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

The presence of disseminated intravascular coagulation (DIC) in the syndrome of haemolysis, elevated liver enzymes and low platelets (HELLP) is debated. We assessed the occurrence of decompensated and compensated DIC (using predefined criteria) in 15 consecutive nulliparous pregnant patients with gestational hypertension combined with the HELLP syndrome and in 12 consecutive nulliparous controls with pregnancy induced hypertension (PIH) but without the HELLP syndrome. A combination of routine coagulation assays revealed the absence of decompensated DIC in all studied patients. However, using more specific and sensitive coagulation assays, compensated DIC was observed in all HELLP patients and in three patients in the control group. The mean values of antithrombin III, thrombin-antithrombin III complexes and protein C in the HELLP and the control group were 66 vs 87% (P = 0.0004), 21 vs 8 ng/ml (P = 0.0008) and 57 vs 90% (P = 0.0018) respectively. We conclude that HELLP patients show evidence of compensated DIC which may have pathophysiological significance for the observed organ damage.
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PMID:Coagulation studies in the syndrome of haemolysis, elevated liver enzymes and low platelets. 199 31

Inhibition of activated clotting factors is an important therapeutic approach in disseminated intravascular coagulation (DIC). We examined the possible protective effect of a purified complex of human antithrombin III (AT III) and heparin in endotoxin-induced DIC in pigs. Two groups of endotoxemic pigs were studied. AT III-heparin group pigs (n = 8) were pretreated with a bolus injection of 500 units AT III-heparin complex, followed by a continuous infusion of 1000 units of the complex for 6 hours given simultaneously with the infusion of 10 micrograms/kgh of S. abortus equi endotoxin. Controls (n = 9) were given saline in addition to the continuous infusion of endotoxin. AT III activity, prothrombin and soluble fibrin in plasma were determined by chromogenic substrate methods. Fibrinogen was measured turbidimetrically. Human AT III antigen in the treated group was 64 +/- 3% at 2 hours and increased to 84 +/- 4% until the end of the experiment. AT III activity in the AT III-heparin group was elevated throughout the whole observation period (greater than 100%), whereas it was significantly lower in the controls. Prothrombin decreased similarly in both groups by approximately 35% until the end of the experiment. AT III-heparin treatment significantly attenuated the endotoxin-induced consumption of fibrinogen and completely prevented the increase in soluble fibrin in plasma. However, no significant effect of AT III-heparin was observed on endotoxin-induced mortality and dysfunction in pulmonary gas exchange. Therefore we conclude that the purified AT III-heparin complex inhibits thrombin effects and prevents development of DIC, but fails to significantly influence clinical outcome in endotoxin shock of the pig.
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PMID:A purified antithrombin III--heparin complex as a potent inhibitor of thrombin in porcine endotoxin shock. 202 Sep 36

Therapy with vincristine (2 mg i.v. weekly) and prednisolone (100 mg p.o. daily) caused a decrease in fibrinogen levels in nine patients treated for lymphoid blast crisis LBC) of chronic myeloid leukemia (CML). During the first days of treatment disseminated intravascular coagulation (DIC), evidence by a positive ethanol gelation test, markedly increased thrombin-antithrombin III complex and fibrin-split product D-dimer levels, and a rapid fall in fibrinogen levels was observed in two patients. The induction of DIC in these two patients caused profuse bleeding in one and necessitated substitution therapy with fibrinogen and platelet concentrates. The remaining seven patients revealed no signs of DIC; nevertheless, four of them showed a moderate increase in D-dimer levels after initiation of therapy. In these patients a well-known side effect of long-term steroid therapy, namely a decrease of fibrinogen levels, was observed within the first week of treatment. Fibrinogen levels did not fall below 150 mg/dl and increased after dose reduction from 100 mg/day to 50 mg/day. We conclude from our results that two types of disturbances in fibrinogen metabolism can be observed during vincristine/prednisolone therapy of LBC of CML: (a) a decrease of fibrinogen levels due to a steroid-mediated impairment of liver synthesis, and (b) a rapid fall in fibrinogen levels in the course of DIC, most likely induced by the release of procoagulants from deteriorating blast cells, leading to severe bleeding in selected cases.
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PMID:Disseminated intravascular coagulation and decrease in fibrinogen levels induced by vincristine/prednisolone therapy of lymphoid blast crisis of chronic myeloid leukemia. 204 63

