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)

Patients received 2,000 ml of dialysate intraperitoneally with five exchanges per day during continuous peritoneal dialysis (CAPD) for the treatment of terminal renal insufficiency. During a dwell time of 4 h the dialysate reached a total protein concentration up to 100 mg/dl by mass transfer of intravascular proteins. The composition is dependent on the molecular weight of the proteins. This results in an intraperitoneal hemostatic system of low concentration and different composition. We found an intraperitoneal fibrinogen cleavage and thrombin-antithrombin III-complex formation leading to increased levels of fibrinopeptide A (FPA: 33.3 +/- 7.0 ng/ml) and thrombin-antithrombin III-complex (TAT: 4.7 +/- 0.4 ng/ml) in plasma by mass transfer from dialysate to plasma. t-PA (tissue plasminogen activator) and PAI-1 (plasminogen activator inhibitor type 1) concentrations in plasma were within the normal range. The dialysate concentrations indicated a low local secretion. The fibrinolytic fibrin fragment D-dimer and the fibrinogen degradation product concentrations in plasma were greater than in dialysate. But the relations of the proteins between plasma and dialysate refer to a local intraperitoneal production as well. The results show that intraperitoneal coagulation predominates over fibrinolysis which is accompanied by an intravascular fibrinolysis in patients undergoing CAPD. Neoantigens produced in dialysate and diffused to plasma are comparable to changes seen in disseminated intravascular coagulation.
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PMID:Relation of intraperitoneal and intravascular coagulation and fibrinolysis related antigens in peritoneal dialysis. 220 48

Patients with acute myeloid leukemia have multiple hemostatic and thrombotic complications, which may or may not result from disseminated intravascular coagulation. Previous studies incorporating routine coagulation analyses failed to detect any clinically useful information in most of these patients. In this study, the first comprehensive evaluation of the various aspects of the hemostatic system in a population of patients with acute myeloid leukemia was performed. Eighteen patients (23-71 years of age) were studied at either diagnosis or relapse. Hemostatic studies were performed at onset and on days 3, 7, and 30 after initiation of therapy. The bone marrow blast counts ranged from 8% to 98%; prothrombin time and activated partial thromboplastin time showed only minor prolongations in a few of these patients. However, in all patients measurement of platelet-associated markers revealed elevated platelet factor 4 and thromboxane B2 and normal 6-keto-prostaglandin F1 alpha levels. Fibrinolytic markers showed an increase in D-dimer and tissue plasminogen activator and a decrease in alpha 2-antiplasmin levels. Plasminogen, plasminogen activator inhibitor, and fibrinogen levels were normal. Coagulation markers demonstrated a decrease in protein C and antithrombin III levels and an elevation of the thrombin-antithrombin complex. The pretreatment values for all hemostatic markers studied were similar to the values obtained on days 3, 7, and 30 during treatment. This investigation demonstrated a subclinical activation of the components of the hemostatic system possibly leading to a hypercoagulable state. Although only six patients (33%) experienced hemorrhagic complications, the risk of bleeding and/or thrombosis was strongly evident in all patients. The significance of finding abnormal levels of specific molecular markers of hemostasis will be established in the future application of such markers in clinical evaluations of leukemic patients known to be at risk for coagulation disorders.
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PMID:Global and molecular hemostatic markers in acute myeloid leukemia. 222 Jun 67

To investigate the effects of extra-corporeal ascites recirculation on coagulation, several coagulation variables were measured in ascitic return fluid and plasma before, during and after this procedure in 16 patients with diuretic resistant ascites. Small but significant reductions in plasma fibrinogen levels and platelet counts and increases in plasma X-oligomer were observed during and after the procedure compared with before. These findings are consistent with the view that ascites recirculation induces disseminated intravascular coagulation although this would appear to be only mild and of no clinical significance in the majority of patients. Although increased levels of activated factor VII were observed in ascitic fluid indicating activation of the extrinsic pathway of coagulation, a significant increase in plasma activated factor VII during the procedure was not demonstrated. Increased fibrinolytic activity was observed in ascitic fluid due to the presence of tissue plasminogen activator. Increased X-oligomer levels were observed in ascitic fluid indicating that lysis of cross-linked fibrin is also an active process within ascites.
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PMID:Coagulation disturbances following ascites recirculation. 233 93

