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)

Five patients with immunopathologic renal disease, 12 with malignant paraproteinaemia and one with myasthenia gravis underwent a total of 179 plasma exchanges on a continuous flow cell separator. Replacement fluids devoid of coagulation factors were used in 160 exchanges while 19 exchanges were replaced with Fresh Frozen Plasma. Coagulation screening was done immediately before and 30 min after each plasma exchange. Plasma fibrinogen concentrations fell to a mean of 25% of initial levels during individual exchanges. Sequential reduction to 10.7% was observed after five consecutive daily exchanges and in one patient fell to 1.2% after 10 daily exchanges. Low levels of fibrinogen could be maintained with daily or alternate daily exchanges. Platelet counts fell to a mean of 50% of pre-exchange levels during individual exchanges. Consecutive daily exchanges resulted in mean reductions to 20.7% after 5 d, but further reductions were not observed with longer periods of exchange. Platelet counts recovered to pre-exchange values during exchange intervals of 2 or more days. Mild clinical bleeding episodes, probably related to low platelet counts, occurred in one exchange in each of three patients. Haemostasis was rapidly achieved in these patients by infusions of platelet concentrates. Coagulation screening, including prothrombin ratio, thrombin time, reptilase time and partial thromboplastin time with kaolin showed progressively greater abnormalities as the intervals between exchanges shortened. The low incidence of clinical haemorrhagic episodes, three of 179 exchanges (2.2%), despite markedly abnormal coagulation parameters, emphasize the safety of the procedure even in moribund patients. We conclude that the use of FFP in intensive exchange programmes solely for the prevention of spontaneous haemorrhagic phenoma is unjustified.
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PMID:Coagulation abnormalities produced by plasma exchange on the cell separator with special reference to fibrinogen and platelet levels. 47 11

The evaluation of excessive hemorrhage was carried out in 774 patients after cardiopulmonary bypass. Excessive hemorrhage was defined in any adult patient as chest tube drainage of more than 600 ml within the first eight hours after operation. Using the prothrombin time, partial thromboplastin time, fibrinogen level, and tri-F titer tests, it was possible to differentiate medical from surgical bleeding. Hyperfibrinolytic bleeding was the most frequently identifiable coagulation disorder and occurred in 159 patients (20%). All these patients were successfully treated with Amicar (epsilon-aminocaproic acid) alone, or with Amicar supplemented with cryoprecipitate or fresh-frozen plasma. Three patients (0.4%) were noted to have residual heparin and required additional protamine sulfate. Five patients (0.6%) had normal coagulation studies and required immediate reexploration. The overall blood consumption per patient was 2.1 units of packed cells. Whole blood and platelets were not used.
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PMID:The treatment of postperfusion bleeding using epsilon-aminocaproic acid, cryoprecipitate, fresh-frozen plasma, and protamine sulfate. 49 96

Controversy continues about the oxygenator preferable for cardiopulmonary bypass (CPB). This prospective study was undertaken in 52 patients undergoing coronary bypass surgery. Oxygenators were alternated each case between model Q-100, Bentley Laboratories Inc, Irvine, Calif, and Travenol Membrane Oxygenator (TMO), Travenol Laboratories Inc, Deerfield, Ill. The Q-100 group required higher CPB O2 flows, but PO2 levels during CPB were similar for both groups. Heparin sodium dosage and activated clotting, bleeding, prothrombin, and partial thromboplastin times were identical in both groups. Blood loss and platelet reduction after CPB were also similar. Postoperative complications in the Q-100 group included one myocardial infarction, and one neurological problem. The TMO group had no myocardial infarction and one neurological problem. The membrane oxygenator took nine minutes longer to set up and was $63 more expensive to purchase. Blood trauma during CPB was less with the membrane oxygenator (lower plasma hemoglobin level), but we conclude that both oxygenators performing adequately during clinical use in open heart surgery.
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PMID:Membrane vs bubble oxygenators: a prospective study of 52 patients. 49 30

