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)

In a prospective randomized study heptest, thrombin-antithrombin complexes (TAT), D-dimer, and t-PA:ag were analysed pre- and postoperatively in 206 consecutive patients undergoing hip arthroplasty during thromboprophylaxis with either a LMW heparin (Enoxaparin) or Dextran 70. Deep vein thrombosis (DVT) developed in 6 of 102 (6%) Enoxaparin and in 21 of 104 (20%) Dextran patients diagnosed by bilateral phelobography. In the Enoxaparin group heptest showed a significant increase from the pre- to the postoperative level opposed to a significant decrease in the Dextran group. Postoperative levels of TAT, D-dimer, and t-PA:ag were significantly increased in both groups, however, TAT was significantly higher in patients in the Dextran group than in the Enoxaparin patients. D-dimer was significantly higher in Dextran patients with DVT postoperatively compared with patients without DVT. No differences concerning TAT or t-PA:ag were observed between patients with and without DVT in any of the groups.
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PMID:Components of coagulation and fibrinolysis during thrombosis prophylaxis with a low molecular weight heparin (Enoxaparin) versus Dextran 70 in hip arthroplasty. 171 55

Thrombolytic treatment of deep vein thrombosis remains controversial. It has never been demonstrated that the late postthrombotic syndrome may be diminished by the faster dissolution of the clots induced by streptokinase or urokinase. On the other hand are the hemorrhagic side effects associated with thrombolysis well described (lethality of 0.6%). Thrombolysis should be performed preferably under controlled conditions of a clinical study. It is indicated only in young patients with symptoms for less than 7 days of a first thrombosis. Initial results from second generation fibrinolytic substances such as rt-PA (alteplase) do not change this view drastically.
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PMID:[Thrombolysis in deep venous thrombosis: critical review]. 178 Jul 95

Five criteria for poor response to a 20 min venous occlusion test were applied to 58 patients 3 months or more after acute deep vein thrombosis (DVT). The criteria were arbitrarily defined as the last 5 percentiles of response distributions in an age- and sex-matched healthy control group of 51 subjects. The criteria were: 1. euglobulin clot lysis time after venous occlusion greater than or equal to 140 min; 2. t-PA activity after venous occlusion less than or equal to 0.04 IU/ml; 3. increase in t-PA antigen above resting value less than or equal to 2-fold; 4. ratio between t-PA antigen increase and resting PAI activity less than or equal to 0.5 ng/IU; 5. PAI activity after venous occlusion greater than or equal to 6 IU/ml. The last criterion of poor response was the only one that was significantly more frequently reached by patients than by controls: 28% (p less than 0.005) of all DVT patients and 35% (p less than 0.005) of the subgroup with idiopathic DVT (N = 34) were found to be poor responders. The percentage of poor responders according to the other four criteria was 7-11% in all patients and 9-15% in the subgroup with idiopathic DVT and thus was not significantly higher than in controls (5% by definition). It was concluded that residual PAI activity after venous occlusion might be a useful criterion for prospective studies on recurrence of DVT.
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PMID:Poor fibrinolytic response to venous occlusion by different criteria in patients with deep vein thrombosis. 178 30

In the present study 57 consecutive patients with a first episode of venographically proven deep vein thrombosis were investigated to evaluate the release of tissue-type plasminogen activator (t-PA) and of urokinase-type plasminogen activator (u-PA) in response to DDAVP stimulation as well as the resting plasminogen activator inhibitor (PAI) concentration, comparing this to the results obtained in 66 similar patients with a clinical suspicion of thrombosis but with a normal venogram. All assays were performed without knowledge of the patient's status. Four patients in the deep vein thrombosis-group (7%) had an absent u-PA antigen response upon DDAVP infusion, while a normal response was observed in all control subjects. Patients and controls showed similar increases in t-PA antigen level upon DDAVP. High resting PAI antigen levels were encountered in 5 patients in the deep vein thrombosis-group (9%) and in 6 subjects in the control group (9%). The results from this controlled study indicate that a defective release of u-PA may occur in patients with deep vein thrombosis and may have pathogenetic significance. Furthermore it is concluded that elevation of PAI levels cannot be considered as a specific risk factor for venous thrombosis.
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PMID:Deep vein thrombosis and fibrinolysis. Defective urokinase type plasminogen activator release. 179 91

Decreased fibrinolytic activity (FA) is considered a risk factor in the development of deep venous thrombosis (DVT). The purpose of this study was to test the hypothesis that an abnormally low FA is more likely in idiopathic DVT as opposed to DVT in the presence of other predisposing risk factors. 156 patients were studied three months after an acute DVT confirmed by venography. In 82 patients a predisposing factor such as trauma, surgery or malignancy was present. In 74, DVT was idiopathic. Fibrinolytic activity was measured in all patients using the following tests: 1. Euglobulin Lysis Time (ELT, in minutes). 2. Global Fibrinolytic activity (FA in mg fibrin lysed per hour). ELT measures plasminogen activator activity (PAA) while FA which is a more global test measures the net effect of the PAA, the plasminogen activator inhibitor (PAI) and the clot structure. PAI was measured in 67 patients from both groups using an Enzyme-Linked immunosorbent assay (ELISA). The results obtained show a significant increase in the incidence of abnormal FA and ELT in the idiopathic group. This supports the hypothesis that low FA is an aetiological factor in the development of idiopathic DVT. The results also demonstrate the importance of associating the FA test to the classical tests such as ELT, PA and PAI for the detection of hypofibrinolysis.
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PMID:Fibrinolytic activity in patients with idiopathic and secondary deep venous thrombosis. 180 59

