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)

A prospective study of hemostatic abnormalities in 108 cancer patients was undertken at an oncology clinic in a university teaching hospital. Tests included Quick prothrombin time, activated partial thromboplastin time, thrombin time, platelet count, modified Ivy bleeding time, fibrinogen, fibrin degradation products (FDP), euglobulin lysis time, protamine sulfate test, and factor V, VII, VIII and X assays. Ninety-eight per cent of the patients had one or more abnormal coagulation tests. The commonest abnormalities were elevated fibrin degradation products and prolonged thrombin time. Thrombocytosis occurred in 57% of patients, hyperfibrinogenemia in 46%, thrombocytopenia in 11%, and non had hypofibrinogenmia. It is suggested that platelet count, fibrinogen concentration, and serum FDP assay are the most useful tests in assessing the hemostatic abnormalities in cancer patients, although thrombin time, factor V assay, and bleeding time may also be helpful. The peripheral blood smears of 53 patients were reviewed, and only one showed microangiopathic hemolytic anemia. The data illustrate that subclinical coagulopathy is relatively frequent in patients with malignancy.
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PMID:Hemostatic abnormalities in malignancy, a prospective study of one hundred eight patients. Part I. Coagulation studies. 42 Jan 61

Recurrent retinal branch artery occlusions, carotid thromboembolism, cerebral venous thrombosis, transient brainstem ischemia, and massive brainstem and cerebral infarction complicated the course of inflammatory bowel disease in 5 patients. Three patients had ulcerative colitis and 2 had regional enteritis. The usual risk factors for stroke were absent. Neuropathological examination in 1 patient showed in situ thrombosis of small cerebral and brainstem arteries and veins. Coagulation studies showed thrombocytosis, short partial thromboplastin times, and elevation of fibrinogen and Factor VIII levels. Platelet counts and coagulation factors returned toward normal after control of intestinal inflammation in each of the 4 surviving patients. Inflammatory bowel disease can be accompanied by a hypercoagulable state that predisposes to stroke.
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PMID:Cerebral and retinal vascular complications of inflammatory bowel disease. 44 68

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

Sera from 23 patients with idiopathic thrombocytopenic purpura (ITP), 14 patients with aplastic anemia with severe thrombocytopenia and healthy control subjects were tested for the presence of fibrinogen/fibrin degradation products (FDP), using the tanned red cell hemagglutination inhibition immunoaassay. The concentrations of circulating FDP of ITP patients (mean 12.01 mug/ml) were significantly higher than those of the patients with aplastic anemia (mean 4.01 mug/ml, p less than 0.05) or normal controls (mean 3.10 mug/ml, p less than 0.001). The patients with untreated ITP with very low platelet counts had higher levels of FDP than those of the treated group (p less than 0.01). Serum FDP and a battery of other coagulation-fibrinolysis tests were serially carried out over a period of 10 weeks in two patients with ITP. The initially high FDP promptly decreased as circulating platelets increased in response to steroid in both patients, while plasma fibrinogen, euglobulin lysis time, prothrombin time and partial thromboplastin time remained essentially normal during the course of observation. The exact source of the increased serum FDP in ITP was not established, but a few possible mechanisms responsible for this abnormality were discussed.
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PMID:Fibrinogen/fibrin degradation products in serum of patients with idiopathic thrombocytopenic purpura: elevated levels during severe thrombocytopenic phase of the disease. 98 69

Both the basal and the collagen plus thrombin-stimulated prothrombinase activities have been measured in platelets from eight patients with essential thrombocythaemia (ET). On a mean basis these activities were significantly lower than the values recorded for a group of age and sex matched control subjects. When the Ca2+ ionophore A23187 was substituted for the agonist mixture the induced expression of prothrombinase activity was essentially the same for the patient and control groups. It is suggested that the defect in prothrombinase expression seen with ET platelets may reside in either membrane signal transduction processes concerned with Ca2+ mobilization or in Ca2+ sensitive cytoskeletal control of membrane phospholipid topography.
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PMID:Basal and induced prothrombinase expression in platelets from patients with essential thrombocythaemia (ET). 209 27

Platelets play a central role in haemostasis. Not only are they involved in aggregatory and agglutination responses but they are also implicated in the clotting system. The conversion of prothrombin to thrombin, in the presence of coagulation factors Va, Xa and calcium ions, is termed prothrombinase activity. For optimal expression of this process a negatively charged phospholipid surface is required. Platelets can provide such an environment, by exposing negatively charged phospholipids at their external plasma membrane, by a 'flip-flop' process whereby negatively charged phospholipids, predominantly phosphatidylserine, move from the inner plasma membrane leaflet to the outer leaflet upon the activation of platelets by certain agonists. Such agonists include collagen and thrombin and the amount of prothrombinase activity expressed is well correlated with the propensity of the agonist to activate platelet calcium-dependent protease, calpain. This enzyme is then thought to act upon platelet cytoskeletal components, thus breaking the restraining action of the cytoskeleton upon the platelet plasma membrane and facilitating 'flip-flop'. The platelet plasma membrane is therefore a dynamic surface capable of catalytic functions in coagulation systems. Recent research has high-lighted abnormalities in platelet prothrombinase expression in certain disease states. These include Bernard-Soulier syndrome, essential thrombocythaemia and conditions where the lupus anticoagulant may be present.
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PMID:Platelet prothrombinase in health and disease. 213 Sep 28

