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)

Thrombolytic therapy is aimed at dissolving thrombi. Streptokinase (SK) and urokinase (UK) are currently used in France but their mode of action has not been completely elucidated, which renders the establishment of therapeutic protocols and the choice of doses difficult. This treatment has a certain number of contraindications which must be strictly respected. The effectiveness of SK and UK in high doses has been demonstrated, in particular in pulmonary embolism and acute arterial obstruction of the limbs, but there is a risk of haemorrhage, whilst UK in moderate doses is usually well tolerated but has yet to prove its effectiveness in randomised double blind trials. Laboratory control has been simplified but it is essential not to forget the importance of clinical monytoring. Finally, drugs have recently been used in association with thrombolytics and more particularly the administration of plasminogen or defibrinating agents before or after thrombolytics.
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PMID:[Thrombolytic treatment (theoretical basis, therapeutic protocols, monitoring)]. 3 Nov 15

This review deals with aspects of fibrinolysis in which significant developments have taken place in the last few years. The structural changes of plasminogen during its activation are now identified precisely; the recent description of a thrombotic tendency in a kindred characterized by a defect of this protein emphasizes its important role in the homeostatic balance. Several activators of plasminogen are now identified; some of them, such as tissue and vascular activators, appear to have an important role in physiology and pathology. The recent characterizations of the alpha 2-antiplasmin and of antiactivators have widened our understanding of the inhibitors of fibrinolysis: a defect of the plasmin inhibitor seems to be associated with an haemorrhagic tendency, whereas high antiactivator levels were encountered in thrombotic conditions. The clinical use of fibrinolytic agents appears to be promising in conditions such as recurrent deep vein thrombosis and in the post-phlebitic syndrome. Thrombolytic therapy with urokinase or streptokinase appears to have elective indications in patients with acute deep vein thrombosis and massive life-threatening pulmonary embolism.
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PMID:Progress in fibrinolysis. 16 15

A 62-year-old man had circulatory failure from massive pulmonary embolism following a road accident. Despite intensive therapy including urokinase infusion, inotropic drugs, and mechanical ventilation, the patient's circulatory status deteriorated. When it became impossible to maintain the mean systemic arterial pressure above 50 mm. Hg and the cardiac index above 1 L. per minute per square meter, circulatory support by partial cardiopulmonary bypass with a membrane lung was begun. Acute circulatory failure and acute pulmonary hypertension were promptly reduced by this procedure, and patient's status necessitated only intravenous heparin infusion and mechanical ventilation. After 60 hours of bypass the patient was weaned from the membrane lung, and 1 month later he was discharged from the hospital.
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PMID:Massive pulmonary embolism with circulatory failure: survival following sixty hours' support with a membrane lung. 68 57

Pulmonary thromboembolism is a widespread problem and is an important cause of death in patients with a variety of medical and surgical conditions. There have been few significant advances in the understanding of the aetiology beyond additional evidence confirming the importance of Virchow's triad. An impressive list of epidemiological associations has been compiled, however. Some knowledge of the natural progression of the disease is required as an aid in the understanding of the application of the therapeutic and prophylactic measures available in the management of pulmonary embolism. It would seem that at least two-thirds of pulmonary emboli are non-fatal, and in these cases the natural resolution, even of comparatively large embolic masses, is very efficient in patients without pre-existing cardiopulmonary disease. Diagnosis may prove difficult and most ancillary investigations are of questionable value. On the other hand, pulmonary radio-isotope scanning is far more specific and pulmonary angiography is a comparatively simple and complication-free diagnostic procedure. Prophylaxis is a real and practical aim, especially following surgery or myocardial infarction. In these groups widespread clinical trials of prophylactic measures have been made possible by the objective radio-iosotope screening techniques. Mechanical means of preventing venous stasis and anticoagulation appear effective. In addition, low-dose subcutaneous heparin seems to be as useful as heparin in conventional dosage. Apart from conventional supportive therapy, there are three major approaches to the treatment of pulmonary embolism. Heparin remains the mainstay, particularly in the less severe cases, hopefully preventing propogation of thrombosis and recurrence of embolism, thus allowing resolution to take place. Thrombolytic therapy with streptokinase or urokinase is capable of producing far more rapid dissolution of pulmonary emboli with consequent theoretical advantages over heparin. No reduction in mortality has been shown using thrombolytic therapy. Patients who fail to respond satisfactorily to acute resuscitative measures may require pulmonary embolectomy.
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PMID:Pulmonary embolism: current therapeutic concepts. 77 78

