Disease relevance of Venous Thrombosis

• BACKGROUND: Low-molecular-weight heparin appears to be at least as effective and safe as standard, unfractionated heparin for the treatment of deep-vein thrombosis, but only limited data are available on the use of low-molecular-weight heparin to treat acute symptomatic pulmonary embolism [1].
• CONCLUSIONS: In acute deep-vein thrombosis, reviparin regimens are more effective than unfractionated heparin in reducing the size of the thrombus [2].
• To assess the risk of venous thrombosis associated with hyperhomocysteinemia, we studied plasma homocysteine levels in patients with a first episode of deep-vein thrombosis and in normal control subjects [3].
• Patients with acute proximal deep-vein thrombosis were randomly assigned to receive either intravenous standard heparin in the hospital (253 patients) or low-molecular-weight heparin (1 mg of enoxaparin per kilogram of body weight subcutaneously twice daily) administered primarily at home (247 patients) [4].
• In non-surgical patients hospitalized with acute myocardial infarction and receiving a low-dose heparin regimen, the findings reflect a significant decrease in deep venous thrombosis, though no observations are yet available concerning reductions in pulmonary emboli, mural thrombi, or systemic emboli [5].

Psychiatry related information on Venous Thrombosis

• RESULTS: Eleven of the 120 patients (9.2%) presented with neurologic complications; 7 suffered from ischemic cerebrovascular events, 3 from cerebral venous thrombosis, and 1 had a transient confusional state during high-dose heparin administration [6].
• For the entire study group, deep vein thrombosis was detected by either venography of non-invasive tests in 37 of 64 patients (58%) in the placebo group and in 11 of 65 patients (17%) in the enoxaparin group, a risk reduction of 71%, P less than 0.0001 [7].
• OBJECTIVE: To demonstrate a clinical decision-making process by which to determine if heparin prophylaxis for deep venous thrombosis (DVT) is appropriate in a specific patient with multiple injuries [8].
• Plasma homocysteine is a risk factor for coronary artery disease, stroke, peripheral arterial disease, extracranial carotid arterial disease, aortic atherosclerosis, deep vein thrombosis, and possibly dementia and Alzheimer's disease in older persons [9].

High impact information on Venous Thrombosis

• Low-molecular-weight heparin in patients with deep-vein thrombosis [10].
• Three months versus one year of oral anticoagulant therapy for idiopathic deep venous thrombosis. Warfarin Optimal Duration Italian Trial Investigators [11].
• METHODS: Patients with a first episode of idiopathic proximal deep venous thrombosis who had completed three months of oral anticoagulant therapy (with warfarin, in 97 percent of the cases and acenocoumarol in 3 percent) were randomly assigned to the discontinuation of oral anticoagulants or to their continuation for nine additional months [11].
• Images in clinical medicine. Cerebral venous thrombosis [12].
• We observed 43 episodes of deep-vein thrombosis and 2 episodes of pulmonary embolism in the placebo group, but only 21 episodes of deep-vein thrombosis and no episodes of pulmonary embolism in the enoxaparin group (incidence of thromboembolism, 39 percent and 18 percent, respectively; P<0.001) [13].

Chemical compound and disease context of Venous Thrombosis

• Unfractionated versus low-molecular-weight heparin for deep venous thrombosis [14].
• Among the 1207 patients with interpretable venograms, 231 of 617 patients (37.4 percent) in the warfarin group and 185 of 590 patients (31.4 percent) in the low-molecular-weight-heparin group had deep-vein thrombosis (P = 0.03) [15].
• The association between elevated homocysteine levels and venous thrombosis was stronger among women than among men and increased with age [3].
• Episodes of tremulousness (n = 5, P less than 0.05), which reversed with a decrease in drug dose, and phlebothrombosis (n = 3, P not significant) were limited to the group given acetohydroxamic acid [16].
• Venous thrombosis results from some phenol injections [17].
• Our findings thus indicate that regulation of TF by NF-kappaB transcription factor p50 is essential for the pathogenesis of deep vein thrombosis and suggest that specific inhibitors of p50, such as Andro, may be therapeutically valuable for preventing and perhaps treating venous thrombosis [18].