Protein C is a potent inhibitor of blood coagulation, and, in addition, appears to be a profibrinolytic agent. In a first step, protein C must be converted to a serine protease. This activation is catalyzed by a complex formed between thrombin and thrombomodulin, an endothelial cell surface protein. Activated protein C exhibits its anticoagulant activity through the proteolytic inactivation of two blood coagulation cofactors, factors Va and VIIIa. This reaction requires phospholipids, originating from platelets or endothelial cells, and a cofactor protein, protein S. Protein S enhances the binding of activated protein C to phospholipids. In addition, activated protein C stimulates fibrinolysis, through the inactivation of the tissue plasminogen activator (tPA) inhibitor. An isolated constitutional, quantitative or qualitative, protein C or protein S deficiency increases the risk of thrombosis, the clinical features are different in the rare cases of homozygous protein C deficiency (neonatal purpura fulminans) or in the heterozygous patients (recurrent venous thrombosis in young adults). Acquired deficiency in protein C and S had been observed in liver disease, during vitamin K antagonists or L-Asparaginase treatment, and in disseminated intravascular coagulation.
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PMID:[Protein C, protein S]. 303 76

A group of 37 patients with myocardial infarction less than 6 hours old was given 5,000 IU of heparin and 0.75 mg/kg of tissue plasminogen activator (rt-PA) (Group A, N = 18) or placebo (Group B, N = 19) intravenously over 90 minutes in a double blind study. Blood sampling was performed before, during and after treatment. The plasma rt-PA concentrations (micrograms/ml) of Group A were as follows: (Table: see text) The concentrations of plasminogen and antiplasmin have decreased significantly as did the fibrinogen level: a concentration of 1 g/l was observed in 7 cases during rt-PA therapy, lasting for 4 to 8 hours after the end of the infusion of rt-PA in 3 cases. The increase of FDP during rt-PA (m = 551 and 222 micrograms/ml at the 60th and 90th minutes) was relatively moderate considering the average level of defibrination (61%). No significant biological changes were observed in Group B. These results support those of our in vitro trials: at comparable thrombolytic activities, the reduction of plasma fibrinogen is less with rt-PA than with streptokinase (SK) or urokinase (UK). However, at concentrations 1 microgram/ml, rt-PA causes almost complete defibrination.
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PMID:[Tissue plasminogen activator (t-PA) in myocardial infarction. Biological aspects]. 310 72

The fibrinolytic response to disseminated intravascular coagulation (DIC) has been considered important both in preventing thrombosis and in contributing to hemorrhage. Detailed studies of fibrinolysis in DIC are lacking, however. We measured tissue plasminogen activator (t-PA) antigen and activity levels in 74 patients with DIC, 53 hospitalized patients with similar illnesses without DIC, and 36 healthy normal subjects, using sensitive, specific assays. Mean t-PA antigen levels were significantly higher in patients with DIC than in either hospitalized control subjects or normal individuals in most disease categories studied. Highest t-PA antigen levels were seen in patients with liver disease, but patients with DIC without liver disease also had significantly elevated t-PA antigen. Detectable free t-PA activity was infrequently seen in patients with DIC, however. No correlation was found with either thrombotic or hemorrhagic complications and levels of t-PA antigen or activity in DIC, with the possible exception of increased t-PA activity in two patients with intracranial hemorrhage. Bleeding complications were seen almost exclusively in patients with underlying anatomic lesions, and thrombotic complications were usually associated with other known predisposing factors. We conclude that t-PA antigen is usually elevated in DIC, but free t-PA activity is infrequently seen, most likely because of increased levels of t-PA inhibitor. The presence or absence of free t-PA activity does not appear to predict which patients with DIC will develop hemorrhage or thrombosis.
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PMID:Tissue plasminogen activator antigen and activity in disseminated intravascular coagulation: clinicopathologic correlations. 311 52

