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)

An enzyme-linked immunosorbent assay for plasminogen activator inhibitor-1 (PAI-1) in biologic fluids was developed on the basis of two murine monoclonal antibodies raised against PAI-1 purified from HT-1080 fibrosarcoma cells. The lower limit of sensitivity of the assay in plasma is 2 ng/mL. The assay is 12 times less sensitive toward the PAI-1/human tissue-type plasminogen activator (t-PA) complex as compared with free PAI-1. The intraassay, interassay, and interdilution coefficients of variation are 5.2%, 8.0%, and 7.1%, respectively. The level of PAI-1 in platelet-poor plasma of healthy subjects is 18 +/- 10 ng/mL (mean +/- SD, n = 45). In platelet-rich plasma after freezing and thawing, 92% of PAI-1 antigen is released from platelets, whereas only 8% is found in the corresponding platelet-poor plasma. In platelet-poor plasma from healthy subjects, a linear correlation (r = 0.80) was found between PAI activity and PAI-1 antigen. In plasma approximately two thirds of the PAI-1 antigen was functionally active, whereas only 5% of the PAI-1 antigen released from platelets was active. During pregnancy a progressive increase of PAI-1 antigen levels up to three- to sixfold the control value was observed. In plasma of patients with recurrent deep vein thrombosis, PAI-1 levels were 44 +/- 20 ng/mL (mean +/- SD, n = 7), during a clinically silent phase. Four of these patients had a level above 38 ng/mL (mean +/- 2 SD of normal). The present assay, based on stable and reproducible reagents, allows the specific determination of PAI-1 antigen in biologic fluids. It may facilitate interlaboratory comparisons and be useful for further investigations of the role of PAI-1 in clinical conditions associated with impaired fibrinolysis and/or a tendency to thrombosis and investigations of the role of PAI-1 in platelets.
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PMID:Measurement of plasminogen activator inhibitor 1 in biologic fluids with a murine monoclonal antibody-based enzyme-linked immunosorbent assay. 325 45

Pulmonary embolism remains a challenging problem in diagnosis and management for the emergency physician. Although its clinical presentation is protean and often ambiguous, risk stratification can be accomplished based on the predictive power of a limited number of physical and historical characteristics. Ventilation-perfusion lung scanning occupies a central position in the work-up of suspected PE; however, evidence exists that it may be misused by many physicians. A low probability V-Q scan does not exclude the diagnosis of PE. Patients with other than normal- or high-probability patterns of pulmonary ventilation and perfusion on lung scanning require further investigation. Noninvasive venous studies are useful when indicative of proximal deep venous thrombosis, but are normal in many patients with acute PE. Heparin remains the standard of treatment for most patients with PE. Vena cava filters effectively reduce the incidence of recurrent PE in patients with contraindications to anticoagulation. Thrombolytic therapy offers potential advantages in the treatment of patients with shock due to their PE. Case reports of PE treated with tissue-type plasminogen activator, a new thrombus-specific fibrinolytic agent, are encouraging but preliminary.
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PMID:Pulmonary embolism. 328 Mar 1

Clinical and laboratory variables were measured on the day before operation in 111 patients who underwent total hip replacement prophylactically treated with acetylsalicylic acid or heparin-dihydroergotamine. Postoperative deep vein thrombosis (DVT) was detected in 16 patients by ascending venography. Stepwise logistic discriminant analysis was used to identify DVT predicting factors. Three such factors, fibrinogen degradation products (FDP), plasminogen activator inhibitor (PA-inhibitor) and tissue type plasminogen activator (t-PA), were found to be significantly associated with DVT and were used to construct a predictive index. The predictive index, I = -2.09 + 0.46 (FDP) + 1.39 (PA-inhibitor) -0.24 (t-PA), was 100% sensitive and 95% specific in the prediction of DVT. This index would allow for identification of those patients in whom routine prophylaxis would be sufficient and for selecting those in whom more effective prophylactic regimens would be necessary.
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PMID:Preoperative identification of patients at high risk of deep venous thrombosis despite prophylaxis in total hip replacement. 336 36

