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Thromboembolism streptokinase

Streptokinase + 35% +++/+ Infusion over 60 minutes 613 Pulmonary embolism, deep vein thrombosis, arterial thromboembol ism, clearance of an occluded arteriovenous catheter... [Pg.97]

Plasminogen, an inactive precursor, is activated to plasmin which as a protease is able to break down fibrin clots. The thrombolytic agents in use promote the conversion of plasminogen to plasmin at the site of a thrombus. Indications include post-myocardial infarction treatment. The thrombolytic must be administered within 6 hours for an optimal effect. Other indications are treatment of acute pulmonary thromboembolism, deep-vein thrombosis, acute arterial thrombosis and thromboembolism, as well as in the clearance of arteriovenous catheters and can-nulae. Agents are streptokinase, anistreplase, urokinase, alteplase, reteplase and tenecteplase. [Pg.374]

The incidence of hemorrhagic complications is particularly high when high doses of streptokinase are used in the treatment of deep venous thrombosis (31). High-dose streptokinase thrombolysis for 2-3 days with an initial dose of 500 000 units followed by a maintenance dose of 3 600 000 U/day led to a 10% rate of major spontaneous bleeding complications, with a fatal outcome in four older subjects out of the total of 98 patients. The fatahty rate of bleeding caused by streptokinase amounts to 7% in patients with peripheral arterial occlusion, but is much lower in younger patients with venous thromboembolism. [Pg.3404]

Streptokinase is administered by intravenous or intra-arterial infusion in the treatment of thromboembolic disorders, e.g. pulmonary embolism, deep vein thrombosis and arterial occlusions. It is also used in acute myocardial infarction. [Pg.446]

A study in coronary patients has shown that fibrinogen levels are Increased over normal controls ° and that fibrinolytic activity is also decreased in these patients.The rate of degradation of fibrinogen is inhibited in rats fed an atherogenic diet. It would seem reasonable then that some control over the clinical outcome of atherosclerosis could be had by the use of fibrinolytic agents. The enzymes streptokinase and urokinase continue to be evaluated with some benefits reported in the therapy of acute Thromboembolism.Phenformin is still the only drug of interest as a fibrinolytic agent other than the enzymes and CPIB mentioned earlier. [Pg.194]

Streptokinase Superoxide dismutase Actynomycete Activates plasminogen to plasmin dissolution of blood clots in thromboembolic patients Convert oxygen free radicals into oxygen and hydrogen peroxide wound healing, potential treatment of several diseases Hoflnieister et al. (1998) Noor et al. (2002) and Paramonov et al. (2005)... [Pg.30]

A variety of clinical states are associated with thrombosis. The present discussion is limited to a few of the more prominent thromboembolic diseases further Information on this subject may be found in several reviews.3,7-9 The most common clinical states which Involve clot-like, venous thrombi are deep vein thrombosis, particularly as a postsurgical complication, and pulmonary embolism. Anticoagulants such as heparin and the coumarins have been known for years to be effective in the prevention of these types of thrombi and more recent experience has demonstrated the efficacy of fibrinolytic agents such as streptokinase for their dissolution.3,9 Platelet aggregation Inhibitors have only recently been evaluated clinically in the prevention of venous thrombosis. These studies are crucial to the resolution of the controversy as to whether platelets play a vital role in the initiation of venous thrombi.10 There is persistent histological evidence that indicates venous thrombi begin as platelet aggregates.H Myocardial infarction and stroke are... [Pg.78]

Although streptokinase is antigenic and frequently pyrogenic, these effects have not been sufficiently deleterious to preclude clinical utility.Clinical experience with this agent has been gained now in most types of thromboembolic diseases,85 with generally favorable results in the treatment of deep vein thrombosis (within 96 hours of onset of symptoms) and pulmonary embolism.9,85,86 A major effort has been expended in recent years to Investigate the usefulness of streptokinase in myocardial infarction, but results in this area are still open to ques tion.13 > 85,87-90... [Pg.85]

A therapeutic regimen that usually controls haemorrhage involves discontinuation of enzyme treatment, administration of e-aminocaproic acid in a dose of 100 mg/kg body weight by slow intravenous injection, and blood transfusion (F). It is important to remember that the risk of thrombolytic therapy is not only haemorrhage but also thromboembolism. In one group of 93 patients with deep vein thrombosis treated by streptokinase infusion, a patient died of pulmonary embolism 8% of the patients in all experienced a less serious embolism (11 ). Eight cases of embolism, 4 of them with a fatal outcome, were seen in a series of 80 treated with streptokinase (18 ). [Pg.243]


See other pages where Thromboembolism streptokinase is mentioned: [Pg.362]    [Pg.362]    [Pg.362]    [Pg.212]    [Pg.459]    [Pg.132]    [Pg.305]   
See also in sourсe #XX -- [ Pg.243 ]




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