The incidence of deep vein thrombosis (DVT) and pulmonary embolism was studied prospectively in patients undergoing elective total hip replacement. 96 patients were randomly allocated to receive either low molecular weight heparin (LMWH) or unfractionated heparin (UFH). All patients had bilateral phlebography and pulmonary perfusion/ventilation scintigraphy 10-12 days after surgery. The following fibrinolytic variables were analysed in plasma and related to thromboembolism: tissue plasminogen activator (t-PA) activity, t-PA antigen (t-PA Ag), plasminogen activator inhibitor (PAI-1) activity and PAI-1 antigen (PAI-1 Ag). No significant difference was found, regarding the fibrinolytic response to surgery, between patients treated with LMWH and UFH. The level of PAI-1 activity was significantly increased before operation in patients developing DVT as compared to non-DVT patients (p less than 0.03). Immediately after surgery and in the morning the first postoperative day the levels of PAI-1 activity, PAI-1 Ag and t-PA Ag were positively correlated to thromboembolism. PAI-1 activity was the only preoperative fibrinolytic variable correlated to thromboembolism.
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PMID:Impaired fibrinolysis and postoperative thromboembolism in orthopedic patients. 185 6

The administration of a radiolabelled monoclonal antibody against tissue plasminogen activator allows detection of areas with increased fibrinolytic activity, i.e. those with an active thrombotic lesion. Eight patients with phlebographically verified deep venous thrombosis were examined. At the time of immunoscintigraphy study they were examined receiving anticoagulant therapy. Some 75-85 MBq indium 111-labelled antibody were injected, and scintigrams were obtained after 30 min and after 24 h. The precise site of the thrombus could not be visualized after 30 min due to high background activity, whereas after 24 h it was detectable in all patients. The thrombus/background ratios achieved are twice as high as those observed in a human antifibrin antibody study. These preliminary data suggest a high sensitivity of our t-PA-specific antibody for the detection of active deep venous thrombosis in man, and our antibody seems to offer theoretical advantages over both platelet and fibrin-specific antibodies.
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PMID:Detection of deep venous thrombosis with indium 111-labelled monoclonal antibody against tissue plasminogen activator. 193 40

91 unrelated patients with idiopathic or familial deep vein thrombosis (DVT) and 72 (34 with DVT) relatives from 26 families were screened for hypofibrinolysis by measuring tissue plasminogen activator antigen (t-PA:Ag) after venous occlusion (VO) for 10 and 20 min and by measuring t-PA inhibitor activity (PAI) at rest. 21 healthy subjects served as controls. Defective release of t-PA:Ag was found in eight out of the 91 patients (9%). A partial family study of six of these eight patients was performed. This study included 10 family members with and 21 without DVT. A defective release of t-PA:Ag was found in 50% (5/10) of the family members with DVT, which is significantly more frequent than the 9% (8/91) prevalence in the unrelated patients (P less than 0.001). Furthermore, 24% (5/21) of asymptomatic members of these families also had defective release of t-PA:Ag. In the 18 families where the propositus had a normal level of t-PA:Ag, none of the 24 studied family members with DVT had defective release of t-PA:Ag. In contrast to the defective release of t-PA:Ag, increased basal level of PAI did not show familial clustering. In conclusion, low release of t-PA during VO shows familial clustering in a proportion of the cases.
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PMID:Familial clustering of defective release of t-PA. 195 88

An inadequate efficiency of the fibrinolytic system was revealed in 50-60% of subjects suffering young age from venous thrombosis or myocardial infarction. In a group of 27 patients with the history of deep venous thrombosis of the idiopathic type the authors revealed a significant relationship between the elevated body weight and inadequate fibrinolysis manifested by a reduced fibrinolytic capacity and excess inhibitor of plasminogen activator and its inadequate decline after desmopressin infusion (DDAVP). In a group of 29 patients, who had suffered a myocardial infarction when young, the authors revealed a significant association between reduced fibrinolytic capacity and elevated body weight, hypertriglyceridaemia and increased immunoreactive insulin secretion after a glucose load. In half the investigated subjects it proved possible to improve the reduced fibrinolytic capacity by a low energy diet.
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PMID:[Disorders of fibrinolysis and thrombophilic states, risk factors and possibilities of dietary effects]. 205 93

Defibrotide, a deoxypolyribonuclide, has been found to modulate endothelial cell function causing increase in t-PA and decrease in PAI levels and also increase in PGI2 production. In addition, it increases platelet c-AMP levels and decreases MDA and TXB2 formation in human. Defibrotide inhibits platelet aggregate formation in vitro experiments as well as end-to-end anostomosis in rats. So, defibrotide inhibits the activation of platelets. Besides an increase of protein C and S levels a synergic action of heparin was observed in animal experiments. A strong antithrombotic effect has been observed in animal models. The drug has a beneficial effect in the cases of DVT, POVD, stroke and thromboembolism. Through its action we may say that the drug acts in a novel fashion in contrast to the other drugs used in this area. Defibrotide is a single-stranded polydeoxyribonucleotide obtained from deoxyribonucleic acid of mammalian lungs by controlled depolimerization. Since 1981 in our laboratory and in the clinical department we have been investigating a newly developed agent defibrotide in vitro experiments, animal experiments, and also its clinical pharmacology and clinical application. Some of our findings are already published and compared with literature (40, 43, 46). Because of the limited space we are not going to review the literature in detail but we are going to summarize our observations on this compound in the following order. I--in vitro experiments, II--Animal experiments, III--clinical pharmacology in human.
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PMID:The pharmacology and clinical pharmacology of defibrotide: a new profibrinolytic, antithrombotic and anti-platelet substance. 210 24


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