Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study we evaluated fibronectin as a marker of endothelial cell injury and antithrombin III as a marker of chronic activation of intravascular coagulation. The aim of the study was to establish to normal trends of plasma antithrombin III and fibronectin in general obstetric population and to determine the value of both in predicting, distinguishing and understanding the pathophysiology of pregnancy induced hypertension. The all cases consisted of 173 pregnant, 19 of them were chronic hypertensive, 45 were pregnancy induced hypertensive and 119 were normotensive at blood sampling. Out of 119 normotensive cases, 109 cases had no adverse outcome during their pregnancy. These cases were used as a control group and for the normal trends of antithrombin III and fibronectin in general obstetric population. Ten out of 119 cases who developed preeclampsia during follow up, 19 cases with chronic hypertension and 45 cases with pregnancy induced hypertension consisted of the study group. In the cases who developed preeclampsia during follow up, the value of plasma fibronectin level (above 95% confidence limit for that gestational week) to predict preeclampsia had 90% sensitivity and 94.4% specificity. In distinguishing hypertensive disorders of pregnancy (chronic hypertension or pregnancy induced hypertension) fibronectin had 71.1% sensitivity and 100% specificity. Plasma antithrombin III level (of antigenicity) measured by immunodiffusion method had no value in predicting and distinguishing pregnancy induced hypertension.
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PMID:The value of antithrombin-III and fibronectin in hypertensive disorders of pregnancy. 803 92

In eight patients with Legg-Perthes disease, we assessed the etiologic roles of thrombophilia caused by protein C and protein S deficiency and hypofibrinolysis mediated by low levels of tissue plasminogen activator activity. We speculated that thrombosis or hypofibrinolysis were common causes of Legg-Perthes disease. Three of the eight patients had protein C deficiency; they came from kindreds with previously undiagnosed protein C deficiency. In one of these three kindreds there were six protein C-deficient family members (beyond the proband child), four of whom had thrombotic events as adults. One of the eight patients had protein S deficiency, as did his brother who had sustained mesenteric vein thrombosis at age 43. One of the eight patients who had normal proteins C, S, and antithrombin III had hypofibrinolysis, failing to elevate tissue plasminogen activator activity after 10 min of venous occlusion at 100 mm Hg. Plasminogen activator inhibitor, alpha 2-antiplasmin, and fibrinogen values were normal in all eight patients. Beyond their Legg-Perthes disease, none of the eight patients had evidence for venous thrombosis. Of the eight patients, four had thrombophilia and one had hypofibrinolysis, disorders that we believe contributed to thrombotic venous occlusion of the femur with subsequent venous hypertension and bone death that characterize Legg-Perthes disease.
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PMID:Protein C and S deficiency, thrombophilia, and hypofibrinolysis: pathophysiologic causes of Legg-Perthes disease. 804 73

The aim of the present study was to investigate the occurrence of changes in the plasma levels of vasoactive prostanoids and inhibitors of blood coagulation in normal pregnancy and in cases of pregnancy induced hypertension. Levels of the coagulation inhibitors antithrombin III, protein C, Protein S as well as the prostaglandin metabolites thromboxane B2 and 6-oxo-prostaglandin F1 alpha were measured between 13 and 37 weeks gestation in 36 primigravidae. In 8 of the examined patients persistently raised blood pressure values of 140/90 and above were measured after 20 weeks of gestation. Our results indicated that an imbalance of vasoactive prostanoids may precede the appearance of clinical symptoms of PIH. The determination of coagulation factors before blood pressure is elevated has no predictive value regarding the later development of PIH. The reduced levels of protein C associated with our PIH group are considered to be the result of an activated coagulation followed by consumption of clotting factors. Reduced measured levels of protein S in normotensive as well as hypertensive pregnancies offer an explanation for the increased risk of thromboembolic disease. This increased susceptibility to thromboembolic disorders is further enhanced by the altered balance between the platelet aggregator and vasoconstrictor thromboxane A2 and its antagonist prostacyclin.
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PMID:[Vasoactive prostanoids and inhibitors of blood coagulation in pregnancy-induced hypertension]. 804 87

