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)

Two patients with acute promyelocytic leukemia and severe bleeding associated with hypofibrinogenemia were studied. The markedly shortened whole blood clot lysis time and dilute clot lysis time suggested that the defect was an increase in fibrinolysis. Although disseminated intravascular coagulation could not be totally excluded as an alternative mechanism, excessive fibrinolysis was confirmed as the pathogenic cause by the prompt response to the administration of tranexamic acid. The low circulating plasminogen, alpha 2 plasmin inhibitor level and the presence of alpha 2 plasmin inhibitor-protease complex in both patients suggested that the increased fibrinolysis probably resulted from the liberation of plasminogen activator from the promyelocyte.
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PMID:Hypofibrinogenemia due to increased fibrinolysis in two patients with acute promyelocytic leukemia. 659 15

Collaborative studies on hemostasis in dengue hemorrhagic fever (DHF) patients by Indonesian and Japanese teams revealed that all DHF patients had manifestations of the acute type of disseminated intravascular coagulation (DIC). Prolongations of activated partial thromboplastin time and prothrombin time and decreases of platelet counts, fibrinogen, prothrombin, factor VIII, plasminogen and antithrombin III activities were observed transiently during the acute stage of DHF. It was also found that alpha 2 antiplasmin was decreased in the acute stage to 32% of the normal level on the average. This may characterize the hemorrhagic diathesis of the DHF patients.
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PMID:Features of DIC in dengue hemorrhagic fever. 666 46

Automated microanalytic chromogenic coagulation assays allow serial monitoring of critically ill newborn infants. In this study 84 premature infants [26 healthy prematures and 58 neonates with idiopathic respiratory distress syndrome (IRDS)] were studied daily during the first week of life, to investigate the possible significance of hemostatic abnormalities in IRDS. In neonates with IRDS, coagulation factors II and X, antithrombin III (AT-III), plasminogen, and alpha 2-antiplasmin were significantly lower than control values. Recovery of the initially low AT-III levels was delayed relative to the other coagulation parameters measured. An AT-III less than or equal to 0.15 U/ml was present within the first 6 h of life in eight patients who developed IRDS, seven of whom died within 48 h. Autopsy of these neonates showed widespread fibrin deposition and hemorrhage in vital organs consistent with intravascular coagulation. These findings indicate that very low levels of AT-III are associated with disseminated intravascular coagulation in neonates with IRDS and suggest that a deficiency of AT-III is predictive of a poor outcome.
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PMID:Low antithrombin III levels in neonates with idiopathic respiratory distress syndrome: poor prognosis. 672 60

Hematin is clinically useful in the treatment of acute intermittent porphyria. Recently, hematin-induced coagulopathy has been reported, and a patient we treated bled during hematin therapy. On 3 separate occasions, infusions of hematin (4 mg/kg) induced thrombocytopenia, prolongation of the prothrombin time, partial thromboplastin time. Reptilase time, and apparent decreases in fibrinogen and increases in fibrin(ogen) degradation products (FDP). However, fibrinogen assayed by heat precipitation was unchanged, the protamine paracoagulation test was negative, there was no red blood cell fragmentation, and plasminogen and antithrombin III remained normal, excluding the presence of disseminated intravascular coagulation. Furthermore, premedication with heparin, 5000 U i.v., failed to prevent the lengthening of the Reptilase time and exacerbated the thrombocytopenia. In vitro studies revealed that hematin, 0.1 mg/ml, aggregated platelets and induced the release of 14C-serotonin and adenosine triphosphate (ATP). Hematin also aggregated washed or gel-filtered platelets but had no effect on formalin-fixed platelets. Aggregation was inhibited by aspirin (0.12 mg/ml), adenosine triphosphate, and apyrase, suggesting that hematin aggregated platelets by inducing adenosine diphosphate (ADP) release. Hematin (0.07 mg/ml) progressively inactivated thrombin and 0.1 mg/ml prolonged the Reptilase time. Thus, hematin is unique in that it both induces platelet aggregation and inhibits coagulation.
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PMID:Hematin: unique effects of hemostasis. 682 96

