Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thromboangiitis obliterans (TAO) and antiphospholipid syndrome (APS) share the clinical characteristics of arterial thrombosis and recurrent thrombophlebitis. Although the association of anticardiolipin antibodies (aCLa) and TAO has been previously recognized, the prevalence and the clinical impact of this association remains unclear. aCLa were measured by double ELISA in patients with TAO (n = 47), premature atherosclerosis (pASO) (n=48) and otherwise healthy individuals (n = 48). Antibody status was then compared to clinical presentation and outcomes in patients meeting the diagnostic criteria for TAO. The prevalence of aCLa was significantly higher in patients with TAO (36%) compared to either pASO (8%; p = 0.01) or healthy individuals (2%; p < 0.001). Patients with TAO and a high antibody titer tended to be younger and suffer a significantly higher rate of major amputations compared to those without the antibody (100% versus 17%; p = 0.003). Clinical features of TAO not significantly altered by the presence of aCLa included upper limb involvement, digital necrosis, superficial thrombophlebitis (or deep venous thrombosis). Protein C, protein S, and anti-thrombin III were normal in all individuals. TAO is associated with an increased prevalence of aCLa. The presence of a high antibody titer in these patients is associated with increased morbidity, including major limb amputation. In patients meeting the diagnostic criteria for TAO, screening for aCLa should be considered. Although attractive, the efficacy of chronic anticoagulation in this setting remains to be proven.
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PMID:Antiphospholipid antibodies in thromboangiitis obliterans. 1271 Aug 39

The aim of this study was to verify the degree of atherosclerosis in a group of subjects affected by secondary deep vein thrombosis and in a matched control group. Sixty-three patients were studied. Of these, 19 were cases (mean age 62.2 +/- 1.2) and 16 were controls (mean age 59.3 +/- 2.7). Twenty-eight were excluded because they were affected by hyperhomocysteinemia. The arterial tree was examined by means of echo color Doppler, and the intima media thickness and the presence of and degree of plaques bilaterally in the carotid and femoral artery and abdominal aorta were measured with a computerized method. No difference was found in the 2 groups as concerns intima media thickness or plaques in the arterial district explored. Secondary deep vein thrombosis is not a greater risk factor for atherosclerosis.
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PMID:Atherosclerosis and secondary deep vein thrombosis: a difficult correlation. 1281 80

As blood clots it goes through predictable stages that reflect the oxygenation state of hemoglobin within the red cells. One of these stages results in the formation of methemoglobin. This substance acts an endogenous contrast agent when imaged using a T1-weighted magnetic resonance sequence (Magnetic Resonance Direct Thrombus Imaging, MRDTI) - appearing as high signal. MRDTI can therefore be used to detect subacute thrombosis. This technique has been applied in a number of clinical settings arising as a result of thrombosis. Deep vein thrombosis and pulmonary embolism are both readily detected using MRDTI, providing a single imaging modality for the detection of venous thromboembolic disease. The technique is also effective in the peripheral arterial tree. Furthermore, thrombosis within vessel wall atherosclerosis is a marker of vulnerable plaque likely to produce symptoms. The MRDTI technique has thus proved useful in identifying complicated plaque in the carotid arteries in the setting of transient and permanent cerebral ischemia. MRDTI therefore holds promise as a technique that is capable of detecting high risk vessel wall disease prior to significant or permanent end organ damage. Because of the non-invasive nature of magnetic resonance imaging (MRI), application of MRDTI in the research setting for the monitoring of therapeutic interventions in a wide number of settings within vascular disease is very appealing.
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PMID:Magnetic resonance direct thrombus imaging. 1287 Dec 74

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. Randomized trials are in progress investigating whether multivitamin therapy with folic acid, vitamin B12, and vitamin B6 to reduce plasma homocysteine levels will reduce the risk for atherosclerotic vascular disease.
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PMID:Homocysteine. The association with atherosclerotic vascular disease in older persons. 1451 74

