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

Prothrombin complex concentrates are used in the treatment of the congenital bleeding disorders associated with Factors II, VII, IX, and X deficiencies. They have also been extensively used to treat acquired coagulation abnormalities secondary to vitamin K deficiency, warfarin ingestion, and various types of liver disease. The reported complications of prothrombin complex concentrates administration include hepatitis, anaphylaxis, and thrombosis. This paper documents the development of disseminated intravascular coagulation in association with the administration of prothrombin complex concentrates to patients with liver disease.
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PMID:Intravascular coagulation with use of human prothrombin complex concentrates. 93 80

A study of coagulation disorders due to hepatitis A infection occurring during pregnancy was undertaken to determine if the unique coagulation status produced by pregnancy (elevated clotting factors and decreased fibrinolytic activity) was responsible for the increased severity of hepatitis A infections reported for pregnant women from various parts of the world. Of 49 patients studied, 12 (24%) developed hepatic failure and 9 (18%) died. A prolonged prothrombin time and low fibrinogen level were found to be as frequent as previously reported for nonpregnant patients with and without hepatic failure. Thrombocytopenia was less common and a long thrombin time was more common. Although intravascular coagulation was suggested by a lower mean fibrinogen level than expected in late pregnancy, mean platelet counts were similar to controls. The frequency of a positive protamine sulfate paracoagulation test for intravascular coagulation (DIC) was similar to that reported for uncomplicated pregnancy, and was of no prognostic value when performed on admission. We conclude that the severe clinical course of hepatitis during pregnancy in this epidemic was not attributable to a predisposition for DIC. However, once fulminant hepatitis occurred, DIC may have been a clinically significant factor.
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PMID:Coagulation studies of viral hepatitis occurring during pregnancy. 100 76

The availability of factor VIII and factor IX concentrates has considerably improved substitution therapy in hemophilia A and B respectively. The desired activity levels and the corresponding factor VIII or factor IX dosage are indicated. Antifibrinolyics have a favorable action when given simultaneously, though hematuria is an absolute contraindication for antifibrinolytic treatment. The administration of factor IX concentrate in case of hemorrhage due to oral anticoagulation or to liver disease, or in newborns, should be used in emergency situations only, since this material may provoke either thrombosis or disseminated intravascular coagulation. Transmission of hepatitis is also possible.
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PMID:[Substitution treatment of hemophilia a and b]. 114 62

A patient developed disseminated intravascular coagulation with purpura fulminans 1 month after starting Dilantin therapy for a seizure disorder. In addition, the patient developed exfoliative dermatitis, hepatitis, cutaneous vasculitis, and microangiopathic hemolytic anemia. She was successfully treated with adrenal steroids and heparin for her purpura fulminans. The hepatitic dermatologic, along with hemorrhagic, complications of Dilantin are reviewed, and the possible origin of the vasculitis and disseminated intravascular coagulation is discussed.
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PMID:Dilantin-induced disseminated intravascular coagulation with purpura fulminans. A case report. 114 59

Factor IX concentrates are of paramount importance in the treatment of hemophilia B. Growing reports of thromboembolic complications and of disseminated intravascular coagulation, coupled with the danger of hepatitis transmission, suggest that the concentrates should be primarily reserved for the treatment of hemophilia B. Concise guidelines for treatment are presented.
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PMID:[Clinical use of factor IX concentrates]. 121 1

The objective of this study was to characterize the hemostatic defect in dogs with infectious canine hepatitis (ICH), a naturally occurring viral disease of dogs. Five littermate dogs were inoculated with 10(3) TCID50 of ICH virus intravenously. Two littermates were controls. The clinicopathologic manifestations of ICH were fever, depression, anorexia, hematemesis, melena, widespread mucocutaneous petechiae, prolonged bleeding from venipunctures, faceial edema, leukopenia, and proteinuria. The hemostatic defect of ICH was characterized by thrombocytopenia, abnormal platelet function, prolonged one-stage prothrombin time and activated partial thromboplastin time, normal thrombin times, depressed factor VIII activity, and increased fibrin-fibrinogen degradation products. These findings suggested that the central pathologic mechanism of the abnormal hemostasis in ICH was disseminated intravascular coagulation (DIC). ICH is an example of DIC induced by viral infection. This disease is a suitable model for investigation of the detection, pathogenesis, and therapy of DIC.
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PMID:Infectious canine hepatitis: animal model for viral-induced disseminated intravascular coagulation. 124 23

