Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma samples of 189 healthy subjects were investigated for antigen levels of the recently reported factor VII- and single-chain plasminogen activator-activating protease (FSAP) and the corresponding pro-urokinase activating potencies. While the age of donors had no significant effect on the investigated parameters, female plasmas revealed a trend to higher antigen contents and activity levels. Surprisingly, as much as 9% of all samples contained significantly reduced single-chain urinary plasminogen activator activating potential, whereas antigen concentrations were normal. Additionally, 1% of the plasmas was found to decrease in both FSAP antigen and activity contents. FSAP of three subjects displaying reduced activities throughout a follow-up period of 6 months were purified from plasmas and were characterized. As compared with pool plasma derived FSAP, investigation of the individual preparations confirmed their reduced potency to activate pro-urokinase. However, factor VII activation was not affected. It is speculated that the FSAP binding site for single-chain plasminogen activators is affected, potentially by as yet unknown polymorphism(s) or mutation(s).
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PMID:Quantitation of the factor VII- and single-chain plasminogen activator-activating protease in plasmas of healthy subjects. 1150 81

Long-term moderate or strenuous physical activity is associated with a considerable reduction in cardiovascular morbidity and mortality in primary and secondary prevention. Various mechanisms, including changes in lipids, lifestyle habits, and other positive physiologic effects, have been suggested to mediate these beneficial effects. In addition, the hemostatic and fibrinolytic systems appear to play an important role. Fibrinogen has been convincingly shown to be an independent cardiovascular risk factor. Other hemostatic and fibrinolytic parameters that are predictive of coronary events include factor VII, platelet hyperreactivity, plasminogen-activator inhibitor 1 (PAI-1), and tissue-plasminogen activator. The effects of exercise on fibrinogen have been intensively studied. Several randomized controlled trials, various other intervention studies and a large number of population-based cross-sectional studies all found an inverse relationship between measures of sport activity or leisure activity and plasma fibrinogen. The magnitude of the effect reported might be associated with a sizeable reduction in major coronary events. Relatively few data are available on the effects of endurance exercise on markers of the fibrinolytic system, with inconsistent results. Acute exercise leads to a transient activation of the coagulation system, which is accompanied by an increase in the fibrinolytic capacity in healthy subjects. Patients with ischemic heart disease, who cannot increase their fibrinolytic potential, however, may be at considerable risk for acute ischemic events if they are exposed to unaccustomed strenuous physical exertion.
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PMID:Exercise and thrombosis. 1157 Jan 12

Several papers concerning abnormalities of blood coagulation and fibrinolysis during hyperthyroidism, have been published. Increased von Willebrand Factor (vWF) activity and high fibrinogen levels have been reported. However, there is controversy concerning the presence of a hypercoagulable state in hyperthyroidism. We investigated various hemostatic parameters in 41 hyperthyroid patients and compared them to 20 euthyroid controls. Prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen, factors V, VII, VIII, IX and X activities, vWF, antithrombin III (AT III), protein C, protein S, tissue plasminogen activator (t-PA) and tissue plasminogen activator inhibitor-1 (PAI-1), as well as common lipid variables, were measured. The relationships between serum thyroid hormones and these hemostatic parameters were examined. Compared with control subjects, fibrinogen, factor IX, vWF, AT III and PAI-1 were significantly increased in patients (p<0.05, p<0.0001, p<0.05, p<0.01 and p<0.0001; respectively), whereas factor X and t-PA were decreased (p<0.05). We showed that free T4 (FT3) levels were correlated with factor VIII activity (r=0.35, p<0.05). FT4, FT3 and TSH did not correlate with fibrinogen, vWF, AT III, t-PA, or PAI-1. AT III was inversely correlated with factor VII activity (r=-0.48, p<0.01). Protein C and S were correlated with vWF levels (r=0.58, p<0.0001; r=0.55, p<0.0001, respectively). Protein C was inversely correlated with t-PA (r=-0.39, p<0.01). There was a negative correlation between triglycerides, LDL-C and F X (r=-0.45, p<0.05; r=-64, p<0.01, respectively). Mean platelet volume (MPV) was correlated with anti-thyroid peroxidase (TPO) antibodies (in Graves'disease) and F IX activity (r=0.57, p<0.05 and r=0.39, p<0.05; respectively). We found important differences in the coagulatory /fibrinolytic parameters between the hyperthyroid patients and healthy controls. Hyperthyroid patients may experience vascular endothelial dysfunction and decreased fibrinolytic activity in blood. This endothelial activation may represent a situation with a higher thromboembolic potential.
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PMID:Blood coagulation and fibrinolysis in patients with hyperthyroidism. 1203 Jun 6

