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)

Six coagulation proteins were measured in 79 consecutive patients referred to the coagulation service for suspected disseminated intravascular coagulation. Antithrombin III, plasminogen, and alpha 2-plasmin inhibitor were measured with fluorescent substrate assays. Fibronectin, prothrombin, and protein C were measured with electroimmunoassays. Using history and physical findings and the results of a coagulation screen (prothrombin time, partial thromboplastin time, fibrinogen, fibrin[ogen] degradation products, platelet count, and peripheral smear), the 79 patients were classified into five categories: no disseminated intravascular coagulation (n = 21), elevated fibrin(ogen) degradation products without other evidence of coagulopathy (n = 44), defibrination syndrome (n = 9), microangiopathic thrombocytopenic purpura (n = 4), and primary fibrinolysis (n = 1). Because the sensitivity and specificity of each of the proteins could not easily be compared, receiver operating characteristic (ROC) curves and areas under the ROC curves were calculated for each of the six proteins as well as for the tests of the coagulation screen. The ROC curves indicated that, apart from plasminogen, the other coagulation proteins provided little additional information about the classification of the coagulopathy.
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PMID:Diagnostic efficacy of six plasma proteins in evaluating consumptive coagulopathies. Use of receiver operating characteristic curves to compare antithrombin III, plasminogen, alpha 2-plasmin inhibitor, fibronectin, prothrombin, and protein C. 376 44

The anticoagulant activity of a partially reduced sulphated alginic acid, a partially reduced aminated and sulphated alginic acid and sulphated guaran have been studied. The anticoagulant activities in the APTT assay were 28, 39 and 70 IU/mg respectively. None showed any activity in anti-factor Xa assay. Studies on binding to Antithrombin III - Sepharose showed that sulphated guaran and a fraction of the aminated and sulphated alginic acid was bound, whereas no binding occurred with sulphated alginic acid. The inhibition of thrombin activity by these polysaccharides was studied in purified systems with or without added Antithrombin III, using both fibrinogen clotting and chromogenic peptide substrate assays. The two alginic acid preparations showed Antithrombin III-dependent inhibition of thrombin, whereas the sulphated guaran inhibits both by Antithrombin III-dependent and independent mechanisms.
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PMID:Mechanisms of anticoagulant effects of some sulphated polysaccharides. 613 65

A prospective investigation was initiated to assess the effect of a low-dose oral contraceptive containing 35 micrograms of ethinyl estradiol and 0.4 mg of norethindrone on blood coagulation and fibrinolysis. Twenty-four women were studied before, during, and after one year of treatment. Positive results included an accelerated activated partial thromboplastin time and an increase in fibrinolytic and anticoagulation factors as measured by alpha 1-antitrypsin antigen and plasminogen antigen and activity. Antithrombin III antigen was decreased but its activity was unaffected. There was no evidence of ongoing intravascular coagulation. No patient had a detectable thromboembolic event. In short, one year's usage of this low-dose oral contraceptive was not associated with a procoagulant hematologic profile.
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PMID:Low-dose oral contraceptive usage and coagulation. 616 2

The effects of treadmill exercise (up to 85% of the predicted maximum heart rate) on platelet functions and coagulating activities were studied in 26 normal men. Blood sampling for the measurements were performed from the antecubital vein at rest, at 3, 6, 9, and 12 min during exercise, immediately postexercise, and at 6 and 30 min after exercise. Measurements for blood analysis included the following: platelet sensitivity and percent aggregation to ADP, platelet counts, plasma thromboxane B2 and 6-keto-prostaglandin F1 alpha levels, plasma epinephrine and norepinephrine levels, plasma fibrinogen level, activity of plasma antithrombin III, and of plasma factors VIII, IX, XI, and XII. No significant changes were induced by dynamic leg exercise in platelet sensitivities and the maximum and 3-min percent aggregation. The platelet counts increased during exercise in platelet-rich plasma without a significant change in that in whole blood. During exercise, plasma thromboxane B2 levels showed a tendency to increase, while plasma 6-keto-prostaglandin F1 alpha levels to decrease. Plasma epinephrine levels showed a tendency to increase and norepinephrine levels increased during exercise. Among coagulating factors, factor VIII activities and fibrinogen levels increased without altering activities of factors IX, XI, and XII. Antithrombin III activities also increased during exercise. In spite of significant changes in several coagulating factors, prothrombin time and partial thromboplastin time were not influenced by exercise. In conclusion, dynamic leg exercise of a moderate to high intensity produced a significantly elevated plasma level of factor VIII, fibrinogen, antithrombin III, and catecholamines without affecting the hemostatic balance in normal subjects.
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PMID:Effects of treadmill exercise on platelet functions and blood coagulating activities in healthy men. 643 Nov 40