We prospectively studied the hemostatic system of ten persons bitten by the Eastern diamondback rattlesnake (Crotalus adamanteus) during 1978-1980. Blood was drawn when the patients arrived in the emergency room and every 6 hr thereafter. All envenomated victims developed incoagulable blood (defined by a thrombin time greater than or equal to 120 sec, normal less than 20 sec). Platelet counts and plasma levels of antithrombin III and factors II and VIII were not drastically altered, which distinguished this disorder from classic disseminated intravascular coagulation. Fibrinogen levels were markedly decreased (mean coagulable level of 0 mg/dl and antigenic levels of 99 mg/dl). Plasminogen levels were 20% of normal, alpha-2-plasminogen inhibitor was 17% of normal, and plasminogen activator was 20 times normal. Levels of fibrin degradation products peaked at a mean of 7,680 micrograms/ml. The magnitude and duration of the coagulopathy were proportional to the clinical severity of envenomation. Treatment with antivenin blunted the coagulopathy. Because venom from the Eastern diamondback rattlesnake does not directly activate plasminogen, we conclude that coagulopathy following envenomation by that reptile appears to be due to partial proteolysis of fibrinogen with secondary activation of plasminogen by released plasminogen activator, probably of endothelial origin.
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PMID:Mechanism of defibrination in humans after envenomation by the Eastern diamondback rattlesnake. 685 33

Coagulation profiles were performed in 30 consecutive alcoholic cirrhotic patients without known infection, malignancy, recent surgery, transfusion, or alcoholic intake. Hemorrhagic phenomena were present in 70% and included gastrointestinal bleeding, oozing from venipuncture sites, bruising, and epistaxis. All 30 patients had multiple liver function and coagulation abnormalities, the most frequent of which were increases in F VIII components and decreases in F XI and F VII. Also decreased in half or more of the 30 patients were Fletcher F, F II, F X, prothrombin time (PT), partial thromboplastin time (APTT), thrombin time (TT), reptilase time (RT), anti-thrombin III, and plasminogen. When comparing cirrhotic bleeders with nonbleeders, four parameters were significantly different in those with a bleeding tendency: F VII, anti-thrombin III, plasminogen, and albumin. The prolonged APTT was associated in four cases with a blocking inhibitor of unknown etiology. The prolonged TT and RT, in the absence of fibrin split products, fibrin monomers, DIC, or shortened euglobulin lysis time in any patient were suggestive of an abnormal fibrinogen, a dysfibrinogen. In three other patients, there was an inhibitor of the TT. Further investigation of the suspected dysfibrinogen in 21 patients by SDS-polyacrylamide gel electrophoresis revealed that the molecular weights of the Aalpha, Bbeta, and gamma polypeptide chains of fibrinogen were not different from normal. Two-dimensional immunoelectrophoresis of the suspected dysfibrinogen was similar to normal in 18 of 21 patients, with loss of the initial shoulder in three.
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PMID:Bleeding and coagulation abnormalities in alcoholic cirrhotic liver disease. 704 81

Presence of chronic DIC (disseminated intravascular coagulation) eliciting an impeded blood coagulation has been postulated of late as one of the etiology causing toxemia of pregnancy, for which studies have been immunologically made. These theories remain unestablished. In this regard, the role of complement in blood coagulation has been noted, and their correlation is being elucidated. The author introduced a concept of complement to etiological theory of an impeded blood coagulation origin, by which toxemia of pregnancy was studied with emphasis placed on their correlation. The results obtained are as follow: 1) Thrombin and thromboplastin allowed in vitro to decreases the potency of complement, and the lowering also was seen even in the case of simultaneous supplement of urokinase and plasminogen. 2) The decrease also was periodically seen in rabbit's DIC experimentally made. 3) An increase in CH50, C3, C4, and factor B of normal pregnancy were of significance when compared with those of the control (p less than 0.001), while C1 inactivator decreased significantly (p less than 0.001). 4) CH50 was 52.2 +/- 2.4U/ml in severe toxemia, a decrease being of significance (p less than 0.01) as compared with that in third trimester of normal pregnancy. Those other parameters which tended to decrease included hemolytic activity of alternative pathway (AP-CH50), C4, and factor B except C1 inactivator with a trend being high.
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PMID:[Studies on relationship between complement and blood coagulation system in toxemia of pregnancy (author's transl)]. 706 48

