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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heparin, a negatively charged sulphated glycosaminoglycan, is clinically the most important antithrombotic drug. Heparin augments the inhibitory activity of antithrombin (AT) towards thrombin, factor Xa (FXa) and other activated clotting enzymes. Tissue factor pathway inhibitor (TFPI) is an endogenous heparin releasable three domain Kunitz-type coagulation inhibitor which inhibits the crucial tissue factor-factor VIIa (TF-FVIIa) dependent coagulation pathway in the presence of FXa. The importance of the TF-FVIIa pathway and TFPI has recently been reviewed (1). TFPI is located to different vascular pools, the largest being the vascular endothelium from where TFPI can be released dose-dependently to the blood by heparins (2). TFPI is speculated to contribute to the anticoagulant properties of heparins, but to which degree is not yet fully understood. In recent years low molecular weight heparins (LMWH) have proven to be effective and safe both for prophylactic (3) and therapeutic treatment (4) of deep vein thrombosis (DVT). Protamine is the least toxic and clinically most commonly used antidote to heparin. However, in vitro and in vivo LMW heparinized blood is not fully neutralized by protamine, as substantial anti-Xa activity remains following neutralization (5). This post-protamine effect has been shown to be partly TFPI dependent when measured in a dilute TF-dependent assay (6,7). We undertook this in vivo study on healthy volunteers in order to investigate whether TFPI released by UH or LMWH (intravenous (iv) or subcutaneous (sc)) remains in the circulation following neutralization of the heparin activity with protamine sulphate (PS). We measured TFPI by three different methods-chromogenic activity, anticlotting activity and a new antigen assay specific for full-length and three-domain TFPI.
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PMID:The effect of protamine sulphate on plasma tissue factor pathway inhibitor released by intravenous and subcutaneous unfractionated and low molecular weight heparin in man. 918 23

Intermittent pneumatic compression has been established as a method of clinically preventing deep vein thrombosis, but the mechanism has not been documented. This study observed the effects of intermittent pneumatic compression of legs on the microcirculation of distant skeletal muscle. The cremaster muscles of 80 male rats were exposed, a specially designed intermittent pneumatic-compression device was applied to both legs for 60 minutes, and the microcirculation of the muscles was assessed by measurement of the vessel diameter in three categories (10-20, 21-40, and 41-70 microm) for 120 minutes. The results showed significant vasodilation in arterial and venous vessels during the application of intermittent pneumatic compression, which disappeared after termination of the compression. The vasodilation reached a maximum 30 minutes after initiation of the compression and could be completely blocked by an inhibitor of nitric oxide synthase, NG-monomethyl-L-arginine (10 micromol/min). A 120-minute infusion of NG-monomethyl-L-arginine, beginning coincident with 60 minutes of intermittent pneumatic compression, resulted in a significant decrease in arterial diameter that remained at almost the same level after termination of the compression. The magnitude of the decrease in diameter in the group treated with intermittent pneumatic compression and NG-monomethyl-L-arginine was comparable with that in the group treated with NG-monomethyl-L-arginine alone. The results imply that the production of nitric oxide is involved in the positive influence of intermittent pneumatic compression on circulation. It is postulated that the rapid increase in venous velocity induced by intermittent pneumatic compression produces strong shear stress on the vascular endothelium, which stimulates an increased release of nitric oxide and thereby causes systemic vasodilation.
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PMID:Intermittent pneumatic compression of legs increases microcirculation in distant skeletal muscle. 1007 52

Deep venous thrombosis is initiated primarily in the pockets of the valves of the veins of the lower limbs and the main pelvic veins. In addition to a genetic predisposition there are several acquired conditions associated with deep venous thrombosis such as major surgery, trauma, cancer, pregnancy, and immobilization. While major diseases as well as hormonal changes have been shown to cause changes in blood coagulation and fibrinolytic factors, the impact of immobilization per se is much less clear. It has been shown that in the absence of intermittent pulsatile flow the blood within the valve pockets became rapidly hypoxic when undisturbed during streamline flow (i.e. when "static"). Hypoxia on the other hand has been shown to cause procoagulatory changes of the vascular endothelium (e.g. production of platelet activating factor [PAF], expression of tissue factor), adhesion and activation of leukocytes and expression of tissue factor on their surface, as well as the activation of platelets. Together with reduced removal and/or inactivation of active clotting factors these mechanisms might contribute to the development of deep venous thrombosis during immobilization.
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PMID:[Pathophysiology of immobilization]. 1037 18

