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)

The results of treatment of pulmonary embolism with heparin (n = 34), streptokinase (n = 28) or embolectomy (n = 25) are presented. The treatment groups represented different degrees of embolization with acute embolic scores (possible maximum: 20, mean +/- SD): 5 +/- 4, 9 +/- 3 and 13 +/- 3, respectively (p less than 0.0001). The post-treatment embolic score (mean +/- SD) for patients with acute massive central emboli (score greater than or equal to 9) was: 6 +/- 4 (n = 7) and 3 +/- 2 (n = 15) in the streptokinase and embolectomy groups, respectively, (p less than 0.01). The hospital mortality was 6% (n = 2), 21% (n = 6) and 20% (n = 5) in the heparin, streptokinase and embolectomy groups, respectively (p less than 0.05). The 5-year cumulative survival (+/- SE) was 68% +/- 10, 64% +/- 10 and 80% +/- 8, respectively (p: NS). The relative survival (hospital and late deaths, observed/expected) stratified according to acute embolic score showed the best results in the embolectomy group. Systolic pulmonary artery pressure greater than 60 mmHg was found in cases with a duration of symptoms greater than 7 days and/or with greater than or equal to 25 anamnestic recurrent embolic episodes before diagnosis, indicative of a gradual increase in pulmonary artery pressure and of partly organized non-lyseable emboli. Embolectomy carried a low risk of complications (8% with cerebral reduction). Streptokinase treatment was associated with serious complications (18% with cerebral reduction/fatal hemorrhage). Pulmonary embolectomy should be recommended in all cases with emboli in the main branches of the pulmonary artery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of pulmonary embolism with full-dose heparin, streptokinase or embolectomy--results and indications. 242 92

Many investigators have reported about beneficial results with thrombolytic therapy in patients with acute pulmonary embolism. Streptokinase and urokinase have been used for more than 15 years, but the conditions of use of these agents still remain controversial. Optimal dosage and treatment schedule are still evolving. For streptokinase most investigators adopt a fixed dosage schedule: a loading dose of 250,000 units followed by a maintenance infusion of 100,000 units per hour for 24 to 72 hours. For urokinase numerous dosage regimens have been used such as: high dosage schedule 4,400 units per kilogram per hour for twelve to 24 hours with or without loading dose; moderate dosage 1,600 to 2,000 units per kilogram per hour for 24 hours and low dosage in bolus. With these treatments there is a trend to reduced in-hospital-mortality in massive pulmonary embolism; the early pulmonary revascularization and the hemodynamic improvement are higher than those noticed with heparin. These results are obtained with a minimum of complication essentially bleeding in 10 or 15%; most bleeding being located at puncture site. More recently, new thrombolytic agents have been used in acute pulmonary embolism. Only four studies have tested rt-PA which is effective and relatively safe, but the optimal dose regimens remain to be determined. Less information is available concerning Anisoylated Plasminogen Streptokinase Activator Complex (APSAC), the angiographic improvement seems to be rapid and important (50% on average) but the decrease of fibrinogen is important too and comparable with streptokinase. Considering the good results of thrombolytic treatment of acute submassive and massive pulmonary embolism, there is a doubt as to whether the pulmonary embolectomy has any place in the pulmonary embolism patients except in those with cardiac arrest. In the near future new thrombolytic drugs could be more efficient on pulmonary embolism and deep venous thrombosis, and thus the bleeding risk might be decreased.
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PMID:Thrombolytic treatment of acute pulmonary embolism. 250 Mar 88