Acute necrotizing (hemorrhagic) pancreatitis was induced in 12 dogs by infusing oleic acid into their pancreatic ducts. There were decreases in blood pH, complement, antithrombin III, blood platelets, 24- and 48-hour plasminogen, and 24-hour haptoglobin and modest decreases in serum albumin. There were increases in fibrinogen, 48- to 120-hour haptoglobin, and 96-hour and 120-hour plasminogen and prolongations of prothrombin and activated partial thromboplastin times. The latter 2 changes together with decreases in antithrombin III, platelet numbers, and complement were indicative of consumption coagulopathy. A clinically innocuous but statistically significant decrease in serum total and ionized calcium despite significant acidosis was noted. This indicates that serum total and ionized calcium is helpful in making the diagnosis of acute necrotizing pancreatitis. Methemalbuminemia of 6 mg/dl at 24 hours and 7 mg/dl at 48 hours indicates that methemalbuminemia is a valuable diagnostic and prognostic finding in association with acute necrotizing pancreatitis.
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PMID:Biochemical and coagulation changes in a canine model of acute necrotizing pancreatitis. 725 99

An analysis was made of 41 cases of disseminated intravascular coagulation in dogs, with the objective of evaluating routine and nonroutine laboratory tests used in making the diagnosis. The dogs were grouped on the basis of underlying disease, which included neoplasia (39%), pancreatitis (30%), chronic active hepatitis (15%), heat stroke (12%), and sepsis (4%). Of the diagnostic tests evaluated, those for determination of activated partial thromboplastin time, antithrombin III activity, prothrombin time, and the platelet count were the most valuable. Of the clotting factors, factor V activity was decreased more frequently than the activity of factor VIII:C (factor VIII: procoagulant). The factor VIII:C activity was in conflict with prevailing dogma that reflects depression of this factor in disseminated intravascular coagulation. Factor VIII:C activity was decreased in only 29% of dogs studied. Activation of the fibrinolytic system was manifested by decreased plasminogen activity in 49% of the dogs studied. Sixty-one percent of the dogs had increased amounts of fibrin (ogen) degradation products.
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PMID:Disseminated intravascular coagulation: antithrombin, plasminogen, and coagulation abnormalities in 41 dogs. 726 67

The influence of haemoperfusion on blood-coagulation and cellular constituents of the blood was studied in three groups of patients. In four patients haemoperfusion was performed using a column containing acrylic-hydrogel coated activated charcoal (Haemocol), in five patients with a column containing uncoated XAD-4 nonionic polystyrene resin (Amberlite) and in five patients with a column containing cellulose coated activated charcoal (Gambro Adsorba 300 C). Perfusion was performed during 4 h with a flow of 300 ml/min. Before the start, 2 h after the start, at the end and 2 h after the end of the perfusion the haemoglobin concentration, haematocrit, leucocyte number, differential white cell count, thrombocyte number and heparin concentration were measured. Before the start and 2 h after the end prothrombin time, thrombin time, partial thromboplastin time, reptilase time, fibrinogen, prothrombin, factors V, VII, X, antithrombin III, bleeding time (Ivy), ethanol gelation test, fibrin split products and plasminogen were measured. The following conclusions can be drawn: haemoperfusion per se causes haemodilution; polystyrene resin causes in some patients a temporary reduction of the leucocyte number during haemoperfusion; polystyrene resin causes a significant reduction of thrombocyte number compared to coated activated charcoal; polystyrene resin and to a lesser extent acrylic-hydrogel-coated activated charcoal causes in some patients a prolongation of bleeding time probably by inducing alteration of thrombocyte function caused by release; polystyrene resin and probably also acrylic-hydrogel-coated activated charcoal causes an increased fibrinolytic activity without signs of disseminated intravascular coagulation.
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PMID:The influence of haemoperfusion on haemostasis and cellular constituents of the blood in the treatment of intoxications: a comparative study of three types of columns (Haemocol, Amberlite XAD-4, Gambro Adsorba 300 C). 727 53


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