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:3.4.21.5 (thrombin)
33,306 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

18 type II diabetes mellitus patients with coronary artery disease (CAD) have been studied. Tissue plasminogen activator (t-PA) antigen and activity, plasminogen activator inhibitor (PAI) antigen and activity, thrombin-antithrombin III (TAT) complexes were determined in blood samples. Diabetic CAD patients showed higher TAT levels with clearly increased PAI levels whereas t-PA levels levels were similar in patients and controls. Long term defibrotide treatment induced marked changes in fibrinolytic parameters of these diabetic patients with CAD with increased t-PA activity, that could be related to an evident reduction of PAI antigen and activity. Drugs able to modulate PAI activity may be useful in clinical conditions at high risk of thrombotic vascular complications like diabetics with stable angina.
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PMID:Effects of defibrotide on fibrinolytic activity in diabetic patients with stable angina pectoris. 157 96

Coagulation in angina pectoris has been analyzed in a normal and elevated level of natural antibodies (nAb) to thrombin. A correlation was found between the level of nAb to thrombin and hemostatic shifts. The correlation of a nAb rise was attempted by means of plasmapheresis (PA) or plasmosorption (PS), altering coagulation potential. PA and PS produced more pronounced anticoagulative effects in patients with a normal baseline level of nAb to thrombin. When the latter levels tended to reduction from initially high, hemostatic processes improved. It is concluded that nAb to thrombin levels have prognostic potential as an indicator of coagulation activity and efficacy of anticoagulant therapy in extracorporeal interventions.
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PMID:[The prognostic significance of changes in the level of natural antibodies to thrombin in stenocardia patients]. 160 2

We here present a Japanese family with type I hereditary heparin cofactor II (HC II) deficiency. The propositus (a 61-year-old man) suffered from angina pectoris and coronary artery disease was confirmed by coronary angiography. He underwent percutaneous transluminal coronary angioplasty (PTCA) four times in one year. Combined use of heparin, aspirin, and nitrates could not prevent the return of his symptoms and restenosis of segment 6 of the left anterior descending artery. His HC II activity and antigen levels were 49% and 50%, respectively, and his daughter also showed similar low levels. Cerebral infarction had occurred in two family members. Argatroban, a selective potent thrombin inhibitor, was administered after the fourth PTCA for the purpose of preventing reocclusion and achieved a successful outcome. A relationship between HC II deficiency and thrombosis has not yet been established. Our case suggests that standard heparin therapy is not effective in preventing restenosis in such individuals, in whom the process is accelerated by thrombin generation at the site where PTCA produces rupture of the atherosclerotic plaque. Argatroban may be more effective under low HC II conditions because of its potent inhibition of thrombin activity at sites of vascular wall damage.
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PMID:Hereditary heparin cofactor II deficiency and coronary artery disease. 161 93

Thrombomodulin (TM) is an endothelial cell membrane glycoprotein which neutralizes thrombin clotting activity and accelerates thrombin-catalyzed activation of plasma protein C. Its role is considered to be very important to prevent thrombosis. Recently, TM has been found in circulating blood and the roles and the functions have been investigated. In this study, we evaluated the reliance and the clinical usefulness of a TM-measuring-kit by enzyme immunoassay (MGC-01-001: Mitsubishi Gas chemical company). Intraassay reproducibility test, dilution linearity test and in vitro recovery test was obtained satisfactory results. A correlation between plasma and serum on TM levels of healthy individuals was very good and the difference between them was not significant. Normal value of plasma TM levels was instituted 15.73 +/- 6.98 ng/ml by measuring 52 healthy adults. The difference between male and female was not significant. Plasma TM levels did not change significantly after venous occlusion test and on circadian fluctuation. Plasma TM levels in patients with occlusion test and on circadian fluctuation. Plasma TM levels in patients with disseminated intravascular coagulation (DIC) was 40.15 +/- 22.68 ng/ml (mean +/- SD, n = 14). It is significantly higher than the levels in healthy adults. However, the levels in patients with angina pectoris, acute myocardial infarction and aortic aneurysm were not significantly different from those of healthy adults. These findings suggest that the precision of this TM-measuring-kit is satisfactory and the measurement of plasma TM can be useful to diagnose of DIC.
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PMID:[Evaluation of an enzyme immunoassay for plasma thrombomodulin]. 165 17

A study was made of changes in the content of natural antibodies (N-AB) to thrombin and alpha 2-macroglobulin in patients with angina pectoris under the influence of plasma perfusion. The content of N-AB being increased, plasma perfusion makes it possible to reduce their content to normal. Provided the content of N-AB is initially normal, plasma perfusion does not produce any changes in their level. In 78% of the patients, a beneficial clinical effect was attained, being more pronounced in initially high content of N-AB.
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PMID:[The effect of plasmasorption on the content of natural antibodies to thrombin and alpha 2-macroglobulin in stenocardia patients]. 171 15

PAI-1 antigen, tPA antigen and thrombin - antithrombin III complexes (TAT) levels were measured in 10 males with stable angina and type-II diabetes mellitus and in 16 males with stable angina without diabetes or other risk factors (hyperfibrinogenaemia, hyperlipidaemia, diabetes, hypertension, smoking and obesity) known to increase PAI levels. Ten healthy men of equivalent age served as controls. Because only diabetics with coronary artery disease (CAD) showed a decreased fibrinolytic capacity, a second study was performed on the 16 non-diabetic CAD patients to determine whether submaximal workload induces significant changes of tPA and PAI levels. TAT levels were increased in CAD, and significantly so in the diabetic group. tPA levels were increased only in the CAD patients without diabetes. PAI levels were significantly increased in diabetic CAD patients (5.26 +/- 1.96 ng/ml) but not in the stable angina patients without diabetes (2.97 +/- 1.44 ng/ml). Immunologically-reactive tPA released after exercise was higher in the 16 CAD patients without diabetes than in controls. Our data could indicate that in stable angina without diabetes there is no chronic latent activation of the clotting system, with no impairment of fibrinolytic activity. On the other hand, the presence of diabetes mellitus seems to influence the fibrinolytic capacity in CAD, particularly increasing PAI levels.
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PMID:Increased plasminogen activator inhibitor antigen levels in diabetic patients with stable angina. 177 97