Low-molecular-weight heparins (LMWH) are widely used as antithrombotic prophylactic pharmaceutical agents in orthopedic and general surgery. Their antithrombotic characteristics are expressed by plasma mediators such as anti-Xa, anti-IIa, and increased release of tissue factor pathway inhibitor (TFPI) from vascular endothelium. The purpose of this clinical research is to study the relation between plasma levels of these mediators and postoperative bleeding. Forty-one consecutive patients undergoing hip or knee arthroplasty (n = 36) and colectomy (n = 5) received the standard enoxaparin (a LMWH) dose preoperatively (general surgery) or immediately postoperatively (orthopedic surgery). Major bleeding was defined as a postoperative drop of > or = 5 g/dL) of hemoglobin. The authors observed that there was a linear relationship between an increase in free/total TFPI ratio levels and postoperative bleeding. When that ratio increased by > 60%, the hemoglobin dropped to > 5 g/dL (n = 17). This relationship between free/total TFPI ratio increase and postoperative bleeding was statistically significant (P < 0.001). Those who did not bleed (hemoglobin drop was less than 5 g/dL) (n = 24) had a ratio increase (if any) of less than 50%. However, the authors did not observe any statistical relationship between anti-Xa, anti-IIa, or prothrombin time and postoperative bleeding in patients receiving LMWH for deep vein thrombosis prophylaxis in orthopedic and general surgery patients. The authors recommend a pre- and postoperative ratio level measurement whenever major bleeding is anticipated, as adjustments of LMWH dose or frequency might be necessary.
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PMID:Plasma tissue factor pathway inhibitor levels as a marker for postoperative bleeding after enoxaparin use in deep vein thrombosis prophylaxis in orthopedics and general surgery. 1119 Sep 8

Patients with cancer are frequently treated with anticoagulants, including heparins, to treat or to prevent thrombosis. Recent randomized trials that compared low molecular weight heparin to unfractionated heparin for the treatment of deep vein thrombosis have indicated that heparins affect survival of patients with cancer. Experimental studies support the hypothesis that cancer progression can be influenced by heparins, but results of these studies are not conclusive. Heparins are negatively charged polysaccharides that can bind to a wide range of proteins and molecules and affect their activity. As a consequence, heparins have a wide variety of biological activities other than their anticoagulant effects, which may interfere with the malignant process. In the present systematic review, we critically evaluate experimental studies in which heparins have been tested as anti-cancer drugs. All animal studies, published between 1960 and 1999, that report effects of heparins on growth of subcutaneously implanted tumors, spontaneous metastasis or experimentally induced metastasis are reviewed. In addition, we discuss mechanisms by which heparins potentially exert their activity on various steps in cancer progression and malignancy related processes. It is shown that heparins can affect proliferation, migration, and invasion of cancer cells in various ways and that heparins can interfere with adherence of cancer cells to vascular endothelium. Moreover, heparins can affect the immune system and have both inhibitory and stimulatory effects on angiogenesis. Because of the wide variety of activities of heparins, it is concluded that the ultimate effect of heparin treatment on cancer progression is uncertain.
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PMID:The complex effects of heparins on cancer progression and metastasis in experimental studies. 1117 40

Low-molecular-weight heparins (LMWH) are widely used as antithrombotic prophylactic pharmaceutical agents in orthopedic and general surgery. Their antithrombotic characteristics are expressed by plasma mediators such as anti-Xa. anti-IIa, and increased release of tissue factor pathway inhibitor (TFPI) from vascular endothelium. The purpose of this clinical research is to study the relation between plasma levels of these mediators and postoperative bleeding. Forty-one consecutive patients undergoing hip or knee arthroplasty (n = 36) and colectomy (n = 5) received the standard enoxaparin (a LMWH) dose preoperatively (general surgery) or immediately postoperatively (orthopedic surgery). Major bleeding was defined as a postoperative drop of > or = 5 g/dL) of hemoglobin. The authors observed that there was a linear relationship between an increase in free/total TFPI ratio levels and postoperative bleeding. When that ratio increased by >60%, the hemoglobin dropped to >5 g/dL (n = 13). This relationship between free/total TFPI ratio increase and postoperative bleeding was statistically significant (P < 0.001). Those who did not bleed (hemoglobin drop was less than 5 g/dL) (n = 28) had a ratio increase (if any) of less than 50%. However, the authors did not observe any statistical relationship between anti-Xa, anti-IIa, or prothrombin time and postoperative bleeding in patients receiving LMWH for deep vein thrombosis prophylaxis in orthopedic and general surgery patients. The authors recommend a pre- and postoperative ratio level measurement whenever major bleeding is anticipated, as adjustments of LMWH dose or frequency might be necessary.
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PMID:Plasma tissue factor pathway inhibitor levels as a marker for postoperative bleeding after enoxaparin use in deep vein thrombosis prophylaxis in orthopedics and general surgery. 1103 May 26

