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At least 19 recordsLinked to original sources
PubMed1975

Radioisotope detection of venous thrombosis. Venous scan vs fibrinogen uptake test.

Experience with the fibrinogen uptake test and the technetium Tc 99m albumin aggregated venous scan in 89 patients showed the latter to be adequate for simultaneous screening for plumonary embolism and venous thrombosis of the lower extremities and pelvis. Because the fibrinogen uptake test differentiated active from inactive venous thrombosis, it is indicated when anticoagulation is considered for patients with a history of thrombophlebitis and equivocal clinical findings of acute activity. It can also be used to monitor high-risk patients and to detect proximal propagation of thrombi. The results of the technetium venous scan were abnormal in 97% of patients with venous thrombosis and the fibrinogen uptake test detected 100% of patients with acute activity. Both tests react to different aspects of the thrombotic disease, thus complementing each other. Because of their reliability, indications for phlebography are now less frequent.

Albumins↗
PubMed2001

Genetic risk factors of venous thrombosis.

Venous thrombosis, whose main clinical presentations include deep vein thrombosis and pulmonary embolism, represents a major health problem worldwide. Numerous conditions are known to predispose to venous thrombosis and these conditions are commonly referred to as risk indicators or risk factors. Generally accepted or "classically" acquired risk factors for venous thromboembolism include advanced age, prolonged immobilisation, surgery, fractures, use of oral contraceptives and hormone replacement therapy, pregnancy, puerperium, cancer and antiphospholipid syndrome. In addition to these well-established risk factors for venous thrombosis, several lines of evidence that have emerged over the past few decades indicate a role of novel genetic risk factors, mainly related to the haemostatic system, in influencing thrombotic risk. The most significant breakthrough has been the confirmation of the concept that inherited hypercoagulable conditions are present in a large proportion of patients with venous thromboembolic disease. These include mutations in the genes that encode antithrombin, protein C and protein S, and the factor V Leiden and factor II G20210 A mutations. Moreover, plasmatic risk indicators, such as hyperhomocysteinemia and elevated concentrations of factors II, VIII, IX, XI and fibrinogen, have also been documented. This extensive list of genetic and acquired factors serves to illustrate that a single cause of venous thrombosis does not exist and that this condition should be considered as a complex or multifactorial trait. Complex traits can be understood by assuming an interaction between different mutations in candidate susceptibility genes. The risk that is associated with each genetic defect may be relatively low in isolation but the simultaneous presence of several mutations may dramatically increase disease susceptibility. Moreover, environmental factors may interact with one or more genetic variations to add further to the risk. The analysis of genetic risk factors and plasmatic factors, together with private life style and environmental factors, has contributed significantly to our understanding of the genetic predisposition to venous thrombosis.

Antithrombins↗
PubMed1986

Epidemiology and pathogenesis of venous thrombosis.

Venous thrombi are intravascular deposits composed predominantly of fibrin and red blood cells with a variable platelet and leukocyte component. They frequently arise in large venous sinuses in the calf, in valve cusp pockets either in the deep veins of the calf or thigh or in venous segments that have been exposed to direct trauma. Venous thrombosis can be produced experimentally by a combination of stasis and systemic hypercoagulability or by stasis and endothelial damage. Thrombosis is augmented if the fibrinolytic mechanism is inhibited or defective. A number of clinical conditions and laboratory abnormalities are associated with and predispose to venous thrombosis and, in many of these, it is possible to identify one or more of the thrombogenic factors discussed. Venous thromboembolism (venous thrombosis and pulmonary embolism) is a serious and potentially fatal disorder that usually complicates the course of sick hospitalized patients, but occasionally affects ambulant and otherwise healthy individuals. Screening studies with iodine-125 fibrinogen leg scanning, impedance plethysmography and perfusion lung scanning have shown that the majority of venous thrombi and pulmonary emboli that occur in hospitalized patients are small and asymptomatic, and it is likely that most are clinically insignificant. In bedridden patients, most thrombi commence in the calf and are asymptomatic. When a calf vein thrombus extends into the proximal venous segment, the risk of clinically significant pulmonary embolism increases. Less is known about the incidence and clinical significance in a nonhospital population; although asymptomatic disease occurs, its frequency is unknown. In contrast to the patients with asymptomatic venous thrombosis, symptomatic patients with venous thrombosis usually have large occulsive thrombi localized in their proximal veins.

