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

Clotting analysis in 30 patients with bleeding complications in malignant hematological diseases revealed the following troubles: The global tests, Quick's index and partial thromboplastin time markedly differed from normal. Activity of clotting factors revealed hypo- or hyperfibrinogenemia, disturbances of the prothrombin complex (factors II, VII, IX and X), decrease of factors V, VIII, XII. Factor XI (= PTA) was not diminished in any case. Regarding the fibrin-stabilizing factor (factor XIII), its activity was significantly decreased in 30 patients with solid tumors and in 30 patients with hemoblastoses. Faulty clotting balance was characterized by hyperfibrinolysis or disseminated intravascular coagulation (DIC) accompanied by reactive hyperfibrinolysis. About one quarter of the patients with malignant disturbances of the hematopoetic system demonstrated (mostly amegacaryocyte) thrombocytopenia. Finally, treatment of bleeding complications in malignant neoplastic diseases is pointed out.
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PMID:[Hemorrhagic diathesis in patients with malignant neoplasms (author's transl)]. 11 27

The relationship between factor VIII (AHF) procoagulant activity and factor VIII-related antigen were examined in patients with disseminated intravascular coagulation (DIC), pulmonary embolism (PE), and coronary artery disease with or without myocardial infarction (MI). It was found that 13 of 13 patients with DIC, 17 of 17 patients with PE, and 10 of 12 patients with MI possessed a significantly elevated factor VIII-related antigen to factor VIII activity ratio (VIII-ratio). The VIII-ratio returned to normal in each of 2 patients with DIC and 1 paitent with PE after treatment with heparin, heparin and alpha-amino-caproic acid, and heparin and coumadin respectively. In contrast, the VIII-ratio was slightly elevated only in 1 of 15 patients with coronary artery insufficiency without MI. In in vitro studies, after treatment of plasma with thrombin or plasmin, factor VIII activity was lost, whereas the amount of factor VIII-related antigen remained the same or was even increased when measured by agarose quantitative immunoelectrophoresis. These observations have led us to conclude that an elevated VIII-ratio is a very sensitive indicator of intravascular coagulation.
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PMID:In vivo and in vitro effects of thrombin and plasmin on human factor VIII (AHF). 13 71

A plasma protein required for the support of ristocetin-induced platelet aggregation was isolated from antihemophilic factor concentrate and radiolabeled with 125I. A double-antibody radioimmunoassay was developed, with use of specific rabbit anti-VIII related antigen serum and goat anti-rabbit globulin. The assay is sensitive, reproducible, and technically simple to perform. Values obtained in normal subjects ranged from 0.65 to 1.53 units, similar to our normal range for VIII coagulant activity (0.67-1.43 units). However, normal or increased values of VIII-related antigen were observed in VIII coagulant-deficient hemophiliacs. Also, concentrations of VII-related antigen significantly exceeded coagulant concentrations in several patients with liver disease or disseminated intravascular coagulation, or both. Of a broad selection of congenital coagulation disorders examined, only patients with von Willebrand's disease had decreased VIII-related antigen concentrations, and these corresponded to the lowered concentration of ristocetin cofactor in the patients. In three transfused patients, VII-related antigen values correlated with the concentration of the cofactor. Our results suggest that the radioimmunoassay of VIII-related antigen is a simple and valuable adjunct in the study of patients with clotting abnormalities.
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PMID:Double-antibody radioimmunoassay for factor VIII-related antigen. 30 60

Tissue factor is an ubiquitous phospholipid-protein complex, which triggers blood coagulation through the so-called extrinsic pathway. Reactions initiated by tissue factor bypass many of the early stages of coagulation (contact phase) and involve factors VII, X, V, II and fibrinogen but also factor IX (and VIII) as it was recently demonstrated. So, it appears that tissue factor has a key-role in the haemostasic process as it has been suggested by the mildness or the absence of haemorrhagic syndrome in contact factors deficiencies. Tissue factor activity has been found in many types of cells, especially in white bloods cells. Experimental studies have demonstrated the presence of tissue factor activity in polymorphonuclears, lymphocytes, monocytes (or macrophages). This activity is enhanced by gram-negative endotoxin stimulation, inflammation, cell mediated immunologic phenomena or malignancy. These data are in good agreement with a wild range of features observed in human pathology: fibrin deposits in inflammatory lesions, disseminated intravascular coagulation (DIC) during the course of gram-negative septicemias or acute promyelocytic leukemias, local thrombi at the early phase of graft rejection. The protective effect of a phospholipase C against DIC induced in rats by tissue factor infusion suggests in the future, a specific therapy would be possible in man that, in the frequent clinical conditions involving clotting activation through tissue factor pathway.
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PMID:[Initiation in vivo of blood coagulation. The role of white blood cells and tissue factor (author's transl)]. 39 57

