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

Hemostatic abnormalities are common in patients with metastatic malignancy and are attributed, in part, to materials secreted by tumor cells. Tumor stimulation might therefore cause further perturbation of hemostasis. This article reports observations on the effects of androgen stimulation on multiple hemostatic parameters in patients with metastatic prostate cancer. Testosterone was given before chemotherapy in an experimental protocol designed to increase tumor sensitivity to cytotoxic agents. The following parameters were measured on day 0 (before) and days 2 and 4 of fluoxymesterone administration: PT, APTT, platelet count, plasma betathromboglobulin (BTG), platelet factor 4 (PF4), fibrinogen, fibrin(ogen) split products (FSP), factor VIII coagulant activity (VIII C), von Willebrand factor antigen (vWF Ag), fibrinopeptide A (FPA), antithrombin III (AT III), and protein C antigen (PC). Ten patients were studied during 17 cycles of hormonal stimulation. Baseline levels of BTG, PF4, fibrinogen, FSP, factor VIII C, vWF Ag, and FPA were significantly elevated compared with normal control. Although androgen stimulation resulted in elevation of BTG, FPA, and FSP levels by day 4 in many patients, the changes for the entire group were not statistically significant. Other parameters remained unchanged or were only slightly elevated. Two patients developed laboratory evidence of disseminated intravascular coagulation (DIC) but were clinically unaffected. Our data suggest that most patients with metastatic prostate cancer show evidence of ongoing activation of platelets, coagulation, and fibrinolysis. In a few individual patients, androgen stimulation of this hormonally dependent tumor may cause further activation of platelets, coagulation, and fibrinolysis.
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PMID:Hemostatic effects of hormonal stimulation in patients with metastatic prostate cancer. 340 35

Disseminated intravascular coagulation invariably accompanies placement of peritoneovenous (LeVeen) shunts, which suggests that ascitic fluid contains procoagulant material capable of activating blood coagulation. In this study, we identified thrombogenic activity in human ascites and the hemostatic pathway by which it acts. Peritoneal fluid was removed percutaneously from patients with ascites due to various causes. Four fractions were prepared by centrifugation: cells, a low-speed, cell-free fluid, a high-speed supernatant, and the precipitate from the high-speed centrifugation. Cellular fractions from all ascitic fluids shortened a one-stage clotting time of normal pooled plasma by 68% in comparison with saline solution and endotoxin controls. Similarly, the cell-free fluids also shortened the clotting time of normal pooled plasma by 41%. The cellular and cell-free fractions shortened the clotting time of factor VIII-deficient plasma but failed to demonstrate procoagulant activity in factor VII-deficient plasma. These fractions had no effect on platelet aggregation or the platelet release reaction. The high-speed precipitate was dissociated by ethylenediaminetetra-acetate (EDTA) into fluid phase and precipitate, both of which demonstrated procoagulant activity. Furthermore, high-speed precipitate contained protein, phospholipid, and sterol in proportions similar to those of plasma membranes and contained membrane-bound vesicles as identified by means of electron microscopy. This material could be rendered inactive by heating to 100 degrees C for 2 minutes or by incubation with phospholipase C for 15 minutes. Finally, the ability of the high-speed precipitate to shorten the clotting time was prevented by preincubation with a monoclonal antibody, which is known to inhibit the procoagulant activity of human tissue factor. We suggest that several entities contribute to the procoagulant properties of human ascites, with procoagulant material deriving at least in part from peritoneal cells. The sedimentable procoagulant factor appears to be associated with cellular membranes or membrane fragments and is thromboplastin-like in its chemical composition, immunoreactivity, and substrate specificity.
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PMID:Preliminary characterization of the procoagulant material in human ascites. 358 68