75 patients with atherosclerosis divided into five disease groups (previous myocardial infarction and cerebral thrombosis, angina pectoris, transient ischemic attacks, arteriosclerosis obliterans) were studied and compared to 20 healthy subjects. Antithrombin III (AT III) concentration was determined by single radial immunodiffusion; AT III and factor Xa-inhibitor (Xa-I) activities were measured by amidolytic methods. No significant difference was found in any group of patients as compared to normal controls by all the methods. A positive correlation was found between AT III concentration and AT III activity, AT III concentration and Xa-I activity, AT III activity and Xa-I activity. Results are discussed in relation to the literature data.
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PMID:Antithrombin III and factor Xa inhibitor in atherosclerosis. 661 88

Coagulation and fibrinolysis profiles of naturally menopausal women receiving conjugated estrogens (0.625 or 1.25 mg for 21 of 28 days) and medroxyprogesterone acetate (10 mg for seven of 28 days) for 18 months were compared with those of similar women receiving no hormone therapy. Tests indicative of the dynamics of the coagulation cascade, ongoing intravascular coagulation, and anticoagulation were performed. Hormone therapy had no effect on prothrombin times, activated partial thromboplastin times, or thrombin times. There was no evidence of intravascular coagulation in any of the groups as assessed by platelet counts, fibrinogen antigen and activity, and fibrin degradation products. Antithrombin III antigen and activity, alpha 1-antitrypsin antigen, and alpha 2-macroglobulin antigen, the natural inhibitors of coagulation, were also unaffected by hormone therapy. Plasminogen antigen levels were unaffected, but plasminogen activity was enhanced in the hormone-treated groups, suggesting a stimulatory effect on fibrinolysis. These data indicate that in terms of the coagulation system, healthy women can safely use a combined regimen of conjugated estrogens and medroxyprogesterone acetate.
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PMID:Combination estrogen and progestogen replacement therapy does not adversely affect coagulation. 662 49

In 57 patients with pregnancy-induced or aggravated hypertension, antithrombin III levels correlated inversely with maternal morbidity. Morbidity was determined by the maximal diastolic blood pressure, disturbance of renal and liver function, and thrombocytopenia. Antithrombin III levels and platelet counts correlated inversely with the degree of placental infarction. Proteinuria (grams per 24 hours) was most predictive of fetal outcome, which was considered to be either favorable if a healthy baby could be discharged with its mother or unfavorable in case of perinatal death or a prolonged stay in the neonatal intensive care unit. Plasma antithrombin III and serum glutamic oxaloacetic transaminase levels, in that order, augmented the number of correct predictions. Antithrombin III inhibits blood coagulation by forming irreversible complexes with activated clotting enzymes, notably with factor Xa and thrombin. Evidence is presented which suggests that antithrombin III levels in preeclampsia are depressed as a result of increased consumption in the maternal vascular tree, rather than decreased synthesis or increased urinary loss.
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PMID:Antithrombin III levels in preeclampsia correlate with maternal and fetal morbidity. 671 44