Biological context of Venous Thrombosis

• Of 170 consecutive symptomatic patients with venographically proven proximal deep-venous thrombosis, 85 received standard heparin (to achieve an activated partial thromboplastin time of 1.5 to 2.0 times the pretreatment value) and 85 LMWH (adjusted only for body weight) for 10 days [19].
• While measurement of BTG in plasma and urine is of limited value in the clinical diagnosis of venous thrombosis, the data indicate platelet activation occurs in venous thrombosis, but is maximal or perhaps limited to the initial phase of thrombus development [20].
• Viral IL-10 gene transfer decreases inflammation and cell adhesion molecule expression in a rat model of venous thrombosis [21].
• BACKGROUND: A low-molecular-weight heparin, enoxaparin sodium, has been shown to be effective and safe in preventing deep vein thrombosis both in general surgery and in high-risk orthopedic surgery [22].
• Two novel (R(-11)C; T394D) and two repeat missense mutations in the protein C gene associated with venous thrombosis in six kindreds [23].

Anatomical context of Venous Thrombosis

• The Leiden factor V mutation is observed in 20% of unexplained lower limb venous thromboses and involves substitution of the arginine residue at position 506 by glutamine (R506Q) [24].
• In the cyclosporin group, 17 thromboembolic complications occurred in 13 patients: 10 pulmonary emboli, 1 renal vein thrombosis, 3 deep vein thromboses, and 3 haemorrhoidal thromboses [25].
• CONCLUSIONS: Administration of the anti-PAI-1 antibody (CLB-2C8) results in increased endogenous thrombolysis and inhibition of thrombus growth in a venous thrombosis model in rabbits and facilitated reperfusion and reduction of reocclusion in a canine model of coronary artery thrombosis [26].
• Central venous catheters and upper-extremity deep-vein thrombosis complicating immune heparin-induced thrombocytopenia [27].
• Three WT mice developed occlusive venous thrombosis an average of 39.7 +/- 1 minutes following the onset of injury, whereas the jugular veins of 4 mice deficient in PAI-1 and 4 deficient in VN occluded 56.7 +/- 5 and 58.7 +/- 2 minutes, respectively, following injury (P <.04 and P <.01 compared to WT mice) [28].

Gene context of Venous Thrombosis

• Using this test, we have now identified six unrelated persons with severe recurrent venous thrombosis who were deficient in protein S, with levels between 15 and 37 per cent while they were not receiving warfarin therapy [29].
• Residual plasminogen activator inhibitor activity after venous stasis as a criterion for hypofibrinolysis: a study in 83 patients with confirmed deep vein thrombosis [30].
• Homozygous cystathionine beta-synthase deficiency, combined with factor V Leiden or thermolabile methylenetetrahydrofolate reductase in the risk of venous thrombosis [31].
• In plasma of patients with recurrent deep vein thrombosis, PAI-1 levels were 44 +/- 20 ng/mL (mean +/- SD, n = 7), during a clinically silent phase [32].
• Sporadic mutations in the thrombomodulin (TM) gene occur in patients with both arterial and venous thrombosis, but the effects of these mutations on expression and function are largely unexplored [33].
• Mildly elevated homocysteine levels as a result of MTHFR 677TT do not seem to cause venous thrombosis [34].

Analytical, diagnostic and therapeutic context of Venous Thrombosis

• Adjusted low-dose heparin prophylaxis appears to be a safe and efficacious method to reduce the frequency of deep-vein thrombosis in patients undergoing total hip replacement [35].
• Sixty-eight patients with acute deep-vein thrombosis confirmed by venography were treated with intravenous heparin and then randomized to secondary prophylaxis [36].
• In 50 patients with suspected deep-vein thrombosis the diagnostic accuracy of standardised clinical examination, doppler ultrasound, impedance plethysmography, and technetium-99m-labelled-fibrinogen scintigraphy (venoscan) was compared with that of X-ray venography [37].
• The application of a completely occlusive tourniquet might be a simple form of prophylaxis against deep-vein thrombosis and would avoid the disadvantages of using heparin [38].
• We did a randomised prospective study of the effect of low-molecular-weight heparin on the incidence of deep-vein thrombosis in patients with minor injuries treated with plaster-cast immobilisation of the leg [39].

References