Clinical experience with thrombolytics in non-coronary disorders is limited to the plasminogen activators streptokinase, urokinase and alteplase; therapeutic trials with anistreplase (APSAC) are almost, and with saruplase completely, limited to acute myocardial infarction. In terms of thrombus clearance, thrombolytic drugs are superior to heparin in patients with recent deep vein thrombosis in the pelvis or lower limbs. In aggregate, thrombi younger than 8 days are lysed in approximately 60% of patients treated with streptokinase, urokinase or alteplase. The results of studies assessing the subsequent development of the postphlebitic syndrome are conflicting, but most suggest that thrombolytic therapy can reduce symptoms of chronic venous insufficiency. Currently, the combination of systemic thrombolytic drugs followed by heparin is recommended for patients with acute major pulmonary embolism who are haemodynamically unstable. Streptokinase, urokinase and alteplase have all been shown to accelerate the lysis of pulmonary emboli and to decrease pulmonary vascular obstruction and pulmonary hypertension. Systemic venous or intrapulmonary infusions of alteplase offers the same benefit in terms of angiographic and haemodynamic improvement. A short infusion of 100 mg alteplase over 2 hours seems to be superior to a 24-hour infusion of urokinase. None of the thrombolytic trials in pulmonary embolism have been large enough to demonstrate a reduction in mortality. It is now generally accepted that, unless contraindicated, thrombolytic therapy is the front-line treatment for patients with massive pulmonary embolism and major haemodynamic disturbance. The local treatment of acute arterial occlusion in limb arteries results in rapid clearing of the artery in 67% of patients treated with streptokinase; the corresponding success rates for urokinase and alteplase are 81% and 88 to 94%, respectively. The main question appears to be the identification of patients in whom local thrombolysis is the treatment of choice, as opposed to established therapeutic modalities. Thrombolytic treatment following a major ischaemic stroke is hazardous, although clinical improvement has been noted in a minority of patients with recanalised cerebral arteries. The safety and efficacy of thrombolytic treatment remains unproven for this indication, and its use must be restricted to experimental protocols. Thrombolytic treatment in retinal artery or vein occlusion has, in practice, been abandoned.
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PMID:Use of thrombolytic drugs in non-coronary disorders. 268 38

A new abnormal plasminogen, Frankfurt I, has been identified in the plasma of a 42 year-old male patients who had recurring thromboses, thrombophlebitis and pulmonary embolism since his age of 29. Reduced functional and also slightly reduced antigen plasminogen concentrations were found in both the proposituts and his mother. Plasmin generation rates carried out by Streptokinase and Urokinase were also abnormal. The plasmin generated was very unstable in the absence of stabilizing ligands and/or substrates. Crossed immunoelectrophoresis of the purified Frankfurt I revealed a peak with normal size and shape, but displaced with respect to normal Glu-plasminogen toward the anode. Isoelectric focusing followed by zymography on an agarose-fibrin plate proved this observation but did not indicate a separation of the normal from the abnormal plasminogen molecular species, also, fewer bands were found in the abnormal plasminogen isozyme pattern. Kinetic studies of Frankfurt I Glu-plasminogen and plasmin showed that most of the functional abnormality is related to absence of active sites in half of the molecules.
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PMID:Congenital abnormal plasminogen, Frankfurt I, a cause for recurrent venous thrombosis. 296 86

The efficacy of low-dose, locally administered streptokinase (SK) combined with full therapeutic systemic doses of heparin was investigated. Seven patients with angiographically proven massive acute pulmonary embolism were treated. Streptokinase, 10,000-20,000 units/hour, was administered directly into the left or right pulmonary artery for 9 to 24 hours. Heparin was administered concurrently. The number of unperfused segments of the infused lung shown on the lung scan decreased from 5 +/- 2 to 2 +/- 1 after 12-24 hours (p less than .01). No change was shown in the contralateral lung. The angiographic index of severity score in the infused lung decreased from 16 +/- 1 to 9 +/- 4 (p less than .01). The partial pressure of oxygen in arterial blood improved within four hours. In spite of the low doses of streptokinase, however, two major bleeding episodes occurred that required blood transfusion. In conclusion, low dose intrapulmonary streptokinase, combined with intravenous heparin, may provide a therapeutic option in patients with life-threatening massive acute pulmonary embolism in whom full dose lytic therapy may be hazardous, although even low dose lytic therapy was associated with risk.
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PMID:Treatment of massive acute pulmonary embolism. The use of low doses of intrapulmonary arterial streptokinase combined with full doses of systemic heparin. 333 89