A case of abdominal aortic aneurysm associated with preoperative signs of disseminated intravascular coagulation is reported. The 69-year-old female patient presented with spontaneously appearing petechiae and bruising. She had 0.95 g.l-1 fibrinogen, 105 G.l-1 platelets, and 100 micrograms.ml-1 fibrin and fibrinogen degradation products. Investigations revealed an 80 mm diameter aneurysm of the abdominal aorta, extending from the coeliac trunk to the iliac arteries. Heparin 7,000 IU.day-1 resulted in a biological improvement for a week only. At that time, levels of coagulation factors were: 92% factor II, 88% factor V, 100% factors VII and X, 100% antithrombin III. Surgical cure of the aneurysm was nevertheless carried out. Twenty standard units of platelets, 8 g fibrinogen, four units of fresh frozen plasma, five homologous and two autologous red cell units were transfused during the procedure. No coagulation factors were necessary during the postoperative course, which was uneventful. The management of coagulation factor infusions, before or after aortic cross-clamping, is discussed.
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PMID:[Aneurysm of the abdominal aorta and preoperative disseminated intravascular coagulation]. 205 33

Disseminated intravascular coagulation (DIC) or renal damage associated with septicemia was induced in rats by ligating the cecum or by injecting endotoxin. In the septicemia model, the number of E. coli and Bacteroides spp in the blood increased concomitantly with an increase of endotoxin. In this model the development of hypercoagulability with mild fibrinolysis was observed. Histopathologic findings in the kidneys, including the formation of microthrombi in the glomeruli and the vacuolization and dilatation of renal tubular cells, suggest the development of mild DIC. In the endotoxin-induced DIC model, both remarkable state of hypercoagulability and fibrinolysis were observed with fibrin thrombi in glomeruli. The administration of the platelet-activating factor antagonist, CV-6209, or of human antithrombin III, ameliorated DIC significantly by limiting the increases in prothrombin time, activated partial thromboplastin time and fibrin degradation products. These agents significantly reduced the deposition of fibrin in the glomeruli and significantly prolonged the survival time of the endotoxin injected rats. These observations suggest that the PAF antagonist CV-6209 and ATIII merit clinical evaluation in the management of DIC caused by septisemia.
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PMID:Effect of a platelet activating factor antagonist and antithrombin III on septicemia and endotoxemia in rats. 206 2

The coagulation system has been examined in 30 women with late toxemia before and after heparin and trental therapy. Pretreatment fibrinogen levels were elevated and antithrombin III levels were reduced. A hemolysate-calcium mixture showed an increase in coagulation at 8 and 10 minutes of incubation. Staphylococcus agglutination and ethanol tests revealed a significant increase in early PDF and other constituents of the fibrinogen pool. These changes were indicative of prolonged-type disseminated intravascular coagulation in late toxemia. Comprehensive therapy comprising heparin and trental leads to a significant reduction in fibrinogen concentration, alleviation of the hypercoagulatory shift and increase in antithrombin III level. Early PDF and fibrin monomer complexes showed a decline. In addition, the therapy had beneficial effects on the maternal and fetal clinical status.
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PMID:[Disorders of the hemostasis system in late pregnancy toxemia and their correction]. 207 11

