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: UNIPROT:P00750 (PLA)
16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous investigations suggested that heparin administration to humans enhances the tissue type plasminogen activator (tPA) levels in blood, but it remains uncertain whether this effect induces fibrinolysis. We studied the effect of therapeutic levels of heparinization on plasma markers for fibrinolysis in patients suspected of pulmonary embolism (PE). Blood samples were taken from 49 consecutive patients; 28 had confirmed PE, 21 had PE excluded. On admission, the plasma levels of plasmin-alpha 2antiplasmin complexes and D-dimer were significantly higher in the patient group with PE compared to those in whom PE was excluded. After heparinization the tPA levels increased in both groups, showing that this effect was not dependent on the initial level of activity of fibrinolysis. In spite of this increment in tPA levels, the concentrations of plasmin-alpha 2antiplasmin complexes and D-dimer decreased. In conclusion, although heparinization in patients with or without pulmonary embolism does lead to elevated tPA:Ag levels, this is not accompanied by enhanced fibrinolysis.
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PMID:Effects of heparin therapy on fibrinolysis in patients with pulmonary embolism. 924 51

The authors report on a 33-year old woman with massive, life-threatening pulmonary embolism at the third trimester of pregnancy. The diagnosis was rapidly accomplished in the Emergency Department by two dimensional-Doppler echocardiography that showed signs of pulmonary hypertension as well as a large, floating thromboembolus in the right atrium. As the hemodynamic deterioration persisted after treatment with iv heparin, the patient received alteplase 50 mg as a bolus over 5 minutes. About 30 minutes later, a further 50 mg infusion of alteplase was given over 60 minutes because clinical conditions were progressively worsening. After an alteplase dose of 75 mg, the woman showed a definite improvement in clinical-hemodynamic status and echocardiography documented a reduction of right ventricular overload and atrial clot disappearance. Two hours later the patient was submitted to cesarean section, because of the onset of uterine contractions, and delivered a vital baby. The occurrence of uterine bleeding was antagonized by the infusion of fresh-frozen plasma and a moderate anemia was subsequently treated with iron preparations. The mother and her baby were discharged on 16th day in fairly good general conditions. The authors emphasize the leading role of early echocardiography in the clinical decision making and the lifesaving potential of full dose thrombolytic therapy without serious adverse effects.
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PMID:[Massive pulmonary embolism during the third trimester of pregnancy: effectiveness of thrombolytic treatment with alteplase]. 924 13

We examined hemostatic abnormalities in 23 patients with acute myocardial infarction (AMI), 10 with pulmonary embolism (PE), and 10 with deep vein thrombosis (DVT). At the onset of AMI, plasma levels of tissue-type plasminogen activator (t-PA), PA inhibitor-I (PAI-I), fibrin-D-dimer, thrombin-antithrombin complex (TAT), and plasmin-plasmin inhibitor complex (PPIC) were significantly increased. Both the plasma total TFPI and free-TFPI levels in the AMI patients were significantly higher than those in the healthy volunteers, PE patients, and DVT patients. There was no significant difference in total TFPI or free-TFPI among patients with PE, those with DVT, and healthy volunteers. One hour after percutaneous transluminal coronary angioplasty (PTCA) in the AMI group, the total TFPI level was further increased, and it was significantly reduced 24 hr after PTCA, to a level similar to that in healthy volunteers. Free-TFPI showed a pattern similar to that of total TFPI. The ratio of free-TFPI/total TFPI was highest 1 hr after PTCA. Increased TFPI in AMI patients might be released from ischemic tissues.
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PMID:Increased tissue factor pathway inhibitor in patients with acute myocardial infarction. 925 77