In 1933 Streptokinase (SK) was isolated from bacterial strains of haemolytic Streptococci. Since then it has become the widest spread drug for fibrinolysis. SK, a protein, consists of 415 aminoacids and has a molecular weight of 47,000u. Together with the plasminogen (PLG) of the blood it forms activator complexes, which then convert other PLG molecules of the blood to plasmin. Plasmin attacks and dissolves fibrin deposits. As a substance produced by bacteria SK stimulates antibody formation in the body, the titer will increase during therapy, and SK lysis should be terminated after 6 days of treatment. Usually SK is administered intravascularly to treat a wide range of diseases, associated with pathological activation of hemostasis, like deep vein thrombosis, pulmonary embolism, myocardial infarction etc.. Contraindications can be traced back to the effects of SK on coagulation and the immune system. Bleeding is the most common side effect, but also a few anaphylactic reactions, caused by massive antigen-antibody precipitation have been observed. The rate of lethality of the treatment was established at 0.7% of the cases. To reduce the incidence of side effects modifications of the drug have been proposed, such as activator complex, light B chain SK, and acylated activator therapy. Compared with Urokinase, SK shows a higher rate of side effects, especially in the field of the immune system. Therapy with Urokinase can be controlled more easily. Nevertheless because of considerable price differences and logistics, SK is preferred in Europe and the USA. If strict guidelines in therapeutic use are followed, the rate of side effects of the drug can be curtailed and will be comparable to those of Urokinase.
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PMID:Review and current status of thrombolytic therapy with streptokinase. 354 44

One hundred and eight patients with phlebographically verified deep venous thrombosis were treated with streptokinase. Total or partial thrombolysis was phlebographically demonstrated in 60 patients (55.6%). Three patients died during treatment, all from pulmonary embolism. Six patients developed clinical signs suggestive of pulmonary embolism. In 16 patients (14.8%), major bleeding complicated the treatment. One patient had anaphylactic shock, while various allergic reactions were recorded in 22. Streptokinase therapy in the routine management of deep venous thrombosis carries an acceptable efficacy and safety similar to what has been achieved under research conditions.
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PMID:Streptokinase therapy in the routine management of deep venous thrombosis in the lower extremities. A retrospective study of phlebographic results and therapeutic complications. 370 3

Streptokinase was given to a patient with an unsuspected left ventricular aneurysm as treatment for acute pulmonary embolism. After 2 days of therapy, a large thrombus dislodged from the left ventricular aneurysm and produced an acute saddle embolic occlusion of the abdominal aorta. Detection of mural thrombi by two-dimensional echocardiography in patients with evidence of previous myocardial infarction might prove helpful in identifying those at risk for this complication of streptokinase therapy.
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PMID:Saddle embolism of the aorta. A complication of streptokinase therapy. 371 1

The case of a young man hospitalised for bilateral lower limb deep vein thrombosis is reported. None of the usual causes were found after systematic wide-ranging investigation. The only abnormality on admission was a spontaneous increase in the cephalin-kaolin time to 65 seconds compared to a control time of 40 seconds. Measurements of the clotting factors showed a moderate and isolated deficiency in factor XII (30 p. 100), also present in a brother (50 p. 100) and a sister (42.5 p. 100). Fibrinolytic therapy was administered : an initial course of Streptokinase was followed by extension of a left femoral vein thrombosis and pulmonary embolism. Two courses of Urokinase were given with an eight day interval without significantly improving the venous circulation. This case is an example of thrombogenic disease due to a deficiency of a clotting factor resulting in non-activation of physiological fibrinolysis.
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PMID:[Thrombophlebitis and pulmonary embolism in congenital factor XII deficiency]. 392 76

Correctly diagnosing pulmonary embolism in the ICU can be very difficult, especially when cardiopulmonary disease is coexistent but unrelated. This study describes four hemodynamically unstable patients in whom pulmonary hypertension and an inability to obtain a wedge pressure during balloon flotation catheterization suggested total embolic occlusion of a major pulmonary artery segment distal to the catheter. The diagnosis was confirmed by angiography performed via the flotation catheter in three patients, and by a perfusion scan in one patient. Streptokinase was infused directly into the pulmonary artery of two patients, resolving the pulmonary hypertension and occlusion in both.
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PMID:"Failure to wedge" and pulmonary hypertension during pulmonary artery catheterization: a sign of totally occlusive pulmonary embolism. 400 94


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