Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.6 (thromboplastin)
13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined components of the coagulation system in 30 neonates (age, 1 to 30 days) undergoing deep hypothermic cardiopulmonary bypass (CPB). A coagulation profile consisting of activated clotting time; prothrombin time; partial thromboplastin time; factors II, V, VII, VIII, IX, X, and I (fibrinogen); antithrombin III; platelet count; and heparin levels was evaluated before bypass, at three intervals during bypass (1 minute after initiation of bypass, stable hypothermic CPB, warm CPB), after weaning from CPB and administration of protamine, and 2 to 3 hours after skin closure. The initiation of CPB resulted in a 50% decrease in circulating coagulation factors and antithrombin III levels. Platelet counts were reduced by 70% with CPB initiation. Neither deep hypothermic temperatures nor prolonged exposure to extracorporeal surfaces had any additional effect on the coagulation profiles. This suggests that the coagulation system of a neonate undergoing CPB is profoundly and globally effected by hemodilution. We believe that treatment of post-CPB coagulopathy in neonates must address these global deficits.
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PMID:Coagulation defects in neonates during cardiopulmonary bypass. 833 80

The hemostatic effects of recombinant human erythropoietin (rHuEP) were investigated in 20 patients with end-stage renal disease (thirteen on hemodialysis, seven without dialysis) receiving this hormone. We studied their hemograms and coagulation profiles before and at 1 month after initiation of rHuEP therapy. One month after rHuEP administration, improvement in anemia (16/20, 80%) and shortening of bleeding time (17/19, 89.5%) were observed. Shortening or correction of bleeding time was achieved in three patients without any increase of the hemoglobin level. This means that factors other than the increased hematocrit level might contribute to shortening bleeding time in uremic patients receiving rHuEP treatment. The platelet count, prothrombin time, partial thromboplastin time, and fibrinogen level did not change over the course of rHuEP therapy. Thrombosis of vascular access was not observed, and heparin doses were not increased in this short-term period. A significant decrease was found in the plasminogen level, from 108.5% to 88.2% (p less than 0.05), in uremic patients on hemodialysis. The antithrombin III level also decreased, from 98.8% to 89.8% (p less than 0.05), and its level dropped to below normal ranges in six of thirteen patients (46%) on hemodialysis after treatment with rHuEP. No significant change was noted in the levels of antithrombin III, plasminogen, and alpha 2-antiplasmin in uremic patients not receiving dialysis. These results suggest that rHuEP administration induces increased extracorporeal dialyzer clotting and consumption coagulopathy, and that this extracorporeal consumption coagulopathy may play a role in the genesis of thrombotic complications.
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PMID:The effect of recombinant human erythropoietin on hemostatic status in chronic uremic patients. 151 Nov 68

Functional antithrombin III levels were measured by factor Xa inhibition in 63 members of a large family with type 2 antithrombin III deficiency and individuals were classified as antithrombin III deficient or non-deficient according to the results. F1 + 2 and TAT complexes were measured using an ELISA and FPA levels were measured by radioimmunoassay. Thirty subjects (48%) were classified as antithrombin III deficient and 33 (52%) as antithrombin III non-deficient. The mean level of F1 + 2 was significantly higher in the deficient adults (0.87 +/- 0.26) compared to both the non-deficient adults (0.70 +/- 0.21) (p = 0.03) and the deficient adults receiving warfarin (0.16 +/- 0.01) (p less than 0.001). The differences in the mean values of TAT complexes and FPA between deficient and non-deficient individuals were not statistically significant. These findings suggest that untreated antithrombin III deficient subjects generate more thrombin than their non-deficient family members and that warfarin inhibits this thrombin formation. In this cross-sectional study, it is not possible to correlate the levels of the surrogate makers with future clinical outcome.
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PMID:Measurement of markers of activated coagulation in antithrombin III deficient subjects. 151 14

The influence of two different methods of autologous transfusion, preoperative donor plasmapheresis (Abbott Autotrans) and postoperative autotransfusion (intraoperative blood salvage, Dideco Autotrans), on the intravascular hemostatic system was investigated. Forty-two patients undergoing total hip surgery and preoperative donor plasmapheresis were prospectively randomized into three groups. For substitution of blood loss, patients in group 1 (control group, n = 12) received in addition to cristalloids and colloids only homologous blood, group 2 (n = 14) autologous blood, and group 3 (n = 16) additionally intra- and postoperative autologous fresh frozen plasma (FFP). The investigation included blood parameters (hemoglobin, hematocrit, thrombocytes), clotting status (prothrombin time, plasma thromboplastin time, thrombin time, fibrinogen, plasminogen, and antithrombin III), and immunological methods such as fibrinopeptide A (FPA), thrombin-antithrombin III (TAT), and protein C. No significant difference was found with respect to total amount of infusion, intraoperative blood loss, autologous transfusion, and blood parameters. Excellent quality of the autologous FFP was demonstrated by investigation of the specimens before administration. The autologous packed red cells showed high levels of TAT and FPA as an indicator of thrombin generation. Their administration caused a significant increase in TAT and FPA levels in groups 2 and 3 compared to group 1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Measures for reducing the use of homologous blood. Effects on blood coagulation during total endoprosthesis]. 144 16