Protein C was measured by means of enzyme-linked immunosorbent assay (ELISA) in plasmas from 58 normal subjects, 39 patients with disseminated intravascular coagulation (DIC) and 5 patients with thrombotic thrombocytopenic purpura (TTP). Protein C levels ranged from 69.7 to 163.6% (95% confidence limits) in normal subjects. In patients with DIC, protein C concentrations were significantly decreased, with a geometric mean value of 42.1%. Protein C concentration was positively correlated with plasma prothrombin, antithrombin III and serum pseudocholinesterase, and was negatively correlated with von Willebrand factor antigen (vWF:Ag) and vWF:Ag/factor VIII ratio. These findings suggest that low protein C concentrations in DIC mean a consumption of protein C probably due to its activation by thrombin and/or impaired liver synthetic function. In patients with TTP, protein C levels were normal with a geometric mean value of 116.7%, indicating that the pathophysiology of TTP is quite different from that of DIC.
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PMID:Protein C levels in disseminated intravascular coagulation and thrombotic thrombocytopenic purpura: its correlation with other coagulation parameters. 384 Dec 32

Factors of coagulation and fibrinolysis have been evaluated in 15 patients with untreated acute nonlymphoblastic leukaemia (ANLL). 10 patients had major bleeding (MB) and 6 had laboratory signs of DIC. 5 patients went into complete remission (CR). Antithrombin III (AT III) was decreased in 7 patients, antiplasmin (AP) in 9, fibronectin (FN) in 6 and factor XIII in 4/12. The ratio between factor VIIIR:Ag and factor VIII:C was over 2.0 in 11 patients, and high values were especially seen in patients with MB and patients with DIC. Spontaneous proteolytic activity, measured with S-2288 was increased in 3 patients who all had MB, and none of whom achieved CR. 2 patients with promyelocytic leukaemia (M3) had low fibrinogen and AP, high FDP and normal AT III, speaking for primary fibrinolysis, which in addition to proteolytic enzymes in the blast cells are important contributing factors regarding MB in ANLL.
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PMID:Factors and inhibitors of blood coagulation and fibrinolysis in acute nonlymphoblastic leukaemia. 385 83

After observing a child with systemic onset juvenile rheumatoid arthritis (S-JRA) who developed purpura fulminans in association with disseminated intravascular coagulation, with subsequent gangrene and autoamputation, we undertook a prospective study of coagulation parameters in children with JRA. Ten consecutive children with S-JRA, 10 children with rheumatoid factor-negative, polyarticular juvenile rheumatoid arthritis (P-JRA), and 10 age- and sex-matched controls were studied. Routine coagulation screening tests were performed, as were tests for plasma fibrinopeptide A (a sensitive measure of intravascular thrombin generation), factor VIII-related antigen (an endothelial cell protein), and platelet factor 4 (a platelet-secreted protein). Our studies suggest that activation of intravascular coagulation is common in systemic onset JRA, but not in rheumatoid factor-negative, polyarticular disease. The coagulopathy may cause severe morbidity. In addition, marked elevations of plasma factor VIII-related antigen suggest perturbation of endothelial cells and vascular involvement in S-JRA, but not in P-JRA. Normal ranges of platelet factor 4 indicate that intravascular platelet consumption does not occur in either type of JRA, despite the thrombocytosis common in both.
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PMID:Evidence for intravascular coagulation in systemic onset, but not polyarticular, juvenile rheumatoid arthritis. 397 74

Protein C is a vitamin-K-dependent plasma glycoprotein that when activated inhibits coagulation by selectively inactivating the active forms of factor V and factor VIII. A specific antiserum to protein C has been raised, and plasma protein C levels have been measured by means of an electroimmunoassay in several physiological and pathological conditions. In 60 healthy adults there were no differences in protein C related to age or sex; protein C levels ranged from 72 to 139% of values in a normal plasma pool. Low levels were found in 12 healthy full-term newborn infants; the levels in 20 women in the last trimester of normal pregnancy were no different from those in healthy non-pregnant women. In 58 patients with chronic liver diseases protein C levels were lower than those in healthy subjects, in degrees roughly proportional to the severity of the disease. Protein C levels were very low in 21 patients with the disseminated intravascular coagulation syndrome, particularly in those who had evidence of consumption coagulopathy. Very low levels were also found, however, in 20 patients with adult respiratory distress syndrome without consumption coagulopathy. Acquired defects of protein C developed after surgery in the patients operated on for malignancies, after major abdominal operations for benign conditions, and also after relatively minor procedures such as appendicectomy and hernia repair. These findings indicate that protein C deficiencies occur in several conditions associated with increased tendency to thrombosis.
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PMID:Deficiencies of protein C, an inhibitor of blood coagulation. 612 39