Impaired fibrinolysis, resulting from increased plasminogen activator inhibitor-1 (PAI-1) or reduced tissue-type plasminogen activator (t-PA) plasma levels, may predispose the individual to subacute thrombosis in sepsis and inflammation. The objective of these studies was to show that adenovirus-mediated gene transfer could increase systemic plasma t-PA levels and thrombolytic capacity in animal model systems. Recombinant adenovirus vectors were constructed that express either human wild type or PAI-1-resistant t-PA from the cytomegalovirus (CMV) promoter. Both t-PA-deficient (t-PA(-/-)) and PAI-1-overexpressing transgenic mice were infected by intravenous injection of these viruses. Intravenous injection of recombinant adenovirus resulted in liver gene transfer, t-PA synthesis, and secretion into the plasma. Virus dose, human t-PA antigen, and activity concentrations in plasma and extent of lysis of a 125I-fibrin-labeled pulmonary embolism were all closely correlated. Plasma t-PA antigen and activity were increased approximately 1,000-fold above normal levels. Clot lysis was significantly increased in mice injected with a t-PA-expressing virus, but not in mice injected with saline or an irrelevant adenovirus. Comparable levels of enzyme activity and clot lysis were obtained with wild type and inhibitor-resistant t-PA viruses. Adenovirus-mediated t-PA gene transfer was found to augment clot lysis as early as 4 hours after infection, but expression levels subsided within 7 days. Adenovirus-mediated transfer of a t-PA gene can effectively increase plasma fibrinolytic activity and either restore (in t-PA-deficient mice) or augment (in PAI-1-overexpressing mice) the thrombolytic capacity in simple animal models of defective fibrinolysis.
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PMID:Adenovirus-mediated transfer of tissue-type plasminogen activator augments thrombolysis in tissue-type plasminogen activator-deficient and plasminogen activator inhibitor-1-overexpressing mice. 926 70

A patient with clinical features consistent with pulmonary embolism showed no improvement despite therapy with tissue-plasminogen activator and full-dose heparin. Transvenous catheter suction biopsy was successful in establishing an antemortem histologic diagnosis of primary pulmonary artery leiomyosarcoma. Urgent surgical intervention was performed.
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PMID:Primary leiomyosarcoma of the pulmonary artery confirmed by catheter suction biopsy. 949 86

A 52-year-old previously healthy man experienced acute severe dyspnoea after suffering from gastroenteritis for 3 days. After arrival of the ambulance, cardiac arrest with an initial rhythm of electro mechanical dissociation occurred. Circulation was restored after 10 min of cardiopulmonary resuscitation but soon cardiac arrest reoccurred. Based on a strong clinical suspicion of massive pulmonary embolism, thrombolytic treatment with heparin 5000 IU and reteplase 20 U, given as single boluses and heparin was continued as an infusion 1000 IU h(-1). After 7 min of continued resuscitation, circulation was restored and after 40 min the vital functions began to stabilize, thus indicating pulmonary reperfusion. The diagnosis of pulmonary embolism was confirmed by a ventilation-perfusion scan and by spiral computerised tomography. The patient was discharged from intensive care after 2 days with a cerebral performance category I. Based on previous calculations, the annual number of patients who present with massive pulmonary embolism leading to cardiac arrest (and thus who would theoretically be candidates for thrombolytic treatment) was estimated to be 0.7/100000 inhabitants in this emergency medical services system.
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PMID:Prehospital thrombolytic treatment of massive pulmonary embolism with reteplase during cardiopulmonary resuscitation. 978 10

Complete resolution of major pulmonary embolism (PE) treated with heparin alone can often take > 3 weeks. Thrombolytic agents effectively resolve pulmonary artery thrombi within a few hours. However, the effect of the 2 types of treatment on recovery of right ventricular function has not yet been followed for periods of > 24 hours. We prospectively examined 40 consecutive patients with documented major PE (symptoms being present for < or = 8 weeks). After diagnosis, 27 patients (68%) were treated with alteplase plus heparin and 13 (32%) with heparin alone. There was no significant difference between the 2 groups with regard to baseline parameters. At 12 hours, systolic pulmonary artery pressure decreased from 56 +/- 20 to 37 +/- 21 mm Hg in the alteplase group, and from 50 +/- 11 to 46 +/- 12 mm Hg in the heparin group (significantly more; p = 0.016). On echocardiographic follow-up, a decrease in end-diastolic dimensions of the right ventricle and an increase in left ventricular dimensions was significantly more pronounced in the alteplase group (p <0.001 and p = 0.05, respectively). The incidence of right ventricular dilation and paradoxical septal wall motion decreased significantly only in the thrombolyis group. However, at 1-week follow-up, no difference was seen between the 2 groups regarding the overall change in right or left ventricular dimensions or the final values of other echocardiographic parameters. Thus, echocardiography is particularly useful for hemodynamic follow-up of major PE. Thrombolysis may rapidly reduce pulmonary artery pressure, but resolution of right ventricular pressure overload also occurs within 1 week in patients treated with heparin alone.
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PMID:Comparison of alteplase versus heparin for resolution of major pulmonary embolism. 979 53