To determine whether there is a correlation between fibrinolytic activity and dyslipidemia, we performed a study of 72 subjects (20 patients with hypercholesterolemia, 20 with hypertriglyceridemia, 12 with isolated low high-density lipoprotein (HDL)-cholesterol (mean age 47.7 +/- 6.3, body mass index 24.7 +/- 0.4) and 20 healthy controls. Plasminogen activator inhibitor-1 (PAI-1), tissue-plasminogen activator activity and plasmin-antiplasmin complexes (PAP) were detected at baseline and after venous occlusion test. We also measured at baseline lipidic pattern, soluble E and P selectins (sE-sel, sP-sel), prothrombin factor 1+2 (F1+2), lipoprotein(a), factor VII, plasma insulin, fibrinogen, homocysteine, and thrombin activable fibrinolysis inhibitor (TAFI) activity. Fibrinolysis was significantly reduced in hypertriglyceridemic patients compared with hypercholesterolemic patients and control subjects (PAP, p < 0.01 and p < 0.001) and was associated with increased PAI-1 (at baseline and after venous occlusion test, p < 0.001). sP-sel, F1 +2 and TAFI were not significantly different compared with controls, while hypercholesterolemic subjects showed a significant increase in these parameters (p < 0.001), which were related to decreased PAP only at the upper low-density lipoprotein (LDL)-cholesterol levels (>160 mg/dl) (p < 0.001, r = -0.76). Moreover, there was no significant difference in PAI-1 activity (at baseline and after venous occlusion test) compared with controls. In conclusion, endothelial dysfunction was the main mechanism of decreased fibrinolysis in subjects with hypertriglyceridemia and low HDL-cholesterol, while enhanced thrombin generation and TAFI activity were the main determinants in hypercholesterolemia.
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PMID:Different mechanisms of fibrinolysis impairment among dyslipidemic subjects. 1206 44

There is increasing evidence that elevated plasma levels of hemostatic factors [fibrinogen, factor VII, von Willebrand factor, fibrin D-dimer, and tissue plasminogen activator (t-PA) antigen] are independently linked to risk for coronary heart disease (CHD). Women with polycystic ovary syndrome (PCOS) are insulin-resistant and have increased risk for CHD and type 2 diabetes, but there are few data on hemostatic markers in women with PCOS. Seventeen women with PCOS (defined on the basis of elevated testosterone and oligomenorrhea) and 15 healthy women matched as a group for body mass index (BMI) were recruited. Insulin sensitivity was assessed using the hyperinsulinemic euglycemic clamp technique. Factor VIIc was determined by a clotting assay; fibrinogen was determined by nephelometry; and t-PA, D-dimer, and von Willebrand factor antigens were measured by ELISA techniques. Of these hemostatic markers, only t-PA concentration was significantly (P = 0.013) elevated in women with PCOS relative to controls. t-PA correlated with BMI in both PCOS and controls (r = 0.428, P < 0.1; and r = 0.686, P < 0.01) and inversely with the insulin sensitivity index (r = -0.590, P < 0.05; and r = -0.620, P < 0.05, respectively). After further adjustment for BMI and insulin sensitivity, there remained a significant difference in t-PA between cases and controls (P = 0.017). Together, age and insulin sensitivity explained 39% of the variance in t-PA in women with PCOS (P < 0.05). Total testosterone did not correlate significantly with t-PA in either group. We conclude that women with PCOS have significantly increased t-PA concentrations relative to women with normal menstrual rhythm and normal androgens. We suggest that elevated t-PA and dysfibrinolysis may be a factor in the increased cardiovascular morbidity seen in PCOS.
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PMID:A specific elevation in tissue plasminogen activator antigen in women with polycystic ovarian syndrome. 1210 38