Blood Circulation↗
PubMed2002

Interaction between hyperhomocysteinemia, mutated methylenetetrahydrofolatereductase (MTHFR) and inherited thrombophilic factors in recurrent venous thrombosis.

Venous thrombosis is a multicausal disease involving acquired and genetic factors. In this study we investigated a possible interaction between hyperhomocysteinemia (fasting or postload) and factor V Leiden or prothrombin G20210A on the risk of recurrent venous thrombosis. We also looked at the risk due to mutations in the MTHFR-gene (C677T and A1298C). We performed a case-control study in 171 patients with a history of recurrent venous thrombosis and 461 control subjects from the general population. Hyperhomocysteinemia (fasting or 6 h after an oral methionine load) was defined as a homocysteine concentration above the 90th percentile of the distributions in the control group. The odds ratio (adjusted for age and sex) for recurrent venous thrombosis was 1.8 (95% CI: 1.1 to 3.0) for fasting hyperhomocysteinemia, 5.1 (95% CI: 3.0 to 8.6) for factor V Leiden and 1.8 (95% CI: 0.7 to 4.2) for prothrombin G20210A. We found 14 patients and 3 controls with both hyperhomocysteinemia and factor V Leiden, which yielded an odds ratio of 11.6 (95% CI: 3.2 to 42.5). We found no interaction between hyperhomocysteinemia and prothrombin G20210A. The relative risk for MTHFR 677CT was 1.6 (95% CI: 1.1 to 2.4) and for MTHFR 677TT was 1.4 (95% CI: 0.7 to 2.8). The combined risk for MTHFR 677TT and factor V Leiden was 18.7 (95% CI: 3.3 to 108). We conclude that hyperhomocysteinemia and factor V Leiden are risk factors for recurrent venous thrombosis. The risk of thrombosis appeared high for individuals who had both risk factors.

Adult↗
PubMed1997

The inherited basis of venous thrombosis.

Venous thrombosis represents a manifestation of disordered hemostatic balance. The classical presentation is of pain and swelling of the lower limb, although clinical history and examination are notoriously misleading in reaching a diagnosis. A number of acquired predispositions have been associated with a tendency to thrombosis, such as immobilisation, surgery, malignancy and certain types of oral contraception, but in at least half of the instances no predisposition can be identified. A variety of genetic risk factors have also been identified. Mutations within the genes for antithrombin, protein C and protein S are associated with a venous thromboembolic phenotype. The commonest thrombophilic predisposition however is a variant of coagulation factor V, factor V Leiden, which results from a single amino acid substitution rendering the factor V molecule resistant to activated protein C. Factor V Leiden is present in approximately 5% of individuals of European origin, and is found in up to 40% of those with confirmed venous thrombosis. Increasingly it is recognised that venous thrombosis should be considered a polygenic disorder, with interactions between the various single gene defects which predispose to thrombosis, as well as normal genetic variation between individuals in the levels of both procoagulant and anticoagulant proteins, all determining which individuals will express the phenotype of venous thrombosis.

Antithrombin III↗
PubMed1987

Ischemic forms of acute venous thrombosis.

Venous thrombosis in an extremity, when extensive, can cause reversible tissue ischemia or frank gangrene even without arterial or capillary occlusion. Patients gradually or abruptly develop severe pain, extensive edema, and cyanosis of the extremity, nearly always in the legs. Gangrene can occur unless the venous obstruction is relieved. Such ischemic venous thrombosis can complicate surgery, trauma, childbirth, or prolonged immobility, but malignant neoplasms, either obvious or occult, are a major predisposing factor. The optimal therapy is anticoagulation and thrombectomy. Patients with venous gangrene may require amputation if extensive, deep-tissue destruction occurs. The mortality rate for ischemic venous thrombosis is about 40%, the cause of death usually being the underlying disease or pulmonary emboli.

Arm↗
PubMed2001

Deep venous thrombosis.