To elucidate the relationship between estrogen and thrombosis, we studied blood coagulation parameters in women whose ovaries were stimulated with human menopausal gonadotropins (hMG). Daily hMG administration over 1 to 2 weeks in seven anovulatory women increased plasma 17 beta-estradiol levels fivefold over the pretreatment value. Of the coagulation parameters, the fibrinogen level increased significantly from an initial value of 248 +/- 11.7 mg/dl (mean +/- SEM) to 353 +/- 32.2 mg/dl after hMG treatment (P less than 0.05), with a significant positive correlation between estrogen and fibrinogen levels (r = +0.762). In addition, a thrombokinetics study showed that the maximal rate of change in optical density of the prothrombin time and activated partial thromboplastin time was significantly increased, suggesting that the coagulation factors involved in extrinsic, intrinsic, and common pathways could be increased by estrogen. Antithrombin III levels decreased gradually during hMG administration. Thus, increased endogenous estrogen levels appear to induce the so-called "hypercoagulable state" through both an increase in coagulation factors in the coagulation cascade system and a decrease in antithrombin III, a potent natural inhibitor of activated coagulation factors. Patients on a regimen of hMG treatment for induction of ovulation serve as excellent models for the study of alteration of "natural" estrogen-mediated coagulation parameters.
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PMID:Response of blood coagulation parameters to elevated endogenous 17 beta-estradiol levels induced by human menopausal gonadotropins. 678 79

Blood coagulation and fibrinolysis were studied in 65 patients with chronic myeloproliferative disorders (MPD). They consisted of 28 patients with chronic granulocytic leukemia (CGL) in chronic phase, 7 with CGL in blast crisis, 9 with polycythemia vera (PV), 13 with primary thrombocythemia (PTh) and 8 with primary myelofibrosis (MF). Hemorrhagic and thrombotic complications were observed in 19 and 8 patients, respectively. Activated partial thromboplastin time and prothrombin time were prolonged in many patients. Low factor II levels were observed in some CGL patients. Factor V was decreased in CGL patients in chronic phase and in PV patients. Fibrinogen was either normal or increased in most patients, but an elevation of fibrin/fibrinogen degradation products (FDP) was found in some patients. The VIIIR: Ag/VIII:C ratio was increased in CGL patients in blast crisis, in PV patients and in PTh patients. Antithrombin III and plasminogen were below normal in some patients. Most patients showed a decrease in alpha 2-plasmin inhibitor. These findings suggest that blood coagulation and fibrinolysis are involved in the pathogenesis of the thrombotic and hemorrhagic complications in these patients. Chronic low-grade intravascular coagulation might be present in some patients with MPD.
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PMID:Profile of blood coagulation and fibrinolysis in chronic myeloproliferative disorders. 695 82

Sensitized and control calves were challenged with an intravenous dose of 0.2 mL/kg horse serum. Changes in the blood pressure, blood cellular components, plasma kaolin activated p-tosyl-1-arginine methyl ester esterase activity, plasma antithrombin III levels and activated partial thromboplastin time were monitored. Anaphylaxis induced a severe drop in carotid arterial pressure and respiratory distress. There was a decrease in the total white blood cell count from a mean of 10,000 to a low of 1,900 per microL, a decrease in the percentage neutrophils and an increase in the percentage of lymphocytes from 57.4% to 94.8%. A drop was observed in the mean platelet count from 463 x 10(3)/microL. The time required for kaolin to produce maximum p-tosyl-1-arginine methyl ester esterase activation increased from two minutes in the controls to three minutes in calves undergoing anaphylaxis and was observed three to 90 minutes after the administration of horse serum. Antithrombin III levels in the plasma appeared to drop during anaphylaxis but were not significantly depressed (p greater than or equal to 0.5). A statistically significant (p < 0.5) drop in the rate of blood coagulation was observed by the activated partial thromboplastin time assay at 15 to 30 minutes after horse serum injection.
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PMID:A study of the effect of acute systemic anaphylaxis on blood coagulation and TAME esterase activity in calves. 699 96


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