Venous thrombosis Subject

In light of earlier evidence that genetic variations in prothrombin of human subjects are clearly associated with the risk of venous thrombosis, and before the results of HERS were known, investigators initiated a case-control study to assess whether prothrombotic mutations modify the association between HRT and the incidence of first MI. Cases were 232 postmenopausal women aged 50 to 79 years who had their first nonfatal MI between 1995 and 1998. 

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. 

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... 

In hormone replacement therapy, the risk of deep vein thrombosis is increased by a factor of 2-4 (35-37). The absolute increase in the treated population as a whole is low, with about one case of venous thromboembolism in 5000 women-years of use of hormone replacement therapy. However, in the subgroup with pre-existing risk factors, such as obesity, varicose veins, smoking, and a prior history of venous thromboembolism or superficial thrombophlebitis, the increase in risk from hormone replacement therapy can be substantial among these women are those with a genetic predisposition to thrombosis, generally due to some form of thrombophilia, such as deficiency of the coagulation inhibitors protein S, protein C, or anti thrombin III. In any of these subjects thrombosis can occur early in hormone replacement therapy. However, this tendency to early occurrence of deep vein thrombosis also seems to be present in all those who take hormone replacement therapy. 

Inhibition of plasminogen by tranexamic acid and aminocaproic acid could theoretically facilitate the development of thrombosis, but whether it actually does so has been the subject of contradictory reports. Episodes of venous and arterial thrombosis have been reported in association with treatment using either tranexamic acid or aminocaproic acid. These include thrombosis at unusual sites such as mesenteric thrombosis (36), the aorta (37), retinal artery occlusion (38), and intracranial arterial thrombosis (39 1), as well as deep-vein thrombosis in the legs (42). 

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