Hypercoagulable states are disorders of blood coagulation, which include deficiencies of natural anticoagulants, disorders of the fibrinolytic system, presence of antiphospholipid antibody and abnormalities of platelet function. These disorders are well known causes of venous thromboembolic disease and are being recognized in association with arterial thromboembolic occurrences with increasing frequency. The performance of standard prosthetic vascular reconstructions may result in disastrous outcomes in patients with unrecognized and untreated hypercoagulable states. From 1986 to 1990, we identified 12 patients with hypercoagulable states, six of whom presented with evidence of arterial thromboembolism. All of the patients were men who smoked and were somewhat younger than the usual patient with atherosclerosis. Their ages ranged from 41 to 62 years. Four patients presented with ischemic rest pain, one patient with blue toe syndrome and one with rapidly progressive claudication. Four patients had undergone prior vascular reconstruction and two had previous pulmonary emboli. Evaluation of these patients to identify hypercoagulability included determinations of prothrombin time (PT) and partial thromboplastin time (PTT), platelet count, antithrombin III, protein C, free protein S and total protein S levels, along with platelet aggregometry. Two patients had protein S deficiency, one had protein C deficiency, one patient had protein C and S deficiency and two patients had hyperaggregable platelets. Four patients had prosthetic reconstructions and two had autogenous reconstructions. Three of the four patients undergoing prosthetic reconstructions had subsequent loss of limb and one patient died. Only one patient with prosthetic reconstruction had a patent graft on long term anticoagulation. Both patients undergoing autogenous procedures had successful revascularization with limb salvage.
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PMID:Hypercoagulable states in arterial thromboembolism. 154 37

Disseminated intravascular coagulation (DIC) secondary to colic was diagnosed in 23 horses. Each horse was categorized retrospectively as to the cause of the colic based on surgical and/or necropsy findings: group 1 consisted of 14 horses with compromised intestine that required resection and anastomosis; group 2 consisted of 3 horses with nonstrangulating intestinal displacement and/or impactions; and group 3 consisted of 6 horses with colic associated with enteritis and/or colitis. Horses were considered to be affected with DIC if at least three of five hemostatic parameters were significantly abnormal: decreased antithrombin III (AT III) values, increased level of fibrin degradation products (FDP), thrombocytopenia, prolonged activated partial thromboplastin time, and prolonged prothrombin time. The most consistent hemostatic abnormalities were decreased AT III activity, increased FDP titers, and thrombocytopenia. Clotting times were more variable and did not always correlate with the presence of excessive hemorrhage. Excessive hemorrhage was present during surgery in seven horses and occurred within 1 to 12 hours after surgery in nine other horses. In addition to treatment of the primary disease, 19 horses received treatment for DIC consisting of heparin and/or plasma or fresh whole blood transfusions. Heparin alone was used in 12 horses. Heparin, in addition to fresh whole blood transfusions or fresh plasma, was administered to four horses. Three horses were treated with plasma alone. Four other horses were not treated specifically for the DIC. Eight horses (34%) survived the acute coagulopathy. Although a greater proportion of the surviving horses received heparin therapy (87.5%; 7/8) than did those that died (60%; 9/15), the difference was not statistically significant (P = 0.345).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Disseminated intravascular coagulation associated with colic in 23 horses (1984-1989). 154 23