The first generation high-dose ( 80 mcg estrogen) oral contraceptives (OCs) were associated with an increased risk of deep venous thrombosis (DVT). So manufacturers removed the high-dose OCs and first replaced them with OCs with 50 mcg estrogen, resulting in a lower incidence of thromboembolic events (40 vs. 20/100,000 users). When they introduced an even lower dose OC (30 mcg estrogen), the incidence fell further (about 8/100,000 users). Yet, women using the lowest-dose OCs still have DVT more often than do control women. Life-style, age, and smoking may be confounding factors, however. It is not clear whether loss of endogenous ovarian steroid production or the effects of the orally administered contraceptive steroids cause significant changes in hemostatic factors (antithrombin III, protein S, protein C, plasminogen, tissue-type plasminogen activator, plasminogen activator inhibitor 1, histidine-rich glycoprotein, and VII, VIII, X, XII coagulation factors) during OC use. These changes tend to be within normal ranges. There is some doubt that these changes have any clinical significance. In nonsmokers, increased activity of anticoagulant factors and fibrinolytic factors counteract the effects on coagulation factors. Progestin-only OCs appear to affect hemostasis but have not increased the risk of thrombosis. There are considerable differences between people in pharmacokinetics and pharmacodynamics of contraceptive steroids. These differences may account for the increased risk of thromboembolic events in some people. Further research should identify methods of individualizing the dose of contraceptive steroids for a single patient. It should also explore the close interrelationship between hemostasis and lipid metabolism, carbohydrate metabolism, and hypertension in the development of cardiovascular disease in OC users. Providers should discourage women with a past history of DVT from using hormonal contraception.
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PMID:Coagulation and anticoagulation effects of contraceptive steroids. 817 1

The coagulation parameters factor VII, fibrin monomers, thrombin-antithrombin III (TAT) complexes and fragment 1.2 (F 1.2) were studied in 43 treated and 11 untreated patients (27 males, 27 females age range 19-70 years) with hypertension of moderate severity. The patients included in this study who were treated with antihypertensive drugs were still hypertensive in spite of their treatment. The median F 1.2 concentrations (interquartile range) in the hypertensive patients were more than double those of the reference group: 1.47 (0.79) nmol/l as against 0.74 (0.49) nmol/l (p < 0.0001). Median concentrations of TAT complexes 2.9 (1.7) micrograms/l versus 2.6 (1.6) micrograms/l (p < 0.02) as well as those of fibrin monomers 14.2 (4.6) nmol/l as against 10.6 (2.0) nmol/l (p < 0.01) also were significantly elevated in the hypertensive patients, but to a lesser extent. For factor VII a significant difference was found between males and females. The median factor VII value in the male patients was 137% (32%) compared with 100% (33%) in the male reference group (p < 0.001). In the hypertensive female patients this median value was 147% (36%) in comparison with 139% (60%) in the female reference group (p < 0.01). By the Spearman rank test, no correlations were found between the coagulation parameters and systolic or diastolic blood pressure, age or duration of hypertension. F 1.2 values were correlated with fibrin monomers (r = 0.33, p < 0.03) but not with the other coagulation parameters studied. The elevated F 1.2 values, together with elevated concentrations of TAT complexes and fibrin monomers, are signs of an activated coagulation system in these hypertensive patients.
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PMID:Prothrombin fragment 1.2 in both treated and untreated hypertensive patients. 830 96

To clarify the effects of correction of anemia with recombinant human erythropoietin (rHuEPO) on blood coagulation, fibrinolysis and endothelium, these markers were examined in 19 regular hemodialysis patients before and 4, 8, 12 weeks on rHuEPO treatment, and 5 weeks after the end of treatment. Hematocrit significantly increased from 22.8 +/- 2.0 to 31.1 +/- 2.7% at 12 week (p < 0.001). Coagulation and fibrinolysis markers did not show significant changes except for minor and transient alteration of protein C, thrombin-antithrombin III complex and alpha 2-plasmin inhibitor plasmin complex (PIC) throughout the treatment. Endothelin and 6-keto-prostaglandin F1 alpha (PGF1 alpha) significantly increased from 6.1 +/- 4.5 to 14.2 +/- 2.9 pg/ml (p < 0.001) and from 51.9 +/- 14.7 to 66.5 +/- 18.5 pg/ml (p < 0.05) at 12 week, respectively. Human atrial natriuretic peptide (ANP) significantly decreased from 277.9 +/- 88.6 to 179.4 +/- 73.3 pg/ml at 12 week (p < 0.001). Endothelin and PGF1 alpha after 6 month treatment with rHuEPO showed high values as same as those of 12 weeks. These data suggests that rHuEPO therapy did not affect blood coagulation and fibrinolysis, however exerts effects on the endothelium. Changes in endothelial function after rHuEPO may be one of the pathogenetic mechanisms of hypertension and may contribute to a decrease in thrombotic complications.
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PMID:[Changes in endothelial vasoactive substances and blood coagulation and fibrinolysis functions under recombinant human erythropoietin therapy in hemodialysis patients]. 831 81

There are a number of predisposing factors to thrombosis. Blood stasis and hypercoagulability are two important factors for the development of venous thrombosis. Several clinical situations are associated with these two factors. Congenital deficiencies in antithrombin III, protein C or protein S, the antiphospholipid antibodies represent well established risk factors. Arterial hypertension, dyslipidemia, tobacco, diabetes and obesity represent risk factors for arterial thrombosis. Hypofibrinolysis high levels fibrinogen and factor VII increases the risk of arterial thrombosis.
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PMID:[Predisposing factors for thrombosis]. 833 21