In Phase I of this study of 160 patients with pulmonary embolism, it was demonstrated that of 12 hours of urokinase accelerated the resolution of pulmonary thromboemboli compared to heparin alone. Phase II compared 12 hours of urokinase, 24 hours of urokinase and 24 hours of streptokinase in 167 patients. All patients had a clinical history and angiographic diagnosis of pulmonary embolism. Patients were randomly allocated to treatment. All physicians making patient observations were unaware of drug assignment. Resolution of the thromboembolism 24-30 hours after therapy had been instituted was determined by pulmonary angiography, lung perfusion scans and cardiopulmonary hemodynamics. Twenty-four hours of urokinase did not demonstrate greater clot resolution than 12 hours of urokinase. Twenty-four hours of urokinase resulted in greater improvement than streptokinase in lung perfusion scans, but not in angiograms. In patients with massive embolism, this difference was statistically significant. Hemodynamic differences varied. Bleeding complications and morbidity due to allergic reactions with streptokinase and urokinase were minimal. There was no statistically significant difference in mortality in the three threatment groups. From the Phase I and Phase II data it is reasonable to conclude that all three regimens of thrombolytic therapy are more effective than heparin alone in accelerating resolution of pulmonary emboli. Thrombolytic therapy offers the clinician an alternative to pulmonary embolectomy.
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PMID:Streptokinase and urokinase in the treatment of pulmonary thromboemboli; from a national cooperative study. 78 89

The defibrinating agent ancrod has had limited clinical trial, but appears to give no advantages over heparin. Intravenous infusion of dextran, a glucose polymer, has been shown to have an antithrombotic effect in many experimental models of thrombosis. However, the evidence that dextran is a clinically valuable antithrombotic drug is conflicting. A number of controlled randomized studies have shown that dextran can prevent postoperative venous thromboembolism when a large volume of dextran 40 or 70 was infused rapidly during and after surgery. However, blood volume expansion during dextran treatment prohibits its use in patients with reduced cardiac reserve, and infrequent though sometimes severe, allergic reactions have been reported. Evidence that dextran is of value for the treatment of venous or arterial thromboembolism comes from uncontrolled studies and is not convincing. Many compounds have been shown to inhibit platelet function in vitro but only five of these drugs have been extensively evaluated as prophylactic or therapeutic antithrombotic agents in man. These are aspirin, sulphinpyrazone, dipyridamole, hydroxychloroquine and clofibrate. They have been evaluated mainly in patients with cerebral vascular disorders, coronary artery disease, peripheral artery ischaemia, venous thromboembolism, prosthetic heart valves, and in patients with arteriovenous shunts. The evaluation of the clinical effect of the platelet function suppressing drugs is in its early stages, but they appear to differ from each other in the spectrum of their clinical effectiveness, and they may be more effective in arterial than in venous thromboembolic disorders. Their role in the management of cerebral vascular disease and coronary artery disease is still uncertain, and should be clarified by the results of a number of multi-centre, prospective, randomized studies which are currently in progress. Three types of thrombolytic drugs have been evaluated clinically; the plasminogen activators streptokinase and urokinase, proteolytic enzymes such as plasmin, and agents which increase the level of endogenous plasminogen activator (e.g. anabolic steroids). Of these, the plasminogen activators now have a definite place in clinical practice. The plasminogen activators accelerate the lysis of recent venous thrombi and pulmonary emboli, and of arterial thrombi or emboli. Thrombolytic therapy with these agents should be considered particularly in patients with recent major pulmonary embolism, as lysis of recent emboli is rapid and substantial. It should also be considered in patients with recent extensive venous thrombosis, because total lysis of venous thrombi has been reported to result in long-term preservation of valve function, and is likely to prevent postphlebitic syndrome, though this has not been proven. However, plasminogen activator therapy carries a higher risk of bleeding than heparin treatment...
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PMID:Antithrombotic drugs: part II. 78 6