Venous thrombosis involving the deep veins is a major US health problem that affects over 2.5 million people annually. The most serious complication of a deep venous thrombosis (DVT) is pulmonary embolism (PE), which is associated with 50,000 to 200,000 deaths each year. DVT and PE are often silent and difficult to detect by clinical examination; however, DVT rarely occurs in the absence of risk factors. This article reviews normal venous anatomy and discusses the etiology of DVT, its clinical manifestations, and diagnosis. Then it reviews treatment of DVT, highlighting the nurse's role. A discussion of DVT prophylaxis based on patient risk follows.

Humans↗
PubMed2001

Mutations at the activated protein C cleavage sites Arg336 and Arg562 of factor VIII in Thai patients with venous thrombosis.

Venous thrombosis is a multicausal disease, more than one genetic risk factor may cooperate to effect thrombotic risk. Factor V Leiden is found to be an important hereditary risk factor for venous thromboembolism. Analogous to factor V Leiden, a point mutation at amino acid positions Arg336 and Arg562 in factor VIII may predispose patients to thrombosis. Eighty-one Thai patients with venous thrombosis and 100 Thai healthy volunteers have been studied. Neither heterozygous nor homozygous mutations were detected both thrombosis patients or normal volunteers. However, further studies with larger samples of venous thrombosis patients are recommended.

Adult↗
PubMed2001

Radiolabeled peptides in the detection of deep venous thrombosis.

Venous thrombosis and pulmonary embolism are major clinical problems that result in significant morbidity and mortality. It is estimated that 600,000 cases of pulmonary embolism occur each year in the United States, resulting in the death of approximately 100,000 patients. Most of these pulmonary emboli arise from deep venous thrombosis (DVT). The clinical diagnosis of DVT is unreliable. Only a third of patients with a clinical suspicion of DVT have objective evidence of the disease, and half of patients with proven DVT do not have any clinical symptoms. Although ascending contrast venography is the present standard for the diagnosis of DVT, duplex ultrasonography, which is increasingly used in combination with color Doppler flow imaging, is accepted as a useful clinical afternative to contrast venography. Both contrast venography and ultrasonography are imaging procedures that detect changes in venous anatomy that are caused by the presence of an intraluminal thrombus that is sufficiently formed either to reduce vascular filling with contrast medium or to resist compression. However, these imaging procedures do not reflect the metabolic activity of the clot, and therefore, they may overestimate the presence of active clots. The sensitivity of ultrasonography is also limited by various disease-related and technical factors. An alternative approach to the diagnosis of acute DVT is to detect a molecular marker of acute DVT that is not present in old, organized DVT. Recent advances in biotechnology permit the use of highly specific synthetic peptide or small molecular markers, which are involved in the acute stages of DVT formation and can be labeled efficiently with 99mTc. 99mTc-apcitide, a glycoprotein (GP IIb/IIIa) receptor antagonist previously known as 99mTc-P280, has been approved recently by the Food and Drug Administration for the clinical detection of acute DVT. Two other agents are currently under clinical investigation: 99mTc-DMP 444, which is another GP IIb/IIIa receptor antagonist, and 99mTc-Fibrin-Binding Domain (FBD), a radio-labeled fibrin-binding domain of fibronectin. Different clinical studies have shown a high diagnostic accuracy with these synthetic 99mTc-labeled peptides in the detection of acute DVT. Although further studies are needed to fully appreciate all of the diagnostic potential of these radiopharmaceuticals, the clinical introduction of 99mTcapcitide scintigraphy will certainly be helpful in expanding the use of nuclear medicine in a specific field in which it used to play a relatively marginal role.

Clinical Trials as Topic↗
PubMed1975

125-I-labeled fibrinogen scanning. Use in the diagnosis of venous thrombosis.

Venous thrombosis is often asymptomatic in patients in whom major pulmonary embolism develops. When used expectantly, iodine 125-labeled fibrinogen scanning is a very sensitive method for detecting subclinical leg vein thrombi. Fibrinogen scanning is less useful for the diagnosis of established venous thrombosis, but is valuable for detecting extension of venographically diagnosed calf vein thrombosis. The technique is safe if fibrinogen is obtained from carefully screened donors. The limitations of the method include its inability to distinguish between superficial and deep venous thrombi, and its sensitivity to fibrin in hematoma and inflammatory exudates. Though the results agree closely with those of phlebography, scanning seems less reliable for detecting femoral vein than calf vein thrombi and is insensitive to thrombi above the inguinal ligament. Screening for these major thrombi may be improved by combining fibrinogen scanning with impedance plethysmography or ultrasonic examination.