In an attempt to discern biological (such as thrombotic or fibrinolytic) risk factors in patients developing restenosis after percutaneous transluminal coronary angioplasty, the following factors were measured prior to angiography in a population of 23 patients (20 men, 3 women, mean age 57 +/- 5 yr) treated by a successful angioplasty (gain > 20% and residual stenosis < 50%) for stable angina pectoris and who had a routine angiographic restudy. The following factors were thus assessed: lipid factors: cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, apolipoprotein AI, apolipoprotein B; coagulation factors: fibrinogen, antithrombin III, fibrinopeptide A, factor VIII coagulant, factor VIII antigen, protein C; factors of physiological fibrinolysis: plasminogen, alpha 2-antiplasmin, tissue plasminogen activator and euglobulin clot lysis time before and after venous occlusion, plasminogen activator inhibitor before venous occlusion; and factors of platelet release: beta-thromboglobulin, platelet factor 4. Also studied were clinical characteristics: age, gender, diabetes, hypertension, smoking habits, previous myocardial infarction; angiographic data: global extent of coronary artery disease, location of the stenosis in a bend or branch point, complexity of the lesion, initial and residual stenosis and treatment during follow-up. The coronary angiograms were analyzed by a computer-assisted method with automatic edge detection. On angiographic criteria, 6 patients (restenosis group) were judged to have developed a restenosis (30% decrease in diameter and/or return to a 50% stenosis). The other 17 patients (those without restenosis) were considered to have a persistent success. Apart from age (group without restenosis: 55 +/- 6; restenosis group 61 +/- 5, p < 0.04), there were no differences in clinical, angiographic or treatment variables. There were no differences in lipid factors, but significant differences were observed in hemostatic variables: fibrinogen (without restenosis: 3.18 +/- 0.83; restenosis: 3.83 +/- 0.51 milligrams, p = 0.05), tissue plasminogen activator before venous occlusion (without restenosis: 10.9 +/- 26.8; restenosis: 232.5 +/- 371.2 IU, p < 0.04), euglobulin clot lysis time after venous occlusion (without restenosis: 176.5 +/- 100.5; restenosis: 78.6 +/- 40.2 min, p < 0.05) and for marker of the platelet release: platelet factor 4 (without restenosis: 10.8 +/- 7.9; restenosis: 20.5 +/- 7.5 ng/l, p < 0.04). These findings indicate that patients developing restenosis after coronary angioplasty tend to have an imbalance in the prothrombotic-antithrombotic equilibrium prior to the procedure.
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PMID:Biological risk factors for restenosis after percutaneous transluminal coronary angioplasty. 844 4

The cardiovascular risk factors blood pressure, overweight, hyperlipidaemia and several coagulation parameters were studied in a group of 54 otherwise healthy patients with essential hypertension of moderate severity. Of the 54 hypertensive patients, 43 were treated with anti-hypertensive drugs and 11 were not. The patients included in this study who were treated with anti-hypertensive drugs were still hypertensive in spite of their treatment. Lipoprotein levels and coagulation parameters did not differ between the untreated and treated hypertensive patients. Substantial percentages of patients were found to have hypertriglyceridaemia (46%), elevated LDL-cholesterol (28%) and elevated lipoprotein(a) concentrations (43%). Coagulation factors F VIIIc, fibrin monomer and factor VII in males were significantly elevated in comparison with a healthy reference group. These data are compatible with a moderate activation of the coagulation system. Correlations were established between systolic blood pressure and serum cholesterol (r = 0.43, p = 0.003), LDL-cholesterol (r = 0.34, p = 0.02) and triglycerides (r = 0.35, p = 0.01); Quetelet-index with fibrinogen (r = 0.37, p = 0.02) and thrombin-antithrombin III (r = 0.30, p = 0.04); and triglycerides with F VIIc (r = 0.34, p = 0.03) and fibrin monomer (r = 0.29, p = 0.04) respectively. These data link hypertension and hyperlipidaemia with increased coagulation activity and may contribute to our understanding of why these two cardiovascular risk factors accelerate atherogenesis.
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PMID:Coagulation factors and lipid composition of the blood in treated and untreated hypertensive patients. 846 17

Undesirable changes of haemostasis induced by some anti-hypertensive drugs can encourage the acceleration of atherogenesis. Therefore, the changes of haemostasis parameters in 22 patients with essential hypertension under long-term celiprolol therapy (> 2 months) were of interest. In the placebo group of 15 essentially hypertensive patients there were no significant changes in platelet activity. On the other hand, the therapeutic dose of celiprolol was shown to reduce total platelet aggregation, without any harmful effects on fibrinolytic activity and coagulation inhibitors such as protein C and antithrombin III. The metabolic neutrality of celiprolol accompanied by the proven platelet-inhibitory tendency is desirable in the new approach to hypertension treatment. Potentially anti-thrombotic or at least neutral prothrombotic properties of celiprolol may be important in terms of the favourable role of anti-hypertensive drugs in cardiovascular morbidity.
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PMID:Effect of long-term celiprolol therapy on haemostasis in essential hypertension. 855 93


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