Deep vein thrombosis (DVT) and pulmonary embolism (PE) are distinct but related aspects of the same dynamic disease process known as venous thromboembolism (VTE). An estimated 200,000 new cases occur in the United States every year, including 94,000 with PE, resulting in an incidence of 23 per 100,000 patients per year-cases. Without treatment, pulmonary embolism is associated with a mortality rate of approximately 30%, causing nearly 50,000 deaths per year. Moreover, based on post-mortem studies, two-thirds of the patients with pulmonary emboli remain undiagnosed. Clinically, PE may present as (1) isolated dyspnea, (2) pleuritic pain and/or hemoptysis, and (3) circulatory collapse. However, clinical history and examination can be notoriously misleading in reaching a diagnosis. A number of acquired etiologic risk factors (predispositions) are associated with a tendency to develop VTE. These include increasing age, immobilization, surgery, trauma, hospital or nursing home confinement, malignancy, neurologic disease with extremity paresis, as well as certain types of oral contraception and hormone replacement therapy. In addition, a variety of genetic risk factors, such as factor V Leiden, protein S or C deficiency have also been identified. However, in at least half of the instances, no predisposing factors can be identified (idiopathic PE). In the majority of cases thromboemboli originate in the deep veins of the calf or pelvis. The pathogenic conditions for VTE comprise a triad of factors and include (1) venous stasis, (2) hypercoagulable states, and (3) vascular endothelium injury. Occlusion of pulmonary arteries has variable and transient clinical and pathophysiologic consequences, involving both mechanical and reflex effects of vascular occlusion with a consecutive perfusion defect as well as the release of vasoactive and other inflammatory mediators. The objectives of this article are to present an overview of the etiologic and pathogenic factors promoting VTE as well as the pathophysiologic and inflammatory processes following PE.
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PMID:Principle mechanisms underlying venous thromboembolism: epidemiology, risk factors, pathophysiology and pathogenesis. 1258 87

Catheter-related deep venous thrombosis is a complication that can occur in patients receiving chemotherapy. Three such cases are described and a review of the literature is made, focusing on recent results regarding possible thrombogenic mechanisms and the high prevalence of non-symptomatic thrombosis as well as the high morbidity and mortality associated with upper extremity deep venous thrombosis. Special emphasis is given to the cytotoxic effects of 5-fluorouracil on vascular endothelium and the likely link to thrombotic complications. The possible differences between two different methods of administering chemotherapy, continuous infusion and bolus dose administration, in this regard are briefly discussed. It is concluded that the first steps towards an understanding of the mechanisms behind the vascular effects of 5-fluorouracil have been taken. Much remains to be done before active interaction with the pathogenic processes leading to vascular and cardiac complications can be realized, yet various forms of anticoagulant therapy could well be an efficient form of prophylaxis.
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PMID:Upper extremity deep venous thrombosis in patients with 5-fluorouracil-containing adjuvant chemotherapy--three case reports and a review. 1506 28

Deep vein thrombosis (DVT) can be the result of coagulation pathway defects at the molecular level or damage to the vascular endothelium. Some of the acquired causes of DVT include malignancy, trauma, prolonged immobilization, and pregnancy (1). Thrombophilia can be owing in part to both acquired and inherited defects. The relative risk for thrombosis is increased by estrogen replacement therapy (2) and homocysteinemia (3). Homocysteine metabolism is influenced by the use of alcohol, anticonvulsant drugs, cyclosporine, methotrexate, inadequate dietary vitamin B(12), folate and pyridoxine intake, organ transplantation, and reduced creatinine clearance (4-8). Similar to venous thrombosis, homocysteinemia has genetic factors that influence susceptibility (9-11).
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PMID:Molecular diagnosis of hereditary thrombotic disorders. 2137 Jan 57

The pathophysiology of venous thrombosis is classically attributed to alterations in one or more components of Virchow's triad: hypercoagulability, stasis, and damage to the vascular endothelium. Deep vein thrombosis (DVT) may lead to pulmonary thromboembolism (PE), and the latter is culpable for many deaths annually in the United States; however, DVT as a complication of uterine leiomyoma has rarely been reported. We report a case of a 57-year-old woman whose death was due to a large pedunculated subserosal leiomyoma externally compressing the pelvic veins resulting in stasis and venous thrombosis leading to fatal PE. The association of large pelvic masses with venous thrombosis has clinical implications, since prophylactic surgery could be life-saving.
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PMID:Sudden Death by Pulmonary Thromboembolism due to a Large Uterine Leiomyoma with a Parasitic Vein to the Mesentery. 2558 72


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