Factor V (Va) is essential for binding of factor Xa to the surface of platelets. After thrombin treatment, normal platelets release at least five times more factor Va activity than is required for maximal factor Xa binding. The concentration of factor V activity obtained after thrombin stimulation of 10(7) normal platelets is sufficient to allow half-maximal factor Xa binding to 10(8) platelets (10% normal, 90% factor-V deficient). Therefore, factor Va activity is not limiting in platelet-surface factor Xa binding and prothrombin activation in normal platelets; some other components limit the number of binding sites. We report studies of a patient (M.S.) with a moderate to severe bleeding abnormality whose platelets are deficient in the platelet-surface component required for the factor Va-factor Xa binding. The patient's platelet factor Va activity released after thrombin treatment is normal, but factor Xa binding is 20%-25% of control values at saturation. Abnormal prothrombin consumption in a patient with normal plasma coagulation factors and platelet function suggests a disorder in platelet-surface thrombin formation.
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PMID:Deficiency of factor Xa-factor Va binding sites on the platelets of a patient with a bleeding disorder. 49 93

The rates of prothrombin activation under initial conditions of invariant concentrations of prothrombin and Factor Xa were studied in the presence of various combinations of Ca2+, homogeneous bovine Factor V, Factor Va, phosphatidylcholine-phosphatidylserine vesicles, and activated bovine platelets. Reactions were monitored continuously through the enhanced fluorescence accompanying the interaction of newly formed thrombin with dansylarginine-N-(3-ethyl-1,5-pentanediyl) amide. The complete prothrombinase (Factor Xa, Ca2+, phospholipid, and Factor Va) behaved as a "typical" enzyme and catalyzed the activation of prothrombin with an apparent Vmax of 2100 mol of thrombin/min/mol of Factor Va or Factor Xa, whichever was the rate-limiting component. Regardless of whether the enzymatic complex was composed of Factor Xa, Ca2+, and plasma Factor Va plus phospholipid vesicles, or activated platelets in the place of the latter components, similar specific activity values were observed. The combination of Factor Va, Ca2+, and phospholipid enhanced the rate of the Factor Xa-catalyzed activation of prothrombin by a factor of 278,000. Factor Va itself when added to Factor Xa, Ca2+, and phospholipid, enhanced the rate of prothrombin activation by a factor of 13,000. Unactivated Factor V appears to possess 0.27% of the procoagulant activity of thrombin-activated Factor Va. From the kinetics of prothrombinase activity, an interaction between Factor Xa and both Factor V and Factor Va was observed, with apparent 1:1 stoichiometries and dissociation constants of 7.3 x 10(-10) M for Factor Va and 2.7 x 10(-9) M for Factor V. The present data, combined with data on the equilibrium binding of prothrombinase components to phospholipid, indicate that the model prothrombinase described in this paper consists of a phospholipid-bound, stoichiometric complex of Factor Va and Factor Xa, with bound Factor Va serving as the "binding site" for Factor Xa, in concert with its proposed role in platelets.
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PMID:The contribution of bovine Factor V and Factor Va to the activity of prothrombinase. 50 Jun 17

Fourteen patients with a documented sudden neurosensory hearing loss and four patients with other diseases causing neurosensory hearing loss were studied. The standardized coagulation workup included hematocrit, activated partial thromboplastin generation time, thrombin generation, prothrombin time, phase platelet count, platelet adhesivity, protamine sulfate, serum antithrombin III activity, fibrinogen, and Factor VIII values. Ony those patients having documented evidence of a neurosensory hearing loss occurring within hours or days were included in this study. Eight of the 14 paitents with a documented sudden neurosensory hearing loss satisfied our laboratory criteria for a diagnosis of in vitro hypercoagulability. Three of these patients had abnormal thrombin generation values, 4 had abnormal serum antithrombin III values, and 1 had an elevated platelet count. Four other patients with other diseases causing neurosensory hearing loss did not show evidence of in vitro hypercoagulability. It would appear from this data that coagulation abnormalities play a role in the pathogenesis of sudden neurosensory hearing loss.
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PMID:Hypercoagulability as a cause of sudden neurosensory hearing loss. 50

Intraoperative hemodilution and retransfusion were used for blood replacement in 30 patients who underwent elective reconstruction of the abdominal aorta, thoracic aorta or femoropopliteal segment. During each operation, 1,000 to 2,000 milliliters of autologous blood were collected through an arterial cannula during induction of anesthesia and the initial stages of operative exposure. Each volume of shed blood was replaced with 1.5 volumes of colloid and crystalloid solutions to maintain a stable intravascular volume despite transient low hematocrit values--mean, 25.8 +/- 2.1 per cent--during the period of maximum blood loss in the surgical field. Collected blood was stored in standard citrate-phosphate-dextrose disposable units and was reinfused at the conclusion of the vascular procedure. Swan-Ganz pulmonary artery catheters were inserted in an initial study group of 15 patients. Serial blood hematocrit and coagulation studies and hemodynamic parameters were measured or calculated before and after induction of anesthesia, during hemodilution, after reinfusion of autologous blood and 24 hours after operation. Improvement in cardiac output and reduction in peripheral vascular resistance maintained adequate systemic oxygen transport during hemodilution. Transient dilution of coagulation factors was documented by abnormal prothrombin and partial thromboplastin times, but serious bleeding tendencies did not occur. Twenty-one of the 30 patients received no homologous blood. Considering the entire series of 30 patients, each required only 0.46 +/- 0.87, S.D., unit of homologous blood during operation and the postoperative period.
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PMID:Intraoperative hemodilution during elective vascular reconstruction. 50 57

