[Pure red cell aplasia complicated with polyarthritis, angitis, and acute renal failure]. 825 11


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