Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Urokinase, a plasminogen activator found in urine is used in the treatment of pulmonary embolism, and is supplied commercially by several companies in Europe, U.S.A. and Japan. It exists in two forms, of molecular weights 50-55 000 and 33 000 daltons, which may differ in their therapeutic efficiency. A variety of assay systems exist to measure plasminogen activator activity--clot lysis, casein hydrolysis, amidolytic cleavage of synthetic peptide substrates. These assays are time-consuming, relatively insensitive, and cannot accurately assess the amount of the two molecular species in any preparation of urokinase. Standardization therefore presents a problem to manufacturers, control agencies, and clinicians. We have prepared a variety of monoclonal antibodies to human urokinase and have assessed their value as standardizing different commercial preparations of urokinase and measurement of urokinase for therapeutic monitoring.
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PMID:Possible use of monoclonal antibodies to standardize the production and use of human urokinase. 654 1

Urokinase treatment, previously employed with success in the declotting of deep venous thrombosis and arteriovenous shunts in patients undergoing regular dialytic treatment (RDT), was used in 23 cases of arteriovenous fistula thrombotic occlusion in 18 RDT patients. The treatment was successful in 65.2% of the cases without any negative side effects, except 1 case which may have developed a pulmonary embolism. Patients with severe hypofibrinolysis may need larger doses or may have a recurrence of the thrombotic episode. All therapeutic failures correlated with the presence of fibrosis or sclerosis.
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PMID:Urokinase treatment for arteriovenous fistulae declotting in dialyzed patients. 669 Oct 3

Urokinase (average 1670 IU/kg X h) and heparin (average 17 IU/kg X h) was infused over several days into the main pulmonary artery of 12 patients with acute massive pulmonary embolism, after diagnostic pulmonary angiography. Pulmonary artery pressures and blood clotting values were serially recorded. There was convincing improvement in the clinical condition of all patients: none died or had a recurrence of embolism. The heart rate and pulmonary vascular obstruction decreased, mean pulmonary artery pressure fell and arterial pO2 rose. There were other, also statistically significant, changes in a decrease of fibrinogen, rise in thrombin time and decrease in haemoglobin concentration. Pulmonary artery pressure after 24 hours had fallen slightly, after 5.8 days significantly. In two patients a haemoglobin fall of more than 3 g/dl required blood transfusion. The findings indicate that after massive pulmonary embolism local continuous infusion of urokinase can, after 5-6 days, normalize pulmonary haemodynamics; the pulmonary angiogram shows almost complete disappearance of the pulmonary vascular obstruction.
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PMID:[Local thrombolysis with urokinase in acute massive pulmonary embolism]. 669 63

Pulmonary embolism is frequently fatal and its treatment and prevention are of vital importance. Curative therapy depends mainly on the use of heparin or urokinase, embolectomy under extracorporeal circulation being reserved for the most severe cases, and Trendelenburg's operation limited in its application at the present time. Prevention of pulmonary embolism is the principal problem and involves, apart from the use of anticoagulants, insertion of a caval clamp by means of a Adams Deweese clip whenever possible, or by the use of an endoluminal filter. Surgical relief of peripheral venous obstruction, apart from very recent proximal phlebitic lesions, is however currently of limited application.
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PMID:[Pulmonary embolism. Medical and surgical treatment (author's transl)]. 705 Feb 72

Urokinase and streptokinase are the two fibrinolytics approved for clinical use. Streptokinase has the broader application, being used to treat deep vein thrombosis (DVT), pulmonary embolism (PE), arterial thromboembolism, and occluded arteriovenous shunts in renal dialysis. Bleeding, the most significant complication of fibrinolytic therapy, arises mostly from invaded sites and can be significantly reduced by minimizing venipuncture and other invasive procedures.
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PMID:Fibrinolytic guidelines in diabetes. 706 Sep 47

The proper place of thrombolytic agents in the management of pulmonary embolism is not yet well defined. A number of survivors of acute massive pulmonary thromboembolism remain in a delicate balance of hemodynamic compensation and where recurrent emboli could frequently be fatal. Successful response to urokinase therapy in such a case is presented and the status of currently available thrombolytic drugs is discussed. We suggest that thrombolytic therapy in massive pulmonary embolism would provide greater hemodynamic reserve, alleviate shock, minimize the chances of recurrent emboli and prevent permanent impairment to the pulmonary vascular bed.
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PMID:Case report. Acute cor pulmonale due to massive pulmonary embolism and successful response to thrombolytic therapy. 706 97