Twenty-seven patients requiring massive transfusions were studied prospectively to determine whether administration of stored, modified whole blood induced a primary disorder of hemostasis evidenced by generalized microvascular oozing. Platelet counts fell in proportion to the number of units of blood transfused. In contrast, the levels of factors V and VIII correlated poorly with the units of blood transfused, 85% of the total variation in the levels being due to influences other than transfused blood. Levels of all other clotting factors were unrelated to the number of units of blood given. Eight patients developed abnormal bleeding. The cause appeared to be dilutional thrombocytopenia in five patients, and DIC in three. In six of the eight, bleeding was controlled with platelet concentrates alone. Two patients were given cryoprecipitate also. The most useful laboratory test for predicting abnormal bleeding was the platelet count. Fibrinogen levels should be followed as an aid in the diagnosis of DIC. The BT, PT, and PTT were not helpful in assessing the cause of bleeding, unless they were greater than 1.5 times the control value. We recommend that any patient receiving massive transfusions who develops diffuse microvascular bleeding be given platelet concentrates. Platelet counts as high as 100,000 may be required to control bleeding from surgical wounds. It is not necessary to supplement transfusions of stored, modified whole blood with fresh blood or fresh frozen plasma.
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PMID:Hemostasis in massively transfused trauma patients. 46 85

The exposure of rats to 100% oxygen at 1 atmosphere leads to a prolongation of prothrombin times and activated partial thromboplastin times. This development is associated with a consumption of factor XII, VIII, and VII activities and with the appearance of fibrin monomers and fibrinogen degradation products. Lead acetate enhances all oxygen-induced changes of the coagulation systems drastically. The O2 survival time of chicks which are naturally deficient in factor XII is greatly increased over that of rats and is not affected by lead acetate. Oxygen survival times of rats suffering from chronic respiratory disease (CRD) are also significantly increased when compared with normal rats. It appears that consumptive coagulopathy and disseminated intravascular coagulation are early events in oxygen exposure, and that their development is accelerated by lead ions.
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PMID:Oxygen-induced consumptive coagulopathy and its enhancement by lead acetate. 57 13

Coagulation and fibrinolysis were studied in a colony of aged Syrian hamsters with spontaneous atrial thrombosis, and the results are consistent with concomitant consumption coagulopathy. In comparison to age- and sex-matched hamsters from the same colony, those with atrial thrombi had significantly prolonged prothrombin and partial thromboplastin times, reduced levels of factors II, VII, VIII and X activities and plasminogen; and concentrations of fibrinogen-fibrin split products in excess of 80 microgram/ml. Hematocrits of the thrombosed animals were significantly decreased, total plasma proteins were increased, leukocyte counts were within normal limits, and platelet counts were about half those of the controls. Thrombosed hamsters had significantly reduced plasma albumin content, increased alpha1-, beta-, and gamma-globulins, and reduced A/G ratios. Aged sick hamsters demonstrable thrombi also had reduced coagulation and fibrinolytic activities and platelet counts, but their fibrinogen levels were markedly elevated, and fibrinogen-fibrin split products were either absent or present in trace amounts. This suggests an earlier and/or less acute form of the thrombotic process.
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PMID:Spontaneous atrial thrombosis in aged Syrian hamsters. II. Hemostasis. 57 88

Bleeding episodes in five haemophiliacs with antibody to F VIII were treated by activated F IX concentrate (FEIBA). Relief of pain and haemostasis in affected muscles and joints were recorded in each case. One patient developed a mild attack of disseminated intravascular coagulation with an uneventful recovery. A substantial rise in natural inhibitors of coagulation was seen in two patients, and all but one experienced a rise in F VIII antibody titer.
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PMID:Activated F IX concentrate (FEIBA) used in the treatment of haemophilic patients with antibody to F VIII. 66 13

As the initial problems of trauma have been resolved, patients may survive the immediate period following critical injury only to succumb later to the effects of sepsis. We previously noted a correlation between multiple organ failure and intravascular clotting. The present study evaluated the incidence of infection complications following proven disseminated intravascular coagulation. Detailed analysis of multiple clotting factor changes following critical surgical illness (Factors I, II, V, VIII, IX, X, XI, and platelets, fibrin degradation products and plasminogen) were carried out prospectively in 48 patients. Twenty-one of the 48 were classified as having a severe degree of intravascular coagulation on the basis of hematologic evidence. Only one survived without evidence of infection; 16 showed changes consistent with a moderate degree of intravascular coagulation, and ten subsequently developed evidence of infection. Of the 11 patients with minimal evidence of intravascular coagulation, infection developed in only one.
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PMID:The relationship between sepsis and disseminated intravascular coagulation. 70 5

Nine patients with severe classic hemophilia and inhibitors against factor VIII were treated for 156 bleeding episodes with 503 infusions of Proplex, Konyne, or Auto-Factor IX, three preparations of prothrombin complex concentrates (PCCs). Approximately two thirds of the bleeding episodes were managed successfully. Although the prothrombin time (PT) and partial thromboplastin time (PTT) were shortened after most PCC infusions, there was no evidence of disseminated intravascular coagulation. The degree of shortening of PT or PTT was not related to the particular PCC preparation used, dose, or cessation of hemorrhage. All PCC preparations contained activated clotting factors, as manifested by their ability to shorten the PTT of normal plasma, factor-VIII-deficient plasma, and factor-IX-deficient plasma. Shortening, which was greater with Auto-Factor IX than with the other products, was inhibited partially by a factor IX antibody and blocked completely by prolonged incubation with plasma. Although the nature of the procoagulant material in PCCs is uncertain, these products are of proven benefit to hemophilic patients with high-titer inhibitors. Side effects have been minimal and inhibitor titers have not risen.
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PMID:Use of prothrombin complex concentrates in hemophiliacs with inhibitors: clinical and laboratory studies. 72 19


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