Thromboendarterectomy is performed to treat chronic thromboembolic pulmonary hypertension with obstruction of main, lobar, or segmental pulmonary arteries. The present study evaluated surgical specimens removed between 1990 and 2001. Medical histories and microscopic slides were reviewed in each case. Study slides were stained with hematoxylin and eosin and Verhoeff-van Gieson and evaluated for thrombus, collagen, elastin, atherosclerosis, hemosiderin, calcification, and inflammation. The study group comprised 54 patients (30 women and 24 men), ranging in age from 33 to 77 years (mean, 58 years). Clinically, 28 (52%) had a history of deep leg vein thrombosis and 42 (78%) had a history of pulmonary embolism; 24 (44%) had both events. Coagulation abnormalities were documented in 15 (28%); autoimmune or hematologic disorders, in 8 (15%). Pulmonary thromboendarterectomy was bilateral in 52 patients (96%) and right-sided in 2. Six patients also had obstructions resected from the main pulmonary arteries. Obstruction limited to segmental arteries occurred only in women. Grossly, right-sided specimens were larger than left-sided ones (P = 0.003). Microscopically, ages of thrombi were uniform in 72% and variable in 28%. Intima was thickened in all patients and consisted of collagen (100%), elastin (67%), hemosiderin (56%), inflammation (53%), atherosclerosis (32%), and calcification (15%). We determined that pulmonary thromboendarterectomy was performed most often in middle-aged and elderly patients with a history of deep venous thrombosis or pulmonary embolism. Less than 50% of the patients had an identifiable coagulation, autoimmune, or hematologic abnormality. Most patients had bilateral disease and resections. Right-sided specimens were significantly larger than left-sided specimens, and lower lobe involvement was more common than involvement elsewhere. Resected tissues most commonly exhibited old organized thrombus.
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PMID:Surgical pathology of pulmonary thromboendarterectomy: a study of 54 cases from 1990 to 2001. 1469 15

Genetic susceptibility tests are already advertised on the Internet to identify individuals at above average risk for cardiovascular disease (CVD), such as deep vein thrombosis, hyperlipidemia, or atherosclerosis, whereas other tests claim to predict response to a particular drug treatment. Some kits are available to the public directly, bypassing a doctor. Their value, however, must be considered carefully, because although a genotype may be strongly and consistently associated with an intermediate trait, and because the intermediate trait is a strong predictor of CVD risk, there may be little or no association of genotype with risk over and above that of the measured trait. This is because multigenic effects and environmental modification (context dependency) of genotype effects determine CVD risk. An individual's personal characteristics and plasma risk-trait levels (which reflect both genotype and exposure) at present are the best predictors of clinical outcome. Only when genetic tests surpass this, possibly by the inclusion of many functional common variants, in conjunction with their context-dependent effects on risk, might their usefulness in clinical management be realized. Here we review some of the particular issues and concerns raised by CVD-risk genetic testing, and suggest areas of further research to address these issues.
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PMID:Genetic testing for cardiovascular disease susceptibility: a useful clinical management tool or possible misinformation? 1471 42

Systemic lupus erythematosus (SLE) is a multifactorial polysystemic autoimmune disorder. Although life expectance in SLE has been improved by adequate immune suppressive therapy, the importance of chronic renal failure has not been reduced. Among late complications of the disease accelerated atherosclerosis attempts increasing attention. Dyslipoproteinemia and increased concentration of lipoproteins are important risk factors of atherosclerotic cardiovascular complication in SLE. Serum lipid parameters of 50 patients with lupus were examined in the present work. Thirty patients had histologically proven lupus nephritis (LN+), while the other group did not have renal involvement (LN-). Serum triglyceride, total cholesterol, LDL-C and apolipoprotein B (apoB) concentrations were significantly higher in the lupus nephritis (LN+) group. On the other hand, HDL-C and apoAI levels were also elevated in patients with LN. As a consequence of that, LDL-C/HDL-C and the apoB/apoAI ratios did not differ between patients with or without kidney involvement. This concluded the authors to measure the concentration of lipoprotein (a) in SLE patients, as Lp(a) is known to be an independent risk factor of atherosclerosis. Results indicated a significantly increased Lp(a) concentration in patients with lupus nephritis as compared to the LN- group. All but 2 patients without kidney involvement had lower than 100 mg/L Lp(a) concentration, while 27% of patients with lupus nephritis has an Lp(a) level between 100-300 mg/L. Further more, Lp(a) concentration was higher than 300 mg/L in 13% of the LN+ group. In a good correlation of these observations patients with nephritis suffered more frequently from deep venous thrombosis and ischaemic heart disease. The frequencies of hypertension and non-insulin dependent diabetes mellitus were slightly elevated in patients with nephritis. Present results suggest the importance of elevated lipoprotein (a) concentration in patients with lupus nephritis, further increasing the risk of athero-thrombotic cardiovascular complications.
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PMID:[Lipid profile in patients with systemic lupus erythematosus, with special focus on lipoprotein(a) in lupus nephritis]. 1502 32