An experimental hepatitis was induced in rabbits by intravenous infusion of 1 g galactosamine per kilogram of body weight. Galactosamine administration caused microclot formation in kidneys, liver, lungs, and spleen in a low percentage. If, however, animals were infused with the fibrinolysis inhibitor epsilon-aminocaproic acid in addition to galactosamine, microclots were generated in a high percentage. The microclots exhibited typical staining characteristics like those observed in the generalized Shwartzman reaction. Some animals developed bilateral renal cortical necrosis. Heparin treatment prevented the occurrence of microclot fromation after galactosamine administration, but it neither prolonged the survival time of the animals nor prevented or reduced liver cell damage. Increases in serum GPT and bilirubin levels were similar in heparin-treated and untreated rabbits. The experiments indicate that disseminated intravascular coagulation is involved in galactosamine-induced hepatitis but does not contribute to the severity of the liver injury.
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PMID:Experimental galactosamine-induced hepatitis. Effect of anticoagulant and antifibrinolytic agents on microclot formation. 125 92

A premature neonate with severe Coxsackie B1 hepatitis acquired in utero developed disseminated intravascular coagulation a few days after birth. The neonate did not respond to conventional treatment. Eradication of aerobic gram-negative bacilli (Enterobacteriaceae) from the gut with oral nonabsorbable polymyxin E and tobramycin (selective decontamination of the digestive tract) was followed by clinical improvement; disseminated intravascular coagulation was controlled. After an unstable convalescence, the neonate recovered and was discharged in good general condition. A correlation between oral feeding, gut carriage of Enterobacteriaceae, fecal endotoxin pool, and platelet counts was observed. The eradication of gut carriage of aerobic gram-negative bacilli was associated with a significant decrease of the intestinal endotoxin pool and paralleled the recovery from thrombocytopenia. Selective decontamination is discussed as a method of possible value for controlling systemic endotoxin-induced symptoms in the critically ill with intestinal endotoxemia.
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PMID:Selective decontamination of the digestive tract contributes to the control of disseminated intravascular coagulation in severe liver impairment. 132 53

Twenty rabbits were inoculated with a suspension of Viral Hemorrhagic Disease virus. Hemostatic functions were assessed every sixth hour from 6 to 60 hours post-inoculation. Tissue samples obtained at the same intervals allowed the study of the development of lesions throughout the experiment. Biological signs of Disseminated Intravascular Coagulation (DIC) were detected on and after 30 h post-inoculation and consisted of prolonged One Stage Prothrombin Time and Activated Partial Thrombin Time, the decrease of factors V, VII, and X and high levels of soluble fibrin monomer complexes and D-dimers. A reduction of thrombocyte numbers, heterophils and lymphocytes was associated. The close association of DIC and necrotizing hepatitis lesions suggested the hepatic lesions to be the most important DIC triggering factor. Other mechanisms are discussed.
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PMID:Hematological parameters and visceral lesions relationships in rabbit viral hemorrhagic disease. 132 5

Seven rabbits experimentally infected with rabbit haemorrhagic disease virus were examined haematologically and histologically. Haematologically, activated partial thromboplastin time and prothrombin time were markedly prolonged in the terminal phase of the disease, just prior to death (all the animals died between 27 and 40 hr after inoculation with rabbit haemorrhagic disease virus). There was an increase in the titre of fibrin degradation products and a decrease in antithrombin III activity during the same interval. Acute necrotic hepatitis and disseminated intravascular coagulation (DIC) in many organs, including the lung, kidney, spleen and heart were the characteristic histopathological changes. Thus, the haematological and histological changes suggested that DIC was induced by rabbit haemorrhagic disease virus infection. Severe liver necrosis was considered to be a factor causing DIC by inducing a hypercoagulable condition in the systemic blood circulation.
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PMID:Disseminated intravascular coagulation (DIC) in rabbit haemorrhagic disease. 133 94


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