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)

Seventy-five cancer patients were evaluated on a scale of coagulation abnormalities related to DIC, one point given for each of the following criteria fulfilled and the score (0 to 4) being used. 1. Platelet count less than 150 x 10(3)/mu 1. 2. PT prolonged more than 1 sec over control or APTT prolonged more than 10 sec over control. 3. Fibrinogen less than 250 mg/dl (mean fibrinogen value of the cancer patients minus 1SD). 4. FDP greater than or equal to 20 micrograms/ml. The patients were distributed with 27% for score 0, 38% for 1, 20% for 2, 7% for 3 and 8% for 4. Platelet mode volume in score 4 was smaller than that of the other groups. Platelet aggregation by epinephrine was decreased in score 3 and 4 (P less than 0.01), while it was increased in score 0 (P less than 0.05). ADP-induced aggregation was increased in score 0 and 1 (P less than 0.01 - 0.05). The mean value of beta-thromboglobulin in cancer patients (44 +/- 24 ng/ml) was significantly higher than that of control (22 +/- 13 ng/ml) (P less than 0.01). These results suggest the existence of hyperfunction of platelets in cancer patients and possibility of a triggering mechanism of such activated platelets in the genesis of DIC in cancer.
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PMID:Activation of platelets in cancer, especially with reference to genesis of disseminated intravascular coagulation. 683 44

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

Thromboembolism of minor vessels in the lungs is almost constantly seen in posttraumtic lung insufficiency. Many investigators consider it as the primary factor in the pathogenesis of this condition. The present paper deals with screening of the coagulation system as part of a more extended project also investigating changes in the fibrinolytic system and the kallikrein-kinin system. The data are also to be compared with morphological findings during the development of experimental posttraumatic lung insufficiency. The experimental syndrome was evoked in Labrador retriever dogs by haemorrhagic hypotension combined with clamping of the portal triad. The surgical procedure was extended to additional thoracotomy in one group of dogs. Group I, without thoracotomy, were followed for 12 hours. Group II, with thoracotomy, were followed until they succumbed (3-14 hours). Thrombotest (TT) showed a steady prolongation of clotting time in both groups, whereas Cephotest did not reveal any alterations, except for a significant prolongation in group II just before collapse. Fibrinogen was markedly reduced in both groups. Platelets and leucocytes were significantly reduced, but only in group II. It is concluded that the present data are indicative of disseminated intravascular coagulation. The involvement of the intrinsic coagulation system is questioned.
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PMID:Blood cells and coagulation during experimental lung insufficiency in dogs. 693 93

This study was designed to examine the effect of selective correction of antithrombin III activity on the increased turnover of fibrinogen, which occurs in patients with liver cirrhosis supposedly due to disseminated intravascular coagulation. Human antithrombin III concentrates were therefore transfused in seven patients with cirrhosis and antithrombin III deficiency (less than 80%). Fibrinogen half-life and the fractional catabolic rate constant were calculated from the turnover of 125I-fibrinogen which was represented by a two-compartment model. Prior to antithrombin III transfusion, 125I-fibrinogen half-life was 76.7 +/- 15.2 h and the fractional catabolic rate constant was 0.33 +/- 0.11 of the plasma fibrinogen pool per day. In six healthy adult controls these values were significantly different: 109.4 +/- 8.8 h and 0.19 +/- 0.01 respectively. Correction of antithrombin III activity with human antithrombin III concentrate reduced the increased turnover of radiolabelled fibrinogen to normal. The 125I-fibrinogen half-life became 108.4 +/- 17.6 h and the fractional catabolic rate constant decreased to 0.23 +/- 0.06. These observations indicate that decreased antithrombin III activity contributes in an important way to the increased 125I-fibrinogen turnover in patients with cirrhosis and this might reflect intravascular coagulation.
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PMID:Antithrombin III transfusion in patients with hepatic cirrhosis. 711 27

The platelet count in 550 patients with gestational hypertension was significantly lower and the mean platelet volume significantly higher than in normal pregnant women. Both the platelet count and volume became increasingly abnormal when hypertension was accompanied by oedema, proteinuria or both, and women with severe pre-eclampsia or eclampsia had the lowest platelet counts and the highest mean platelet volume. The proportion of patients with thrombocytopenia and/or macrothrombocytosis also varied with the severity of the clinical presentation. Fibrinogen degradation products were found mainly in fully developed pre-eclampsia. These findings confirm the concept of a rapid platelet turnover caused by low-grade disseminated intravascular coagulation in gestational hypertension. The platelet pattern in essential hypertension is similar to that seen in normal pregnancy.
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PMID:Thrombocytopenia and macrothrombocytosis in gestational hypertension. 729 1

Coagulation disorders, including thromboembolic phenomena and disseminated intravascular coagulation are recognised as a complication of neoplastic disease. In the present study the Fibrinogen Degradation Products (F.D.P.) were determined in 26 patients with Advanced Ovarian Cancer (stage III and IV FIGO) (mean = 38.1; S.D. = 37.6) and in ten healthy patients considered as controls (mean = 2.7; S.D. = 13). The significative difference (p less than 0.05) between the two groups points in evidence an increasing activation of Ffibrynolytic processes. The F.D.P. determination has revealed a good correlation (p less than 0.001) with the tumor extension as showed by the difference between third stage with large tumor masses (late) (mean = 44.5; S.D. = 24.5) and third stage with minimal residual disease after reductive surgery (early) (mean = 6.7; S.D. = 5.7).
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PMID:Fibrinolysis in ovarian cancer. 733 61