The effects of progestogens on hemostatic function seems to be minimal, however, in this longterm surveillance study of the effects of Norplant among 100 healthy, nonsmoking, nonalcohol drinking, and nonlactating Singaporean women indicates the possibility of an increased predisposition of thrombosis. Clinical assessment and blood sampling were taken prior to insertion and at 6, 12, 24, 36, and 48 months. Laboratory tests included prothrombin time (PT), activated partial thromboplastic time (APTT), hematocrit and platelet count as hemostatic measures. Also measured were fibrinogen, coagulation factor II, a 1-stage assay for factors V and VII, factor VII, factor X, antithrombin III, plasminogen activator activity on the fibrin plate and FDP, platelet aggregation, factor VIIIR. 20 normal controls not on any medication were used and international standards were applied in most cases. The coefficients of variation of the various tests with reference control plasma or sera are summarized. The paired t test was used to assess statistical differences. Skewed results were analyzed with the Wilcoxon signed rank test. % changes between pre- and postinsertion levels were also utilized. The results were that the hemoglobin concentration increased from 12.1 gm/dl to 13.4 gm/dl in the 1st year, and then decreased to preinsertion levels within 3 years, and increased to 13.3 gm/dl in the 4th year. The 4th year also reflected no menstrual disorder. PT and APTT appeared significantly shortened in year 1. PT continued to shorten in 3 more years, while APTT increased to the preinsertion mean. Vitamin K dependent factors II and VII decreased significantly in year 1, while factors V and X increased significantly. Factor II increased minimally within 2 more years, but decreased again in year 4. Factor VII continued to decrease over the 4 years. The concentration of factors II and VII were significantly lower after 4 years. Factor V increased 14.4% in year 1, but decreased below preinsertion levels in the next 3 years, and then decreased to preinsertion levels in year 4. No significant changes in fibrinolytic activity occurred in 4 years. Major changes occurred in mean platelet count, which rose significantly in year 1 and increased concentration in year 4. In 4 years, platelet aggregation using ADP or equine collagen rose significantly. Serious thought must be given to the risk of thrombosis and potential for hypercoagulation.
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PMID:Haemostatic function changes in Singapore women using Norplant implants: a four year review. 1228 17

Cholesterol lowering therapy markedly reduces the frequency of subsequent cardiovascular events and is associated with a modest degree of angiographic regression of atherosclerotic lesions. There is a strong association between lipids and fibrinogen, plasminogen activator-1, and activated factor VII levels. Low density lipoprotein may be thrombogenic whereas high density lipoprotein protects against thrombosis. Lipoprotein (a) may affect atherosclerosis and thrombosis mainly by binding to fibrin and attenuating the fibrin-enhanced plasminogen activation. Tissue factor-complex initiates coagulation by activating factor X and factor IX leading in the presence of calcium to the generation of thrombin. Lipid lowering treatment with statins stabilizes atheromatous plaque and has antithrombotic effects. Therefore there are links between lipids and the haemostatic mechanisms which affect atherosclerotic, vasomotor and thrombotic components of ischemic heart disease.
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PMID:Effects of lipids on thrombotic mechanisms in atherosclerosis. 1241 62

Abnormalities in coagulation and haemostasis represent a well-known link between obesity and thrombosis (both arterial and venous). Several studies have shown that obese patients have higher plasma concentrations of all pro-thrombotic factors (fibrinogen, vonWillebrand factor (vWF), and factor VII), as compared to non-obese controls, with a positive association with central fat. Similarly, plasma concentrations of plasminogen activator inhibitor-1 (PAI-1) have been shown to be higher in obese patients as compared to non-obese controls and to be directly correlated with visceral fat. Furthermore, obesity is characterized by higher plasma concentrations of anti-thrombotic factors, such as tissue-type plasminogen activator (t-PA) and protein C, as compared to non-obese controls, the increase in these factors being likely to represent a protective response partly counteracting the increase in pro-thrombotic factors. The issue of whether adipose tissue contributes directly to plasma PAI-1, its products stimulating other cells to produce PAI-1, or whether it primarily contributes indirectly has not yet been resolved. It has been proposed that the secretion of interleukin-6 (IL-6) by adipose tissue, combined with the actions of adipose tissue-expressed TNF-alpha in obesity, could underlie the association of insulin resistance with endothelial dysfunction, coagulopathy, and coronary heart disease. The role of leptin in impairing haemostasis and promoting thrombosis has been recently reported. Finally, some hormonal abnormalities (androgen, F, catecholamines) associated with the accumulation of body fat may contribute to the impairment of coagulative pathway in obesity. As to intervention strategies, dietary (i.e., low-fat high-fiber diet) and lifestyle (i.e., physical activity) measures have been demonstrated to be effective in improving the obesity-associated pro-thrombotic risk profile.
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PMID:Coagulation and fibrinolysis abnormalities in obesity. 1250 53