Ischemic optic neuropathy and retinal arterial occlusion are 2 forms of arterial occlusive disease affecting the eye. Reports in the literature suggest platelet hyperactivity in acute arterial occlusive diseases affecting other organ systems. Therefore, 14 patients with ischemic optic neuropathy and 17 patients with central or branch retinal artery occlusion were studied to determine whether platelets have a role in the pathogenesis of these vascular occlusive disorders. The results of the following investigations were no different in these patients compared with those in 18 control patients with non-vascular eye diseases: prothrombin times, partial thromboplastin times, plasma fibrinogen, factor V, factor VIII, platelet counts and threshold concentrations of ADP, epinephrine and collagen resulting in secondary platelet aggregation and serotonin release. In contrast, platelet coagulant activities concerned with the early stages of intrinsic coagulation were significantly increased in patients with retinal artery occlusion without hypertension or type IV hyperlipoproteinemia, but generally normal in patients with ischemic optic neuropathy and in patients with retinal artery occlusion associated with hypertension, type IV hyperlipoproteinemia, diabetes mellitus and generalized atherosclerosis. These results are consistent with a platelet contribution to retinal arterial occlusive disease in patients without other known contributing factors such as hypertension, serum lipid abnormalities, diabetes mellitus and generalized atherosclerosis and may have implications regarding prophylaxis.
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PMID:Platelet coagulant activities in arterial occlusive disease of the eye. 50 1

Bovine platelets that have been activated by thrombin facilitate the conversion of prothrombin to thrombin in the presence of calcium ions and factor Xa. Activated protein C, a vitamin-K-dependent plasma protein, inhibits this platelet prothrombin-converting activity. The inhibition is time dependent and is not reversed by increasing concentrations of factor Xa. However, factor Xa is able to protect the platelet prothrombin-converting activity from inactivation by activated protein C. The activated protein C causes a parallel loss of factor Xa receptor sites and platelet prothrombin-converting activity. Activated protein C may contribute to the regulation of clotting through inactivation of the platelet prothrombin-converting activity.
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PMID:Activated protein C inhibits platelet prothrombin-converting activity. 50 37

1. Activated factor XIII is the enzyme that covalently cross-links fibrin monomers into fibrin polymers and results in increased clot strength and resistance of the clot to fibrinolysis. 2. Small amounts (greater than 1% of normal) of factor XIII are necessary for normal in vitro and in vivo activity. 3. Factor XIII deficiency is a rare autosomal recessive illness in which a hemorrhagic diathesis is caused by the virtual absence of the active a subunit of factor XIII. Approximately 100 cases have been described. 4. The disease in homozygotes is characterized by umbilical stump bleeding, a high incidence of fetal wastage, delayed soft tissue hemorrhage, and a high incidence of intracranial bleeding. The heterozygote is asymptomatic. 5. This paper calls attention to the apparent high incidence of oligospermia and small testes seen in homozygote males. Otherwise secondary sex characterics are normal. 6. Because there is no abnormality in thrombin generation and conversion of fibrinogen to fibrin, route coagulation tests (prothrombin time, partial thromboplastin time, thrombin time, etc.) are normal. Platelet function tests are normal. 7. Clots made from recalcified plasma severely deficient in factor XIII are soluble in 5 M urea or 1% monochloroacetic acid. These screening tests are simple and nearly pathognomonic of the illness. 8. More sophisticated and quantitative tests (e.g., dansylcadaverine incorporation) are available for definitive diagnosis and heterozygote detection. 9. Replacement treatment of the illness is simple, effective, and relatively inexpensive. Due to the long half-life of infused factor XIII and the small amounts necessary for normal hemostasis, prophylaxis is feasible and encouraged.
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PMID:Factor XIII. 51 66


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