Blood Donors↗
PubMedDate not supplied

[Experimental observations on posttraumatic venous thrombosis].

Venous thrombosis had been experimentally induced in dogs by two different ways of trauma: contusion of whole venous wall and stripping of intimal layer. Both ways produced thrombosis in 33% of cases. The Authors describent histological findings of venous wall and thrombi with attention to genesis and evolution of these post-traumatic venous thrombosis.

Animals↗
PubMed2004

Deep venous thrombosis.

Venous thromboembolism (VTE), manifested as either deep venous thrombosis (DVT) or pulmonary embolism (PE), is an extremely common medical problem, occurring either in isolation or as a complication of other diseases or procedures. Yet, despite its frequency, much remains to be learned regarding the pathogenic mechanisms that initiate VTE, about tailoring its treatment to the individual with her/his specific set of risk factors for recurrence, and about its medical management when associated with specific disease entities, such as cancer. These three topics are addressed in this chapter. In Section I, Drs. López and Conde discuss the mechanisms by which venous thrombi may be initiated on the vessel wall in the absence of anatomically overt vessel wall injury. The authors propose a model whereby tissue factor (TF)-bearing microvesicles that arise from cells of monocyte/macrophage lineage can fuse with activated endothelial cells in regions of vessel activation or inflammation and initiate blood coagulation. Key components of this model include docking of the microvesicles to the stimulated endothelium through P-selectin glycoprotein ligand-1 on their surfaces binding to either P-selectin or E-selectin on the endothelium, and the role of hypoxia during blood stasis in initiating local endothelial activation. Elevations in the levels of TF-bearing microvesicles associated with inflammatory conditions would help to explain the increased risk of thrombosis associated with infections and inflammatory states such as inflammatory bowel disease. In Section II, Dr. Clive Kearon discusses the risk factors for recurrent thrombosis and strategies for determining length of therapy and tailoring specific therapies through risk stratification. Those patients who experience VTE in association with a major reversible risk factor such as surgery are much less likely to experience a recurrence when anticoagulation is discontinued than are patients with a persistent risk factor, such as thrombophilia or cancer unresponsive to therapy. Those with a minor reversible risk factor, such as prolonged air travel, have an intermediate risk of recurrence after discontinuance of anticoagulant therapy. The author provides an algorithm for using risk assessment as a means of determining the length and type of therapy to be used to minimize the rate of recurrence while simultaneously diminishing the risk of bleeding associated with anticoagulation. In Section III, Dr. Agnes Lee updates the topic of VTE associated with malignancy. Patients with cancer make up approximately 20% of those presenting with first time VTE, and the presence of VTE forebodes a much poorer prognosis for patients with cancer, likely because of the morbidity associated with VTE itself and because VTE may herald a more aggressive cancer. Recent evidence indicates that low-molecular weight heparins (LMWHs) improve survival in patients with advanced cancer through mechanisms beyond their effect as anticoagulants. Because of their improved efficacy and safety and potential anti-neoplastic effect, the LMWHs have become the anticoagulants of choice for treating VTE associated with cancer.

Heparin, Low-Molecular-Weight↗
PubMed1999

Use of the Amplatz thrombectomy device for severe deep venous thrombosis.

Venous thromboembolism is a significant cause of morbidity in the United States. Thrombectomy devices are not currently the standard of treatment in deep venous thromboses. The Amplatz thrombectomy device is used for arterial occlusions and pulmonary emboli, but its regular use in venous thromboses has not been documented in the literature. We report a unique case of treatment of lower extremity deep venous thrombosis with the Amplatz thrombectomy device.

Catheterization↗
PubMed2005

Inherited risk factors for venous thrombosis.