Factor VIII concentrates have been shown to have reduced ability to correct the bleeding time defect in von Willebrand's disease and to have abnormal mobility of their VIIIR:Ag on crossed immunoelectrophoresis. This report concerns the partial characterization of a fragment of VIIIR:Ag that lacks some of the normal antigenic determinants present on VIIIR:Ag. It is present in commercial factor VIII concentrates, but not in cryoprecipitate, and is recovered from the plasma of hemophilic patients who have been infused with these concentrates. The fragment is also produced during disseminated intravascular coagulation. Although it has a similar mobility on SDS agarose electrophoresis to the smallest multimer of VIIIR:Ag, they are not immunologically identical.
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PMID:Specific factor VIII-related antigen fragmentation: an in vivo and in vitro phenomenon. 618 Jul 85

A fast migrating protein (FMP) was detected by agarose radio-crossed immunoelectrophoresis, in addition to factor VIII antigen (VIII:RAg), using antiserum to human factor VIII (FVIII). FMP had partial immunochemical identity with FVIII, migrated as an alpha-protein, and was distinct from alpha-2 macroglobulin, fibronectin or IgM. FMP was precipitated by concanavalin A and was separable from the bulk of VIII:RAg by ammonium sulphate fractionation. A significant amount of FMP was seen in normal serum (n = 12), plasma from patients with: (a) disseminated intravascular coagulation (n = 12) and (b) severe haemophilia A (n = 6). Trace amounts of FMP were observed in plasma from normal donors (n = 12), but neither VIII:ARg nor FMP was detectable in the plasma or serum from patients with severe von Willebrand's disease (n = 3). Freshly prepared cryoprecipitate contained trace amounts of FMP, similar to normal plasma, but increased levels were observed in antihaemophilic factor concentrates prepared for patient use. Significant levels of FMP were also seen in cryoprecipitate after storage at 4 degrees C for 7 d and this generation of FMP was diminished by the addition of protease inhibitors. The presence of significant levels of FMP in situations where proteolytic enzymes may be activated and inhibition of its generation by protease inhibitors, suggest that this protein is produced by proteolytic action of enzyme(s) on the FVIII molecule.
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PMID:Fast migrating protein, immunochemically related to human factor VIII, studied by crossed immunoelectrophoresis in agarose. 640 77

Coagulation factors were measured in 50 patients presenting with acute renal failure on the day of their admission (D1) and seven days later (D7). A number of changes were observed, particularly in those patients with a poor prognosis (decreased platelet counts and plasminogen concentrations and increased factor VIII related antigen concentrations). In the majority of cases it would appear that disseminated intravascular coagulation remains sub-clinical.
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PMID:Factor VIII related antigen, coagulation tests and acute renal failure. 641 Mar 77

In 24 cirrhotic patients at different stages of hepatic failure, factor VIII:C (F VIII:C), factor VIIIR:AG (F VIIIR:AG), factor VIII AG/C ratio (F VIII AG/C), and serum fibrin-fibrinogen degradation products (FDP) were investigated. In 11 of the 24 patients, several instances of gastrointestinal bleeding due to esophageal varices rupture were documented and 5 patients died of unarrestable bleeding. In our study, we evaluated whether the cause of bleeding was the development of intravascular coagulation or the severity of hepatic failure. A statistically significant difference between F VIII:C, F VIIIR:AG/C ratio, and serum FDP was found in bleeding in comparison with non-bleeding patients. An inverse correlation between the F VIII:C plasma level and serum FDP as well as a direct correlation between F VIII AG/C ratio and serum FDP in the group of bleeding patients were also found. These data seem to suggest a hypercoagulable state which was more significant in the 5 patients who died owing to bleeding. Furthermore, only 1 of these patients had severe hepatic failure. From this study it appears that, in cirrhotic patients, bleeding is related more to the appearance of disseminated intravascular coagulation, as a consequence of both hemodynamic and endothelial changes, than to the degree of hepatic failure itself.
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PMID:Bleeding in cirrhotic patients: a precipitating factor due to intravascular coagulation or to hepatic failure? 641 23


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