Fibrinolytic therapy was carried out in 59 patients suffering from a total of 60 deep venous thromboses of the iliac segment (n = 24), the femoropopliteal segment (n = 18), the deep calf veins (n = 2), or the subclavian vein (n = 16). 46 patients received streptokinase (SK), 4 were given urokinase (UK), and 10 were treated with streptokinase followed by urokinase (SK + UK). The duration of fibrinolytic therapy was between 19 and 596 hours (x = 166 +/- 111 hrs). Phlebographic examination was used to determine the location of the thrombotic occlusion as well as to evaluate therapeutic results. To assure sufficient anticoagulatory protection during therapy with streptokinase the dose of streptokinase was either reduced by steps of 20,000 U/hr to a minimum of 40,000 U/hr or heparin was added as a continuous infusion. Urokinase was administered with a mean loading dose of 75,000 IU followed by an average maintenance dose of 40,000 IU/hr; it was always given in combination with heparin. When therapeutic success was graded as complete/partial/no recanalisation, the following results were obtained: thrombotic occlusion up to 1 week old 35%/48%/17%; up to 2 weeks old 57%/14%/29%; 3 or 4 weeks old 12%/38%/50%; older than 4 weeks 13%/37%/50%. The two most common side effects were a fall of the hemoglobin and a rise of body temperature. Treatment with SK had to be interrupted for bleeding in two cases. One patient diet after rupture of the liver and of the spleen following development of subcapsular hematoma in these organs, 3 patients survived pulmonary embolism without major long-term impairment. Considering medical and social aspects (preservation of capability for working in young adults) it appears justified to administer fibrinolytic agents up to a thrombus age of 14 days, in some cases even up to a thrombus age of 28 days. Good results in cases of deep vein thrombosis of the lower limbs are often obtained only when fibrinolytic therapy is extended beyond 96 hours. It should be performed in intensive care units only. Follow-up examinations of the venous drainage capacity up to 2 years after fibrinolytic therapy document the good therapeutic effect that is warrented by streptokinase or urokinase induced complete recanalisation.
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PMID:[Fibrinolytic therapy in deep venous thrombosis of the upper and lower extremity]. 84 72

Two fibrinolytic drugs, streptokinase and urokinase, have undergone extensive clinical evaluation in the past fifteen years. Current evidence suggests that these agents may become the drugs of choice in the treatment of certain patients with venous thrombosis and pulmonary embolism. The ultimate usefulness of fibrinolytic therapy in the treatment of thrombotic conditions other than venous thrombosis and pulmonary embolism has not yet been determined.
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PMID:The clinical use of fibrinolytic agents. 88 35

A case of unexpected cardiac arrest occurring in a 17-year-old male patient is reported. The patient had been admitted after sustaining hand trauma. A first emergency surgical procedure was carried out, followed about three weeks later by another one. No incidents occurred during or after either of these two operations. A third procedure was required about two months after the accident (free toe graft to the thumb of the left hand). The twelve-hour operation was carried out under general anaesthesia and axillary block. The patient was given intravenous heparin (800 IU.h-1) during the procedure on the arm. The patient recovered quickly, and was extubated before his transfer to the recovery room. Fifteen minutes later, the patient's heart rate decreased to 40 b.min-1, followed by a transient cardiorespiratory arrest. The suspicion of pulmonary embolism was confirmed by pulmonary scintigraphy. Thrombolysis was carried out with 2,000 IU.kg-1.h-1 of urokinase for a 72 h period, combined with continuous heparin administration (16 to 36 x 10(3) IU.day-1). The patient recovered after one week. No thrombophlebitis was found for origin of the emboli. Biological investigations carried out both before and after 10 minutes of anoxia revealed a normal fibrinolytic system, but a deficit in protein C (62% antigen, 64% activity). Two years after the episode of pulmonary embolism, the patient, still taking acenocoumarol, remained free from any sequela. Current perioperative management of patients with a known protein C deficit is discussed.
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PMID:[Disclosure of protein C deficiency with pulmonary embolism followed by cardiac arrest during the recovery period]. 144 21

The use of thrombolytic agents in the treatment of postoperative pulmonary embolism presents a dilemma to the surgeon. On one hand, postoperative pulmonary embolism usually occurs within 2 weeks of surgery. On the other hand, recent surgery is considered a contraindication for the use of thrombolytics. We developed a protocol for treating pulmonary embolism patients who have recently undergone surgery. Urokinase, at a dose of 2,200 U/kg wt, is injected directly into the clot via a catheter positioned in the pulmonary artery. This is followed by continuous infusions of urokinase at 2,200 U/kg wt/hr until the clot is lysed (up to 24 hrs). Simultaneously, heparin is administered peripherally at 500 U/hr. The level of serum fibrinogen is monitored every 6 hours and maintained at no less than 0.2 g/dL to prevent bleeding. Thirteen patients were treated for angiographically proven pulmonary embolism within 14 days of surgery. Complete lysis of every embolus was achieved, and no deaths or bleeding complications occurred. Two patients received inferior vena cava filters, and nine patients no longer needed chronic anticoagulants within 3 months after the embolic event.
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PMID:Thrombolytic therapy for postoperative pulmonary embolism. 155 78


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