Three patients with karyotype XYY who had presented with deep vein thrombosis and leg ulcers (plus pulmonary embolism in two of them) were investigated for: (1) androgens (plasma testosterone measurement, testosterone oestradiol binding globulin (TeBG) assay, GnRH 50 micrograms test), and (2) haemostasis by fibrinolysis tests (euglobulin lysis time and area, antigenic plasminogen activator assay before and after 10 min venostasis). Full evaluation of haemostasis failed to demonstrate the presence of circulating anticoagulant or of antithrombin III, protein C and protein S deficiencies. One patient had neither hormonal nor fibrinolytic abnormality. The other two patients shared some clinical features with male hypogonadism (gynoid morphotype in both, hypotrophy of the testes in one, gynaecomastia in the other). They also had hormonal disorders ("over-response" to the GnRH test in one case, elevated TeGB in the other case) and abnormalities of fibrinolysis (poor response to venostasis, high baseline level of plasminogen activator). Response to venostasis became normal after 3 months of treatment with percutaneous dihydrosterone 125 mg per day in the two patients with initially poor response. The mechanism of venous pathology in XYY subjects is discussed. A genetic defect not involving the fibrinolysis system is possible since fibrinolysis was normal in one patient; however, abnormal fibrinolysis may have been responsible for the venous pathology in the other 2 patients. The role played by abnormalities of fibrinolysis in the pathogenesis of deep vein thrombosis and leg ulcers is recalled, and the possible implication of these abnormalities in patients with XYY karyotype is emphasized.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Post-phlebitic leg ulcers and XYY karyotype: fibrinolysis and androgenic function tests. Apropos of 3 cases]. 343 47

The fibrinolytic activity of blood was measured in control subjects and patients with idiopathic deep venous thrombosis by a new method, which was based on the rate of release of radioactivity in vitro from clotted blood to which 125I-fibrinogen was previously added. Blood was obtained without application of a venous tourniquet. The results are expressed as the amount of fibrin lysed per unit of time and are not affected by the fibrinogen concentration, a drawback inherent in previous techniques. The mean value (+/- standard deviation) of fibrinolytic activity was 0.464 +/- 0.158 mg of fibrin lysed per hour in the control subjects and 0.194 +/- 0.089 mg of fibrin lysed per hour in the patients. This difference is significant (p less than 0.01) and indicates a considerable reduction in fibrinolytic activity in patients with idiopathic deep venous thrombosis. This has been demonstrated without the need to stimulate the release of plasminogen activator by applying a venous tourniquet as done in previous studies.
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PMID:Estimation of fibrinolytic activity of whole blood in patients with recurrent idiopathic deep venous thrombosis. 372 86

Plasminogen, fibrinogen, antithrombin III, euglobulin lysis time, tissue plasminogen activator (t-PA) and fast-acting t-PA inhibitor were measured in 21 patients receiving either stanozolol (10 mg orally given for 14 days preoperatively) or subcutaneous heparin, during a continuing comparative trial in the prevention of postoperative deep vein thrombosis. Stanozolol treatment resulted in significant (p less than 0.01) increases between the 14th and 1st preoperative days in the plasma concentrations of plasminogen (3.4 to 4.9 Cu/ml) and antithrombin III (107% to 132%); t-PA levels did not increase significantly (6.0 to 16.0 mU/ml; p greater than 0.1). There were significant (p less than 0.02) falls in fast-acting t-PA inhibitor (132% to 75%) and fibrinogen (2.4 to 1.8 g/l). Surgery reversed the changes in fibrinolytic activity seen preoperatively in the stanozolol-treated patients, and similar changes were seen in the heparin-treated group. In this dosage, stanozolol does not appear to prevent the fibrinolytic shutdown which occurs after elective major surgery.
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PMID:Effects of oral stanozolol used in the prevention of postoperative deep vein thrombosis on fibrinolytic activity. 387 18

The aim of these studies was to investigate different regimens of thrombolytic therapy and oral anticoagulation, and to evaluate the effects of streptokinase (SK), heparin and warfarin in the treatment of deep vein thrombosis (DVT). Low-dose SK, although controlled according to the fibrinogen levels, did not provide improved thrombolysis compared to conventional high-dose SK, and more postthrombotic changes were registered after an average of 3 years. Furthermore, serious hemorrhagic side-effects occurred, which makes this regimen inexpedient. Various regimens of local venous infusion of SK were tried, and with a dose of 4,000 IU/h for 72 h in combination with heparin a thrombolytic effect was achieved, albeit not greater than usually observed with conventional SK. Systemic hypofibrinogenemia and hemorrhage were not avoided. A hitherto not described side-effect with bullous dermatitis was reported. Venographic severity of calf vein thrombosis displayed a statistically significant correlation to long-term hemodynamic changes, as assessed with foot volumetry, after an average of 5 years. This correlation was stronger for the size of the thrombus after initial treatment than for the size at diagnosis. Thus it seems important to treat calf vein thrombosis with heparin in order to limit the extent of the thrombus, thereby reducing long-term sequelae. During heparin treatment, an average reduction of the thrombi of 17% was observed. This reduction was significantly correlated to a short duration of symptoms but not to parameters of heparin therapy or fibrinolytic components. However, patients with substantial thrombolysis had high plasmin-alpha 2-antiplasmin (PAP) levels, and those with high tissue plasminogen activator (t-PA) inhibitor levels and remarkably also those with high t-PA antigen levels had no lysis. The concentration of t-PA antigen showed a significant increase during heparin infusion, whereas that of PAP and t-PA inhibitor was not influenced. By applying more intensive initial oral anticoagulation, stable therapeutic prothrombin time (PT)-levels were achieved one day earlier and the duration of heparin infusion could be equally reduced compared to the conventional regimen (4.4-5 days vs 5.4-6 days). The activity of coagulation factors II, VII, IX and X had dropped to the same level with both regimens the day heparin was discontinued, observed. The effectiveness of oral anticoagulation after DVT was studied in 596 patients treated for a total of 4450 months.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Studies on the medical treatment of deep vein thrombosis. 391 82