Ascitic fluid reinfusion in severe cirrhosis has frequently been associated with intravascular coagulation (DIC). A low-grade DIC has been postulated to be present in liver cirrhosis. PT, APTT, fibrinogen, plasminogen, antiplasmin, fibrin degradation producers (FDP), euglobulin lysis time, tissue plasminogen activator, and fibrinopeptide A were investigated both in the plasma and ascitic fluid of cirrhotic patients before and after the concentration-reinfusion technique. Our results indicate that increased thrombin formation associated with hyperfibrinolysis is present in the plasma of cirrhotic patients. In ascitic fluid very high levels of thrombin and fibrinolysis activation were found. We conclude that (1) a DIC-like picture exists in ascites and (2) after ascites reinfusion procedures, ascitic fluid is the principal factor in the pathogenesis of DIC. During ascitic fluid reinfusion heparin treatment could be used successfully.
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PMID:A DIC-like picture on plasma and ascitic fluid of cirrhotic patients. 314 1

Influence of acute portal vein occlusion on blood coagulation and fibrinolysis have not been fully clarified. In this experimental study in mongrel dogs, 1) changes of blood coagulation and fibrinolysis in portal vein and peripheral vein, 2) histological changes in small intestine and 3) activity of plasminogen activator in small intestine were investigated periodically after acute portal vein ligation with or without heparinized hydrophilic catheter-bypass between portal and femoral vein. All five dogs died 81-130 minutes (mean 105 minutes) after portal vein ligation. On the other hand, all five bypassed dogs survived in good condition for more than four hours. Acute portal venous congestion caused hypercoagulable state in portal system and apparent DIC occurred in portal system 10 minutes after portal vein ligation. Activity of tissue plasminogen activator which was observed mostly in the endothelial cells of vessels in submucosal layers of small intestine decreased rapidly and disappeared within 20 minutes after portal vein ligation. To the contrary, with the use of the catheter-bypass procedure, no significant changes of blood coagulation and fibrinolysis were observed. These results indicate clearly that portal venous congestion is the trigger of hypercoagulable state in portal system, which progresses to irreversible DIC in 20 minutes. With the use of the catheter-bypass procedure, portal vein shut-down is performed without any abnormal coagulation and fibrinolysis in portal bed and systemic circulation.
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PMID:[The experimental study of blood coagulation and fibrinolysis in acute portal vein occlusion]. 668 31

A patient undergoing intracranial surgery developed disseminated intravascular coagulation with life threatening peroperative bleeding. Thromboelastography established the diagnosis of hyperfibrinolysis, usually a fatal complication of a neurosurgical operation. With the administration of a high dose regimen of aprotinin (Trasylol) the haemorrhage was controlled and the hyperfibrinolytic state reversed. Evaluation of blood samples from the jugular bulb suggested that there was a pronounced local release of tissue plasminogen activator into the circulation.
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PMID:Hyperfibrinolysis during intracranial surgery: effect of high dose aprotinin. 752 19

Abnormal fibrinolysis and thrombotic complications have been often observed in patients who had undergone surgery for meningioma. Fourteen patients, affected by meningioma, were studied before surgery, during surgery and 24 h after surgery in order to evaluate the modifications of the fibrinolysis system and the coagulation physiological inhibitors. Before surgery, no patient showed hyperfibrinolysis and/or modifications of coagulation physiological inhibitors. During surgery, an activation of fibrinolysis with pathological levels of tissue plasminogen activator activity (mean = 6.33 U/dl, SD = 7.9, p = 0.02) and increased levels of fibrin degradation products (mean = 0.21, SD = 0.18, p = 0.002) was noted. Modifications of the fibrinolysis parameters occurred only in 9/14 patients (64%). These patients presented a more vascularized tumour, revealed before surgery by computerized tomography scan and cerebral arteriography and directly confirmed during the resection. Twenty-four hours after surgery no patient presented fibrinolysis activation. There was no evidence of disseminated intravascular coagulation in our patients. None of them presented pathological decrease of the physiological coagulation inhibitors or thrombotic complications. In conclusion, during surgery, fibrinolysis parameters show important modifications in patients with vascularized meningioma suggesting an ongoing tumour-host interaction. These variations must be taken in account, in order to plan timely a correct therapeutic approach.
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PMID:Coagulation study in patients who had undergone surgery for meningioma. 803 35


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