We aimed to investigate significant correlations of insulin resistance with thrombotic factors in South Asians with stroke. Correlations of Homeostasis Model Assessment (HOMA)(as a surrogate of insulin resistance) were analysed with 6 thrombotic factors in 140 South Asian patients with a history of confirmed (by computerised tomography) ischaemic stroke. Age and sex adjusted HOMA was correlated to waist-hip ratio (r = 0.38, p = 0.0001), triglycerides (r = 0.22, p = 0.03), systolic blood pressure (r = 0.21, p = 0.04), tissue plasminogen activator (t-PA) (r = 0.22, p = 0.04); plasminogen activator inhibitor 1(PAI-1) (r = 0.26, p = 0.02); fibrinogen (r = 0.25, p = 0.02); and factor VII antigen (r = 0.21, p = 0.06). On regression analysis, with HOMA as dependent variable and significant correlates as independent variables in the model, HOMA was independently associated with PAI-1 antigen. There is extensive clustering of metabolic and thrombotic factors with insulin resistance in South Asian patients with ischaemic stroke, which may contribute to high prevalence of vascular disease in this population.
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PMID:Clustering of thrombotic factors with insulin resistance in South Asian patients with ischaemic stroke. 1252 44

The aim of this study was to evaluate hemostatic variables in women according to different body mass index (BMI) values, and then correlate them with some metabolic parameters - fasting insulin and glucose, total cholesterol, high-density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol and triglycerides. Eighty-four female patients aged 18-39 years were recruited, and agreed to participate in the study. The study group was divided into three subgroups according to BMI: low BMI (BMI < 18.5 kg/m2; n = 43), normal-weight (control) (BMI 18.5-24.99 kg/m2; n = 21) and overweight/obese (BMI > 25 kg/m2; n = 20). BMI was calculated, and the following measurements were taken: International Normalized Ratio, antithrombin III, tissue plasminogen activator (t-PA) activity, t-PA-antigen, plasma fibrinogen level, factor VII, Plasminogen activator inhibitor (PAI)-1 activity and antigen and metabolic parameters: fasting insulin and glucose, total cholesterol, HDL-cholesterol, LDL-cholesterol and triglycerides. The results were statistically analyzed. In the low BMI group, a negative correlation between fasting insulin and PAI-1 activity, and a positive correlation between fasting glucose and PAI-1 antigen were observed. Also, a strong negative correlation between PAI-1 activity and insulin/glucose index was found. Plasma insulin levels were significantly lower in the low-BMI women than in the overweight/obese group (p < 0.001) and with no difference compared to the control group. We did not find any difference in fasting glucose level between all groups. HDL-cholesterol showed the highest levels in the normal BMI group and was significantly higher than in the low BMI and obese groups (p < 0.05 and p < 0.01, respectively). PAI-1 activity in the low BMI women revealed increased activity in comparison to control and overweight/obese women (p < 0.001 and p < 0.05, respectively). Lower antigen levels were also shown as compared to both these groups (p < 0.001 and p < 0.001, respectively). Similar results were obtained with t-PA antigen levels (p < 0.001 and p < 0.001, respectively). There were no differences in activity of t-PA in all groups. Obese women showed significantly higher fibrinogen levels than other BMI groups (p < 0.001 and p < 0.001 respectively). Analysis of hemostatic variables in women with a low BMI testify to the impaired fibrinolysis in this group, also showing a strong correlation with carbohydrate metabolism.
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PMID:Hemostatic variables, carbohydrate metabolism and lipid profile in women with low body mass index. 1274 26


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