Some aspects of the function of the fibrinolytic system have been investigated in 37 patients with a recent incident of symptomatic and confirmed deep vein thrombosis and compared with findings in 20 healthy persons. New specific methods to measure tissue plasminogen activator (t-PA) activity and antigen before and after venous occlusion and the recently discovered fast inhibitor to t-PA were employed. Thirteen of the patients with deep vein thrombosis (35%) had t-PA activity less than 0.5 IU/ml after venous occlusion, whereas the lowest activity found among the healthy individuals was 0.56 IU/ml. The t-PA inhibitor level in the total patient group was 3.8 +/- 3.7 U/ml (range 0 to 15.0 U/ml; median 2.9 U/ml) as compared with 0.7 +/- 0.7 U/ml in the healthy (median 0.5, range 0 to 2.4 U/ml). In the 13 patients with low t-PA activity in postocclusion plasma samples the inhibitor level was 6.0 +/- 4.4 U/ml. Furthermore, in this group of patients a significantly lesser release of t-PA antigen (3.7 +/- 2.8 micrograms/L) was found as compared with that in the healthy individuals (9.5 +/- 6.0 micrograms/L). Thus, two months after their first incident of symptomatic deep vein thrombosis many of the patients (35%) were found to have decreased fibrinolytic activity. This is the result of highly increased plasma levels of a novel fast inhibitor toward t-PA in combination with a poor ability to release t-PA. Possibly the decreased fibrinolytic activity did play a role in the pathogenesis of deep vein thrombosis in these patients.
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PMID:The role of the fibrinolytic system in deep vein thrombosis. 391 25

An assay system for determination of the "fast"-acting inhibitor (antiactivator, AA) of tissue-type plasminogen activator (tPA) in human plasma was developed. The system is based on incubation of plasma samples with various amounts of vessel wall-derived tPA for 8 minutes at 25 degrees C, followed by acidification and determination of the residual tPA activity by an indirect spectrophotometric assay. One unit of AA was defined as the amount inhibiting 1 U of tPA. AA levels in normal controls (n = 26) were 1.4 to 17.4 U/ml (median 3.0 U/ml) and 0.9 to 17.5 U/ml (median 3.0 U/ml) in patients with a history of deep venous thrombosis (n = 26). When plasma was subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis followed by reverse fibrin autography, AA activity appeared as an inhibitory band corresponding to a relative molecular mass of 50,000. In six samples the inhibitory activity of this band was directly correlated to the functional AA activity of the plasma samples.
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PMID:Tissue plasminogen activator inhibitor in human plasma: development of a functional assay system and demonstration of a correlating Mr = 50,000 antiactivator. 392 46

Fibrinogen, euglobulin lysis time (ELT), tissue-type plasminogen activator (t-PA) antigen, plasminogen activator inhibitor activity (PA-inhibitor) and alpha 2-antiplasmin (alpha 2-AP) were measured pre- and postoperatively in 60 patients undergoing total hip replacement. Reduced fibrinolytic activity as assessed by the prolongation of euglobulin lysis time, decrease of t-PA and increase of PA-inhibitor and alpha 2-AP could be demonstrated. These changes did not correlate with the postoperative deep vein thrombosis (DVT) diagnosed with the 125I-fibrinogen test. However, preoperative PA-inhibitor activity was significantly higher in patients with postoperative DVT (p less than 0.01). The prophylactic treatment with aspirin (20 patients) and with heparin plus dihydroergotamine (20 patients) induced significant changes in some of those parameters. This study shows that the decrease of t-PA and the increase of PA-inhibitor may contribute to the reduced postoperative fibrinolytic activity after total hip replacement. PA-inhibitor level might be a useful marker in evaluating the risk of developing DVT in patients undergoing total hip replacement.
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PMID:Postoperative changes in the plasmatic levels of tissue-type plasminogen activator and its fast-acting inhibitor--relationship to deep vein thrombosis and influence of prophylaxis. 393 69


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