Venous thrombosis occurs as a consequence of genetic and environmental risk factors. Since the discovery of factor V Leiden, the most common genetic risk factor, there has been intense interest in clarifying the roles of genes and the environment with thrombosis risk. The translation of this risk information to clinical practice is a challenging one in the setting of a rapidly expanding knowledge base that includes application of genetic medicine. There are benefits, but also potential harms, of testing for inherited disorders associated with thrombosis. This paper reviews inherited risk factors for thrombosis and discuss clinical applications of testing.

Environment↗
PubMed2003

Prevalence of factor V Leiden, FII G20210A, FXIII Val34Leu and MTHFR C677T polymorphisms in cancer patients with and without venous thrombosis.

Venous thromboembolism (VTE) is a common complication in patients with malignant disease. In addition to well-established acquired risk factors for VTE, several genetic risk factors, mainly related to the haemostatic system, are known to influence thrombotic risk. However, the contribution of gene abnormalities to thrombotic tendency in cancer patients remains poorly explored. We performed a prospective study to evaluate the prevalence and clinical significance of four gene variations (factor V Leiden [FVL], factor II G20210A, factor XIII Val34Leu and MTHFR C677T) in cancer patients, with and without VTE. Enrolled were 211 unrelated and unselected patients (M/F ratio 0.5, mean age 57 years, range 12-91 years) with a diagnosis of cancer, admitted to two University Oncology Clinics in the city of São Paulo, Southeastern Brazil. After admission, all patients were evaluated for the presence of symptoms and signs of VTE. Sixty-four patients (30.3%) had an episode of deep venous thrombosis (DVT) or pulmonary embolism (PE), which has been objectively verified; 147 patients (69.7%) had no evidence of VTE. FVL was found with a frequency of 1.5% and 2.7% in the VTE and non-VTE group, respectively (odds ratio [OR] for VTE 0.6, 95% CI: 0.06-5.3). FII G20210A was found in 1.5% and 1.3% of thrombotic and nonthrombotic patients, respectively, yielding an OR of 1.2 (95% CI: 0.1-13.1). FXIII Val34Leu was detected in 29.6% of the thrombotic patients and in 28.5% of the non-thrombotic patients (OR 1.1, 95% CI: 0.5-2). MTHFR 677T was present in 53.1% and 60.5% of patients with and without thrombosis, respectively (OR 0.8, 95% CI: 0.4-1.4). The present data do not point to an association between the four polymorphisms here investigated and the risk of VTE in cancer patients.

Adolescent↗
PubMed2005

Venous thromboembolism: diagnosis and management of deep venous thrombosis.

Venous thromboembolism (VTE) affects 1-2 per 1000 people in the general population each year. Clinical diagnosis of deep venous thrombosis (DVT) is unreliable, and must be confirmed by compression ultrasonography or venography. A low clinical pretest probability of DVT and negative D-dimer result reliably exclude the diagnosis, with no need for diagnostic imaging. Initial treatment of DVT is with low-molecular-weight heparin or unfractionated heparin for at least 5 days, followed by warfarin (target INR, 2.0-3.0) for at least 3 months. A vena cava filter is indicated in patients who are ineligible for anticoagulant therapy or who experience embolism despite therapeutic anticoagulation. Thrombolysis or surgical embolectomy may be used as a limb-saving measure in patients with extensive proximal DVT and circulatory compromise that threatens the viability of the leg. Decisions regarding the optimal duration of anticoagulation to prevent recurrent VTE should be individualised and balance the risk of recurrence if warfarin is stopped against the risk of major bleeding and inconvenience of continuing treatment. The risk of recurrence is highest in people with recurrent unprovoked DVT or chronic predisposing factors (eg, cancer) who require indefinite anticoagulant treatment.

Algorithms↗
PubMed2004

Massive deep venous thrombosis and venous gangrene in a 29-year-old case: metastatic epidermoid carcinoma with an unknown primary.

Cancer-associated venous thromboembolism is a severe form of paraneoplastic syndrome. It rarely leads to venous gangrene. We report a case who presented with multiple deep venous thrombosis and venous gangrene of the lower extremity. During the follow-up period, the patient developed bilateral cervical and right supraclavicular lymphadenopathies. The fine needle aspiration of the lymph nodes revealed metastatic epidermoid carcinoma of an unknown primary. Thrombotic manifestations may complicate the clinicopathological course of malignancies.

Adult↗