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Deep venous thrombosis anticoagulants

Of 256 patients with myeloma randomized to thahdomide or not, 221 received no prophylactic anticoagulation and 35 received low-dose warfarin 1 mg/day (31). The incidence of deep venous thrombosis was higher in those who took thahdomide (hazard ratio 4.5). Warfarin did not reduce the risk, and prophylactic subcutaneous enoxa-parin 40 mg/day was therefore introduced in 68 patients of a subsequent group of 130 patients who received thalidomide. This intervention eliminated the difference in the incidence of deep venous thrombosis between those who took thalidomide and those who did not. [Pg.3345]

Agnelli G, Prandoni R Gabriella M, et al. Three months versus one year of oral anticoagulant therapy for idiopathic deep venous thrombosis. N Engl J Med 2001 345 165-169. [Pg.412]

Heparin is an anticoagulant that inhibits reactions that lead to clotting. It is indicated in prophylaxis and treatment of venous thrombosis and its extensions, pulmonary embolism (PE), peripheral arterial embolism, and atrial fibrillation with embolization diagnosis and treatment of acute and chronic consumption coagulopathies (DIC) and prevention of postoperative deep venous thrombosis. [Pg.320]

Anticoagulants are given to patients who are at risk for deep venous thrombosis and pulmonary embolism. These patients may have had a myocardial infarction (MI, heart attack), a cerebrovascular accident (CVA or stroke), or have an artificial heart valve. [Pg.388]

In 14 clinical trials of prothrombin complex concentrates for reversal of oral anticoagulation therapy, seven of 460 patients (1.5%) had thrombotic events, three thrombotic strokes, two cases of deep venous thrombosis, and two non-Q-wave myocardial infarctions [31 ]. However, in 40 patients taking oral anticoagulants, who needed cardiopulmonary bypass surgery, and of whom 20 were treated with prothrombin complex concentrates, no thrombotic events occurred [35 ]. [Pg.519]

Anabolic androgenic steroids have been reported to have anticoagulant and profibrinolytic effects in people with protein C deficiency. However, despite these supposed antithrombotic effects, a 19-year-old male athlete with protein C deficiency developed proximal deep venous thrombosis and pulmonary embolism while abusing anabolic androgenic steroids and had repeated venous thromboembolic events during treatment with low-molecular-weight heparin [36 ]. [Pg.672]

Superficial venous thrombosis, which is also known as superficial thrombophlebitis, refers to thrombus located in the large or small saphenous veins or in superficial varicosities. This condition does not have the same clinical implications as deep venous thrombosis and, when the deep system is not involved, can be treated with only heat and anticoagulation drugs (aspirin). The thrombosis of the superficial venous system is more easily recog-... [Pg.768]

Venous thrombi (red thrombi) are formed mainly from fibrin in simations where vascular stasis exists or in hypercoagulability states. Here the symptoms consist of deep vein thrombosis with the risks of pulmonary embolism and the mainstay of therapy is anti-coagulation with heparin and oral anticoagulants. [Pg.370]

The anticlotting drugs are used in the treatment of myocardial infarction and other acute coronary syndromes, atrial fibrillation, ischemic stroke, and deep vein thrombosis (DVT). The anticoagulant and thrombolytic drugs ate effective in treatment of both venous and arterial thrombosis. Antiplatelet dmgs are used primarily for treatment of arterial disease. [Pg.304]

Venous thromboembolism (VTE) is a complicating condition responsible for high morbidity and mortality in North America and Europe. This disease commonly is linked to advanced age but has both hereditary and acquired risk factors, such as surgery, any form of trauma, and childbirth, associated with it. It encompasses the conditions of deep vein thrombosis (DVT) and pulmonary embolism. In excess of 60,000 deaths annually are attributed to pulmonary embolism. Preventative therapy consists of the use of two different classes of antithrombotic agents, namely anticoagulants and antiplatelet drugs (1,2). [Pg.1209]

Comparative studies Rivaroxaban has been compared with standard anticoagulation (low-molecular-weight heparin followed by warfarin) in patients with acute deep vein thrombosis, who were randomized either to rivaroxaban 15 mg bd for 3 weeks followed by 20 mg/day or to standard anticoagulation for 3-12 months [47. Rivaroxaban was non-inferior to standard anticoagulation in preventing recurrent venous thrombosis (HR=0.68 95% Cl=0.44,1.04). The principal safety outcome was a combination of major or chnically relevant non-major bleeding, and this end-point occurred at a similar rate in patients t ing rivaroxaban or standard anticoagulant therapy (HR =0.97 95% Cl = 0.76,1.2). [Pg.546]

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]


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See also in sourсe #XX -- [ Pg.576 ]




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Anticoagulation

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Thrombosis, anticoagulation

Venous thrombosis

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