A case of disseminated intravascular coagulation (DIC) and fatal myocardial infarction in a haemophilia B patient is described. DIC occurred after 4 days of therapy with unactivated prothrombin complex concentrates during the post-operative period. Therapy with fresh frozen plasma, heparin and antithrombin III concentrates was started without efficacy; after autopsy myocardial infarction was evident.
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PMID:Disseminated intravascular coagulation and myocardial infarction in a haemophilia B patient during therapy with prothrombin complex concentrates. 210 59

It has been recently suggested that an acquired deficiency of proteins C and S could contribute to the pathogenesis of meningococcemic purpura fulminans (PF) in children. Our study was designed to measure the levels of antithrombin III (AT III), protein C, and protein S during adult PF and to determine the effects of an early infusion of high doses of AT III concentrates on clinical and biological alterations of PF. We studied five consecutive adult patients with meningococcemia (type B) and PF. The levels of AT III, protein C (antigen and activity), and protein S (total and free) were measured at admission and 24 h and 1 month later. The treatment included in each case: amoxycillin, dobutamine and high doses of AT III concentrates. All patients survived and were discharged without any sequelae. At admission, biological data were consistent with severely depressed protein C and protein S levels and moderately decreased AT III levels, without any discrepancy between protein C antigen and activity. After 24 h, AT III and protein S levels were within normal ranges, whereas protein C levels were still depressed. These data are consistent with the theory of a particular imbalance in the anticoagulant systems during meningococcemic PF, contrasting with the usual findings observed during septic disseminated intravascular coagulation. The possibility must be considered that high doses of one anticoagulant (AT III concentrates) could compensate for the acute decrease in the other (protein C system).
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PMID:Meningococcemia and purpura fulminans in adults: acute deficiencies of proteins C and S and early treatment with antithrombin III concentrates. 213 71

Thrombin-antithrombin III complex (TAT) and Plasmin-alpha 2 plasmin inhibitor complex (PIC) were examined in fifty two cases of various chronic liver diseases. TAT was significantly elevated in cases of hepatocellular carcinoma (HCC), but PIC did not show significant changes in any chronic liver diseases. Elevations of TAT and PIC were seen in cases of HCC accompanied by tumor enlargement and extensive tumor thrombosis. In cases of HCC undergoing transcatheter arterial embolization (TAE), TAT and PIC increased on the next day after TAE, and tended to recover with time, returning to almost normal at fourth week. Prolongation of prothrombin time, elevation of FDP and positive FM test were noted more often in liver cirrhosis with disseminated intravascular coagulation (DIC) than in severe liver dysfunction without DIC. Of five cases confirmed as DIC, only three cases were diagnosed as DIC by DIC score. On the other hand, TAT and PIC were significantly elevated in DIC cases. Especially, TAT exceeded 30 ng/ml in all DIC cases. TAT was regarded to be useful for the diagnosis of DIC in severe liver dysfunction.
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PMID:[Clinical significance of thrombin-antithrombin III complex and plasmin-alpha 2 plasmin inhibitor complex in chronic liver diseases]. 214 51

Disseminated intravascular coagulation (DIC) after hepatic resection is a serious complication that leads to a fatal outcome unless prompt treatment is instituted. Between April 1973 and June 1988, DIC occurred postoperatively in 18 of 192 patients who underwent hepatic resection because of a variety of diseases of the liver and biliary tract. The diagnosis was made on the basis of changes in platelet count, fibrinogen level, serum level of fibrin degradation product (FDP), and protamine sulfate test. Heparin was used in an earlier series but has been discontinued because of difficulty in determining the optimal dose in patients undergoing liver resection. Instead, we now use gabexate mesilate, which blocks the coagulation cascade without the aid of antithrombin III and works as an anticoagulant. Fifteen patients had uneventful recoveries, but three died. Two died of aggravation of DIC, which was a result of reoperation performed under the diagnosis of surgical bleeding. The other patient died of liver failure after fever of unknown cause persisted for 4 months. The rationale for the diagnosis and treatment of DIC after liver resection is documented, and the problems involved are discussed.
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PMID:Disseminated intravascular coagulation after hepatic resection. 204 3


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