We measured D-dimer and plasminogen activator inhibitor-1 (PAI-1) activity in 45 trauma patients to assess their efficacy in predicting the post-traumatic hemostatic perturbations. We found the correlation between D-dimer measured by Simpli Red test and ELISA to be highly significant (p=0.0001). The D-dimer ELISA indicated that the serial changes of D-dimer after trauma were variable. However, the increases of D-dimer were associated with clinical conditions of the patient, such as trauma surgery, infections, or thrombotic complications. A significant correlation was found for D-dimer levels measured by ELISA versus the injury severity score (ISS) in all the trauma patients on day 1 (p=0.0153) and on day 2 (p=0.0495). The PAI-1 activity was increased at admission and showed a progessive decline from day 2 onward, and the correlation for the daily decline of PAI-1 was highly significant (p=0.0001). The PAI-1 activity and plasminogen activator activity showed a significant negative correlation on days 1, 2, and 3. PAI-1 activity correlated moderately with D-dimer level only on day 1 (p=0.0569). Three out of forty-five patients developed thrombotic complications: one patient who died from pulmonary embolism and two patients who developed adult respiratory distress syndrome (ARDS). In summary: 1) PAI-1 activity and D-dimer exhibited contrasting serial changes after trauma. 2) There was also a negative correlation between PAI-1 activity and PA activity. 3) A significant correlation of D-dimer with ISS confirms, as might be anticipated, that there is increased activation of the coagulation mechanism in severe injury, and suggests that D-dimer levels may prove useful to screen for patients at strong risks of thrombotic complications.
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PMID:Contrasting post-traumatic serial changes for D-dimer and PAI-1 in critically injured patients. 1032 64

The clinical usefulness of catheter fragmentation and aspiration therapy was studied in 8 patients with acute pulmonary embolism who received thrombolytic therapy using urokinase or tissue-type plasminogen activator (t-PA) (thrombolysis group) and 8 patients who underwent catheter fragmentation and aspiration therapy using a percutaneous transluminal coronary angioplasty (PTCA) guide catheter (catheter group). The patients were selected from 20 patients with a definite diagnosis of acute pulmonary embolism based on pulmonary arteriography and nuclear imaging. Urokinase (48 x 10(4) to 96 x 10(4) unit/day) or t-PA (12 x 10(6) unit/day) was administered intravenously for mean 4 days in the thrombolysis group. Pulmonary artery pressure was first measured using a Swan-Ganz catheter via the jugular vein or the femoral vein in the catheter group. Then, a PTCA guide catheter was advanced into the pulmonary artery, and the thrombus was disrupted repeatedly using a Radifocus wire, followed by manual aspiration. Subsequent treatment consisted of intravenous infusion of heparin (10,000 to 15,000 unit/day) and urokinase (24 x 10(4) to 48 x 10(4) unit/day) for mean 6 days. Partial revascularization was achieved in all patients in both groups. Five patients in the thrombolysis group died within 1 month due to respiratory failure, re-embolization, and/or hemorrhagic complications. One patient in the catheter group died of hemorrhagic shock. Pulmonary artery systolic pressure in the catheter group was significantly reduced from 47.4 to 26.5 mmHg (p < 0.01). Catheter treatment of acute pulmonary embolism associated with acute circulatory failure such as shock can lead to rapid hemodynamic improvement. In contrast, thrombolysis is an effective treatment, but bleeding problems are common and caution is required. Catheter fragmentation and aspiration therapy is effective for acute pulmonary embolism, is minimally invasive, and should be considered the treatment of first choice.
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PMID:[Clinical outcome of catheter fragmentation and aspiration therapy in patients with acute pulmonary embolism]. 1046 88

Thrombolytic drugs, streptokinase and urokinase, were initially used in pulmonary embolism. More recently, new drugs like alteplase, reteplase, lanoteplase and saruplase have been a breakthrough in the treatment of acute myocardial infarction. Their efficacy has been demonstrated when treatment is initiated before the 6th hour of infarction onset. A 50% reduction of death rate is expected, if treatment starts within the 1st hour. Alteplase and reteplase are the most efficient thrombolytics despite a higher risk of cerebral bleeding. In pulmonary embolism with clinical signs of severity, thrombolysis is clearly indicated. In deep vein thrombosis of the lower limbs, therapeutic thrombolysis is still controversial. Some acute ischemic strokes (before the 3rd hour) could be treated with alteplase if there is no absolute or relative contraindication for thrombolysis. In prosthetic heart valve thrombosis, thrombolysis may be used if surgical treatment is contraindicated but the risk of bleeding and embolism should be taken into account.
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PMID:[Indications for thrombolytics]. 1058 97


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