Plasma levels and 24-hour urine excretion of fibrinopeptide A were measured in a consecutive series of 179 patients with angina pectoris. Sixty-four patients had stable angina and 115 patients had unstable angina. Urine was collected over 24 hours the day before coronary arteriography, and blood samples were taken at the end of urine collection. When the values of fibrinopeptide A in plasma and in the 24-hour urine specimens were compared, no significant correlation was found in patients with either stable (rs = 0.16, difference not significant) and unstable (rs = 0.07, difference not significant) angina. The concentrations of fibrinopeptide A in the plasma did not differ significantly when patients with stable angina (range 0.1 to 82.6, median 7.4 ng/mL) were compared with patients with unstable angina (range 0.2 to 61.7, median 14 ng/mL, p = 0.055), whereas fibrinopeptide A 24-hour urinary excretion was significantly higher in patients with unstable angina (range 0.3 to 38.1, median 11.8 micrograms/24 hr) than in patients with stable angina (range 0.4 to 38.1, median 3.8 micrograms/24 hr, p less than 0.001). Twenty-four-hour urine excretion of fibrinopeptide A in patients with unstable angina and angiographically documented intracoronary thrombi were higher than the corresponding values in patients with unstable angina without such angiographic characteristic (p less than 0.001). The largest increase in plasma and urine concentration of fibrinopeptide A was observed in patients whose first episode of angina at rest occurred within the previous 48 hours. We conclude that the cumulative thrombin activity, assessed by 24-hour urinary excretion of fibrinopeptide A, is a more useful index, compared with single fibrinopeptide A measurement in plasma, for discriminating between patients with stable and with unstable angina pectoris.
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PMID:Fibrinopeptide A excretion in urine: a marker of the cumulative thrombin activity in stable versus unstable angina patients. 189 68

The impact of 6-week strenuous exercise training (SET) on blood coagulative and fibrinolytic parameters (levels of fibrinogen, soluble fibrin, fibrinogen-fibrin degradation products, activities of plasminogen and plasmin) was studied in 28 patients with first angina pectoris, in 16 of whom in the first 3 months of onset of the disease, but angina pectoris lasting 3-4 prior to SET. The 6-week strenuous exercises in patients with first angina were found to cause a decrease in fibrinogen levels, exert no action on thrombin and fibrin formation. They did not diminish plasminogen activator release during exercise in patients with pre-exercise unstable angina.
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PMID:[Newly developed stenocardia: effect of intensive physical training on the indicators of the blood coagulation system and fibrinolysis]. 189 56

The Caerphilly Collaborative Heart Disease Study is based on a large cohort of men (2,398) aged 49-66 years at the time of study. Platelet aggregation induced by collagen, thrombin, and ADP was measured in fasting blood samples and was related to prevalent angina, past myocardial infarction, and electrocardiographic evidence of ischemic heart disease. A number of subjects had taken aspirin, other nonsteroidal anti-inflammatory drugs, or other drugs affecting platelet aggregation 7 days before blood sample collection; after the exclusion of these subjects, data were available for 1,811 men. No relations were demonstrated with angina, but significant relations were shown between past myocardial infarctions and electrocardiographic evidence of ischemia and ADP-induced aggregation (both primary and secondary) and between electrocardiographic evidence of ischemia and thrombin-induced aggregation. The strongest relation indicated more than a twofold increase in the odds of a past myocardial infarction in subjects of the highest fifth of ADP-induced primary platelet aggregation compared with the lowest fifth. No significant relations were detected with collagen-induced aggregation. Accounting for a number of possible confounding factors had a relatively small impact on the relations between platelet aggregation and ischemic heart disease. Other evidence, including the well-established effect of aspirin on reducing the incidence of ischemic heart disease, indicates that the relations we describe are unlikely to be simply an effect of IHD on platelets.
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PMID:Ischemic heart disease and platelet aggregation. The Caerphilly Collaborative Heart Disease Study. 198 96

Plasma antithrombin III was measured by an immunological approach (AT III:Ag) using an antiserum developed in our laboratory and by its ability to inhibit thrombin (functional assay) using a chromogenic synthetic substrate in 12 patients with myocardial infarction, 9 patients with angina pectoris and 10 healthy control subjects. In the early stage (3 to 24 hours after the onset of pain) of an acute myocardial infarction AT III:Ag (115.67% +/- 21.23) was found to be significantly (p less than 0.01) higher than functional (free) AT III (92% +/- 10.27). This difference was less obvious 10 days later (AT III:Ag 118% +/- 18.93; functional AT III 104.94 +/- 14.45). There was also no significant difference between AT III:Ag and functional AT III in patients with angina pectoris as well as in controls. Since AT III:Ag represents total plasma AT III while functional AT III represents only free AT III the difference between these two variables could provide informations about the amount of the anticoagulant forming complexes with activated clotting factors. It is therefore considered that the significant increase in the difference between AT III:Ag and functional AT III in the early stage of acute myocardial infarction is likely to suggest an intravascular activation of coagulation.
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PMID:Functional and antigenic antithrombin III in angina pectoris and acute myocardial infarction patients. 210 Aug 76


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