Recent deep vein thrombosis of the iliofemoral segment often leads to pulmonary embolism and to impaired valve function. Although more common, occlusions in the calf veins are less dangerous, and often a self-limiting disorder as almost half of these thrombi lyse spontaneously. Approximately 70% of fresh deep venous thrombi dissolve under intensive and prolonged thrombolytic treatment with streptokinase and long-term follow-up studies indicate that normal valve function is preserved in those patients in whom thrombus clearance was obtained. Thrombosis with streptokinase or urokinase appears to be the current treatment of choice for most cases of massive and severe, life-threatening pulmonary embolism; those patients surviving more than an hour or so after massive infarction comprise a prognostically better group, in whom the chances of surviving embolectomy is today smaller than the probability of survival without surgery but with thrombolytic treatment. Obviously there are problems in the evaluation but also in the thrombolytic treatment with streptokinase and urokinase of deep venous thrombosis and pulmonary embolism. These problems do not concern the principle of thrombolysis, but are largely due to the fact that the drugs so far used also induce a systemic fibrinogenolysis resulting in a bleeding risk. There is already good evidence that tissue activator of plasminogen is highly specific for fibrin and can induce thrombolysis in experimental animals without inducing systemic fibrinogenolysis.
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PMID:[Actual state of thrombolytic treatment of recent vein thrombosis and pulmonary embolism (author's transl)]. 719 77

Thirty-eight patients admitted to hospital for pulmonary embolism of recent onset were divides into four treatment groups. Group I patients (10) received streptokinase in does of 250,000 units over 20 minutes, followed by 100,000 units/hour for a total of 24 hours. Group II patients (8) received urinary urokinase 4,500 CTA units/kg/hour during 12 hours. Group III patients (10) were treated with urinary urokinase (112,500 CTA) units/hour during 24 hours) and heparin (500 units/kg/24 hours). Group IV patients (10) were given tissue urokinase and heparin, both in the same dosage as in group III patients. Pulmonary angiography and cavography were performed in all patients before treatment and within 24 hours of its termination. With regard to pulmonary emboli, improvement was most pronounced with streptokinase, with a gain of 15.7 points on Miller's index of severity, as against 9.6, 10.5 and 5.7 points for Group II, III and IV patients respectively. In peripheral venous thrombosis, streptokinase showed even greater superiority over other treatment, with a gain of 16 points of Marder's index, as against zero, 4.5 and 11.2 points for patients in Groups II, III and IV respectively. On biochemical tests, the decrease in fibrinaemia was more pronounced in Group I patients than in other groups.
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PMID:[Effects of thrombolytic agents on pulmonary and venous clots in severe pulmonary embolism (author's transl)]. 722 Feb 91

Although low-dose heparin therapy is the technique most commonly used for prophylaxis of pulmonary thromboembolism, its usefulness is being questioned. Platelet deaggregation prophylaxis with either aspirin or dipyridamole, or both, apparently is a reasonable alternative, but further studies are needed. For treatment of pulmonary thromboembolism, continuous conventional-dose heparin therapy is the approach of choice. It has the highest therapeutic/toxic ratio and is the most effective technique for prevention of clot propagation. The patient's fibrinolytic network must be intact, however, if clot degradation is to occur. Fibrinolytic therapy with urokinase or streptokinase should be restricted to use in patients with massive pulmonary embolism in whom hemodynamics are unstable. Caval interruption and pulmonary embolectomy have lower benefit/risk ratios than do the medical alternatives and are rarely used for pulmonary thromboembolism.
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PMID:Pulmonary thromboembolism. 2. New trends in prophylaxis and therapy. 737 11

The history and physical examination were assessed in 215 patients with acute pulmonary embolism uncomplicated by preexisting cardiac or pulmonary disease. The patients had been included in the Urokinase Pulmonary Embolism Trial or the Urokinase-Streptokinase Embolism Trial. Presenting syndromes were (1) circulatory collapse with shock (10 percent) or syncope (9 percent); (2) pulmonary infarction with hemoptysis (25 percent) or pleuritic pain and no hemoptysis (41 percent); (3) uncomplicated embolism characterized by dyspnea (12 percent) or nonpleuritic pain usually with tachypnea (3 percent) or deep venous thrombosis with tachypnea (0.5 percent). The most frequent symptoms were dyspnea (84 percent), pleuritic pain (74 percent), apprehension (63 percent) and cough (50 percent). Hemoptysis occurred in only 28 percent. Dyspnea, hemoptysis or pleuritic pain occurred separately or in combination in 94 percent. All three occurred in only 22 percent. The most frequent signs were tachypnea (respiration ate 20/min or more) (85 percent), tachycardia (heart rate 100 beats/min or more) (58 percent), accentuated pulmonary component of the second heart sound (57 percent) and rales (56 percent). Signs of deep venous thrombosis were present in only 41 percent and a pleural friction rub was present in only 18 percent. Either dyspnea or tachypnea occurred in 96 percent. Dyspnea, tachypnea or deep venous thrombosis occurred in 99 percent. As a group, the identified clinical manifestations, although nonspecific, are strongly suggestive of acute pulmonary embolism. Conversely, acute pulmonary embolism was rarely identified in the absence of dyspnea, tachypnea or deep venous thrombosis.
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PMID:History and physical examination in acute pulmonary embolism in patients without preexisting cardiac or pulmonary disease. 746 69


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