High fibrinogen is recognised as a risk factor for atherosclerosis. It seems that high fibrinogen is also a risk factor for deep vein thrombosis (DVT). It has been shown that certain polymorphisms in fibrinogen genes can influence the fibrinogen level. In this study, fibrinogen levels and the frequency of the polymorphisms TaqI, HaeIII and BclI were studied in 114 patients with DVT and 244 healthy subjects. In non-smokers, fibrinogen levels above 5 g/l were associated with an increased risk of DVT (odds ratio 3.3, 95% confidence interval 1.6-7.0). The frequencies of common alleles were similar in patients and healthy subjects for all polymorphisms. An association between fibrinogen levels and the polymorphisms TaqI, HaeIII and BclI was found in healthy subjects, but not in the patients. It was concluded from these data that the polymorphisms TaqI, HaeIII and BclI are not major risk factors for DVT.
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PMID:Fibrinogen polymorphisms TaqI, HaeIII and BclI are not associated with a higher risk of deep vein thrombosis. 1517 Mar 97

Venous thromboembolism is an important cause of maternal morbidity and mortality throughout the developed world with an incidence of about 1 per 1000 deliveries, of which 1-2% are fatal. Two thirds of women who have a pregnancy-associated deep vein thrombosis develop the post-thrombotic syndrome and suffer long-term morbidity. The risk of venous thromboembolism is greater in older women and in women who have an operative delivery. Other risk factors include obesity, high parity, and immobilization. Acquired or inherited thrombophilias augment the risk, and some women with a previous history of venous thromboembolism may be at increased risk of a recurrence associated with pregnancy. Arterial thrombosis is uncommon in pregnancy but may have devastating consequences. The incidence of ischemic stroke associated with pregnancy is unknown but is estimated to be about 0.18 per 1000 deliveries-the majority being the result of arterial occlusion. Myocardial infarction is estimated to occur in 0.1 per 1000 women in association with pregnancy. Events occur most frequently peripartum or postpartum. Risk factors include maternal age, atherosclerosis, obesity, hypertension, and smoking.
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PMID:Venous and arterial thrombosis during pregnancy: epidemiology. 1519 90

Tissue factor (TF) is a transmembrane glycoprotein that binds its zymogen cofactor, Factor VIIa (FVIIa) on the cell surface. Together (TF/FVIIa) they activate Factor X (FX) and Factor IX (FIX) and start the extrinsic pathway of blood coagulation. As such, the TF/FVIIa complex plays an important role in normal physiology as well as in thrombotic diseases such as unstable angina (UA), disseminated intravascular coagulation (DIC), and deep vein thrombosis (DVT). In addition to its function as an initiator of coagulation, TF/FVIIa plays an important role in inflammation. Expression of TF on the cell surface and its appearance as a soluble molecule are characteristic features of acute and chronic inflammation in conditions such as sepsis and atherosclerosis. Here we demonstrate that BCX-3607, a small molecule potent inhibitor of TF/FVIIa, reduces thrombus weight in an animal model of DVT. BCX-3607 also decreases the level of interleukin-6 (IL-6) in a LPS-stimulated mouse model of endotoxemia. Additionally, in vitro studies indicate that BCX-3607 blocks the generation of TF/FVIIa-induced IL-8 mRNA in human keratinocytes and reduces the TF/FVIIa-mediated generation of IL-6 and IL-8 in human umbilical vein endothelial cells (HUVEC). Therefore, BCX-3607 might block the TF/FVIIa-mediated coagulation and inflammation associated with pathological conditions.
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PMID:The antithrombotic and anti-inflammatory effects of BCX-3607, a small molecule tissue factor/factor VIIa inhibitor. 1637 35


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