The effects of intraamniotic instillation of saline solution for abortion induction on blood coagulation were studied in 81 women in the 16-24th week of pregnancy. Activity of blood coagulation system was estimated by changes in plasma fibrinogen concentration. Depending upon the time period between saline instillation and the onset of abortion, the women could be divided into 3 groups. Group 1 included 37 women in whom abortion occurred 24 hours after instillation, group 2 consisted of 28 women in whom abortion occurred 24-48 hours after instillation, and group 3 included 16 women in whom abortion occurred 48 hours after saline instillation. The women in all 3 groups showed decrease in fibrinogen concentration within the 1st 24 hours after saline administration. The maximum decrease in fibrinogen concentration was observed in group 1. Fibrinogen concentrations returned to normal values within 48-64 hours after abortion. It was concluded that transient hypofibrinogenemia induced by intraamniotic saline instillation can play a role in the pathogenesis of disseminated intravascular coagulation.
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PMID:[Changes in the fibrinogen level and the risk of defibrination after the intra-amniotic instillation of a saline solution used for abortion purposes]. 738 74

Seventeen adult patients who underwent surgery for the thoracic or thoracoabdominal aortic disease by the use of left heart bypass with the Bio-Pump were divided into untreated, low-dose heparin treated and argatroban treated groups so as to evaluate the effects of systemic infusion of a newly synthesized antithrombin agent, argatroban, for the prevention of platelet loss and consumption coagulopathy. ACT reached 150 to 250 seconds at doses 0.5-7.5 micrograms/kg/min of argatroban and maximum ACT prolongation was limited to around 250 seconds. ACT spontaneously recovered below 150 seconds within 60 minutes following the end of bypass during which no excessive blood loss developed. In argartoban group, platelet loss during and immediately after surgery was effectively prevented as compared to other groups with significance. Fibrinogen was also preserved to some extent by argatroban treatment without evidence of systemic embolization. Argatroban, as an antithrombotic agent, is worthy of further trial of clinical use in bypass with a centrifugal pump.
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PMID:[Left heart bypass with the bio-medicus centrifugal pump by the use of an antithrombin agent, argatroban]. 793 35

Fibrinogen (Fg), plasminogen (Plg), alpha 2-antiplasmin (alpha 2-AP), plasminogen activator (PA), tissue plasminogen activator (tPA), plasminogen activator inhibitor (PAI), D-dimer (DD) and fibrin(ogen) degradation products (FDP) were studied in 60 subjects: 40 patients with endemic hepatosplenomegaly (20 during acute haematemesis from ruptured oesophageal varices, 20 with endemic hepatosplenomegaly assigned to the same grade of oesophageal varices but with no history of haematemesis) and 20 normal controls. All parameters were markedly altered in the disease groups. Reduced levels of Fg, Plg, alpha 2-AP and PAI were associated with increasing levels of PA, t-PA, DD and FDP. Alterations were most marked in the group complicated by acute bleeding. It was concluded that these patients have an enhanced fibrinolytic state. This was probably aggravated in the haematemesis group by an acute haemostatic imbalance that superimposed the low grade chronic DIC reported in cases of hepatosplenic schistosomiasis.
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PMID:Fibrinolytic parameters during acute haematemesis in endemic hepatosplenomegaly. 814 81

Ancrod is a purified coagulant venom which renders blood incoagulable by cleaving fibrinopeptide A (FPA) from fibrinogen, but the mechanism involved in the clearance of fibrin from the circulation is unknown. To investigate the fibrinolytic response to ancrod, and to increase understanding of clearance mechanisms, six patients with peripheral vascular disease causing claudication were infused with ancrod at 2 u/kg over 6 h followed by 2 u/kg at 12 h intervals for 38 h. Venous blood samples were taken at time 0, 3, 6, 25 and 49 h for assay of fibrinogen (Fbg), fibrinopeptide A (FPA), total fibrin(ogen) degradation products (TDP), fibrin degradation products (FbDP), fibrinogen degradation products (FgDP), cross-linked fibrin degradation products (XL-FDP), tissue plasminogen activator (tPA), urinary type plasminogen activator (u-PA), plasminogen, alpha 2 antiplasmin (alpha 2 AP) and plasminogen activator inhibitor-1 (PAI-1). Fibrinogen (median and range) was 2.3 (1.4-3.90) g/l at time 0 and thereafter was undetectable. FPA rose from 2.5 (1.8-3.6) to 600 and 188 pmol/l at 3 h and 6 h and remained elevated. TDP, FbDP and FgDP increased greatly following ancrod while there was no evidence of XL-FDP. The surprising increase in FgDP during defibrination suggests either that fibrinogen is digested following its incorporation into circulating fibrin protofibrils or that some of the fibrin subunits in the photofibril retain one of the two fibrinopeptide A's. tPA and uPA remained unchanged. Plasminogen fell from 125 (100-155)% to 79 (40-118)% at 49 h and alpha 2 AP fell from 91 (75-107)% to 24 (10-35)% at 49 h. The level of PAI-1 was depressed during defibrination, with the exception of the 6 h data. The results demonstrate that ancrod removes FPA from fibrinogen to produce non-cross-linked (soluble) fibrin. This is cleared from the circulation without evidence of an increase in the circulating activities of the plasminogen activators, tPA or UK, but with evidence of plasminogen activation and consumption.
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PMID:The fibrinolytic response to ancrod therapy: characterization of fibrinogen and fibrin degradation products. 845 76


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