We have investigated whether or not tissue factor (TF) which is present in the supernatant of isolated glomeruli, is responsible for the stimulatory activity of TXB2 production by isolated human platelets. Reconstituted TF stimulated TXB2 synthesis in platelets in a dose-dependent manner. This effect was potentiated in the presence of a mixture of the major fatty acids found in glomerular supernatants. Addition of a neutralizing anti-TF monoclonal antibody abolished both the procoagulant activity and the platelet-TXB2 stimulatory activity of reconstituted TF and of glomerular supernatants. Anti-factor VII/VIIa (F VII/VIIa) Fab inhibited in a dose-dependent manner the platelet-TXB2 stimulatory activity of an identical dilution of reconstituted TF and of glomerular supernatants, providing evidence that the functional complex TF. VIIa and not TF itself was the active agent. Pretreatment of platelets, TF or glomerular supernatant by hirudin, an inhibitor of thrombin, as well as by antithrombin III heparin, which inhibits both activated factor X and thrombin also markedly inhibited the synthesis of TXB2 by platelets in the presence of either TF or glomerular supernatant. Taken together, these results demonstrate that the stimulatory activity for TXB2 production by platelets which is released by the glomerular cells is attributable to TF. TF does not act directly. Its effect is mediated by thrombin which is formed de novo at the platelet surface in the presence of even traces of the plasma coagulation proteins associated with platelets. TXB2 formation in platelets correlates well with TF concentration in the glomerular supernatant. The possibility of a similar set of mechanisms associated with glomerular injury may require consideration.
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PMID:Glomerular tissue factor stimulates thromboxane synthesis in human platelets via thrombin generation. 155 9

Various haemostatic analytes were systematically evaluated for four months pre-partum and five months post partum in 14 healthy mares. The plasma fibrinogen concentration and both Factor VIII:C and von Willebrand factor activity showed gradual increases from mid-gestation and reached maximal, or near maximal activity at parturition. These increases were paralleled by an increase in plasma fibronectin concentration, the appearance of fibrinogen degradation products, and a modest rise in antithrombin III concentration. In contrast, the activity of Factor VII and Factor IX, and the one-stage prothrombin (PT) time and the activated partial thromboplastin (APTT) time remained relatively constant throughout the pre- and post parturient period.
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PMID:Evaluation of the haemostatic profile in the pre- and post parturient mare, with particular focus on the perinatal period. 155 43

We retrospectively evaluated the hemostatic system of 13 patients during implantation (2 to 35 days) of the Jarvik 7-70 total artificial heart (TAH). Although all patients were clinically manageable while on the TAH, 5 had excessive generalized bleeding. After the heart transplant procedure, 2 patients had neurological events and 1 patient, thrombosis of the leg. While the patients were supported by the TAH, the routine coagulation assays (prothrombin time, activated partial thromboplastin time, fibrinogen, factor assays, and platelet count) showed slight abnormalities but no correlation to hemorrhagic or thrombotic events. In contrast, plasma and cellular activation markers, which are highly sensitive and specific for hypercoagulability, fibrinolysis, or platelet activation, revealed activation in all patients. Most striking was the marked activation of the fibrinolytic system (p less than 0.05 to 0.001). Correlations of individual patient data compared with the average TAH group response could be made between excessive enhancement of fibrinolysis (increased D-dimer and tissue plasminogen activator and decreased plasminogen activator inhibitor) and bleeding. A hypercoagulable state (increased fibrinogen and thrombin-antithrombin complex and decreased antithrombin III and protein C), decreased fibrinolysis (decreased tissue plasminogen activator and D-dimer), activated platelets (increased thromboxane B2), or combinations of these were associated with thrombosis. The hemostatic activation returned to normal 1 day after removal of the TAH. These data suggest that the patient with a TAH requires more sophisticated laboratory monitoring and individualized treatment for excessive fibrinolysis, hypercoagulable state, or platelet activation to avoid thrombotic and hemorrhagic complications.
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PMID:Hemostatic abnormalities in total artificial heart patients as detected by specific blood markers. 157 Sep 81

A 48-year-old female received serial combination chemotherapy including L-asparaginase (L-ASP) for acute lymphoblastic leukemia. After administration of L-ASP, the prothrombin time and activated partial thromboplastin time were prolonged, while fibrinogen and antithrombin III levels markedly decreased, so she was given fresh frozen plasma (FFP). But subsequently, she developed cerebral infarction in the left parietal region and further hemorrhagic infarction in the right parietal region, and died. Autopsy revealed superior sagittal sinus thrombosis and bilateral cerebral infarction, but no obvious thrombus in other organs. Coagulopathy following L-ASP therapy is well-known. In this case, the coagulation studies at the first attack showed that the plasma protein levels of coagulation and fibrinolysis factors decreased in spite of administration of FFP. Fibrin-fibrinogen degradation products (FDP) slightly increased. However there were no significant abnormalities in the platelet count, nor soluble fibrin monomer, which suggested no evidence of disseminated intravascular coagulation. Thus, these findings suggest that L-ASP might be associated with the pathogenesis of thrombosis in this case.
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PMID:[Superior sagittal sinus thrombosis following L-asparaginase therapy of acute lymphoblastic leukemia]. 157 39


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