Two aspects of the activation of factor X by the intrinsic clotting pathway have been studied in purified human systems, in the presence of either purified phosphatidylserine:phosphatidylcholine vesicles (PS:PC) or platelets activated with ionophore A23187: (1) the activation of factor VIII by factor Xa and by thrombin, and (2) the activation of factor X by the factor IXa/VIIIa complex. Factor VIII activation by thrombin was unaffected in either rate or extent by the presence of PS:PC or activated platelets. In contrast, factor VIII activation by factor Xa required either PS:PC or platelets. The products of optimal factor VIII activation by the two enzymes, designated factor VIIIa(T) and factor VIIIa(Xa), are kinetically different in the activation of factor X by factor IXa, factor VIIIa(T) being approximately twice as active (in factor X activation) as factor VIIIa(Xa) in the presence of PS:PC or platelets. Factor VIIIa(Xa) can be converted to the more active VIIIa(T) by thrombin treatment, but the activity of factor VIIIa(T) is unchanged by factor Xa treatment. Factor X activation was also studied with optimally activated factor VIIIa(T), in the presence of PS:PC or activated platelets, as a function of factor IXa concentration in order to determine the apparent dissociation constant for the factor IXa-VIIIa interaction in the two cases. Activated platelets increased the apparent affinity more than fivefold.
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PMID:A comparison of phospholipid and platelets in the activation of human factor VIII by thrombin and factor Xa, and in the activation of factor X. 314 Sep 13

Membrane assembly of complement proteins C5b-9 on human platelets results in a dose-dependent increase in the binding of coagulation factors Va and Xa to the plasma membrane, concomitant with a marked increase in platelet prothrombinase activity. Factor Va binding increased by 6-15-fold in platelets treated with the C5b-9 proteins as compared to controls. In the presence of near-saturating concentrations of factor Xa, factor Va binding to C5b-9-treated platelets approximately doubled. In the absence of added factor Va, C5b-9-treated platelets bound 1700 molecules of factor Xa versus 50 molecules/cell bound to controls, suggesting that C5b-9 assembly on the platelet surface initiates the release of platelet factor V from the alpha-granules. The capacity of the C5b-9 proteins to initiate the nonlytic release of the platelet alpha-granule storage pool was confirmed by assay for platelet factor 4. When measured in the presence of exogenous factor Va (2 micrograms/ml), factor Xa uptake by C5b-9 platelets increased to approximately 5500 molecules/cell (versus 330 molecules/cell for controls). Removal of external Ca2+ inhibited the C5b-9-initiated release of the alpha-granule storage pool and reduced by approximately 50% the expression of new factor Va binding sites, suggesting that these two events contributing to increased platelet prothrombinase activity are mediated in part by the influx of Ca2+ across the C5b-9 pore.
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PMID:On the mechanism by which complement proteins C5b-9 increase platelet prothrombinase activity. 315 19

The effect of splenectomy on hemostatic tests was studied in 10 patients with agnogenic myeloid metaplasia. Prolonged partial thromboplastin time and abnormal prothrombin consumption were found before splenectomy and were normalized postoperatively in the majority of patients. Prolonged bleeding time and prothrombin time were normalized in some patients. While platelet counts and fibrinogen levels rose significantly following splenectomy, platelet aggregation remained impaired. Thrombocytosis and increased fibrinogen level after splenectomy in patients with agnogenic myeloid metaplasia can enhance a thromboembolic tendency.
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PMID:Influence of splenectomy on hemostasis in agnogenic myeloid metaplasia. 360 15

Intraabdominal pseudotumor of the plasma cell granuloma type in a 19-year-old man is reported. The patient presented with fever and weight loss lasting months, and the laboratory findings revealed high sedimentation rate, hypochromic, microcytic anemia, thrombocytosis, elevated alkaline phosphatase, decreased thromboplastin time and polyclonal hypergammaglobulinemia. When the plasma cell granuloma was removed, all laboratory findings returned to normal within 3 months and the patient remained asymptomatic during the two-year follow-up.
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PMID:[Abdominal inflammatory pseudotumor (plasma cell granuloma) with anemia and hypergammaglobulinemia]. 370 10


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