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)

Alteplase is the product of recombinant DNA technology and is chemically identical to endogenous tissue-type plasminogen activator: Plasminogen is converted to plasmin by alteplase, and fibrinolysis of blood thrombi is subsequently stimulated. Alteplase is now firmly established as a treatment of choice in the management of acute myocardial infarction. The efficacy of intravenous alteplase in the treatment of pulmonary thromboembolism has also been established and appears to be similar to that of streptokinase and urokinase in this indication and in arterial thrombotic occlusion. However, its use in this latter indication and in other vascular disorders has not been as extensively documented. Although trials demonstrating the efficacy of intravenous alteplase in patients with deep vein thrombosis and intra-arterial alteplase in patients with arterial thrombotic occlusion exist, reliable data on the efficacy of the fibrinolytic in ischaemic stroke and intracranial haemorrhage are scarce. Little clinical benefit is apparent in patients with unstable angina, although careful use may be warranted in those with definite pretreatment coronary thrombi. Of concern, there is a suggestion that general use of alteplase in patients with unstable angina may be associated with increased incidence of myocardial infarction. The incidence of major haemorrhage associated with alteplase therapy increases with increasing dose and appears to be similar to that seen with other fibrinolytic agents. Thus, further well-designed studies of the use of alteplase in ischaemic stroke and cerebral haemorrhage are required. However, a small subset of patients with unstable angina and definite pretreatment coronary thrombi may benefit from alteplase therapy. Further, preliminary data suggest efficacy in the therapy of deep vein thrombosis and arterial thrombotic occlusion, and alteplase has a proven place in the fibrinolytic treatment of pulmonary thromboembolism.
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PMID:Alteplase. A reappraisal of its pharmacology and therapeutic use in vascular disorders other than acute myocardial infarction. 852 60

Thrombolytic therapy provides clinical benefit in patients with vascular occlusions, depending upon the organ or limb that is threatened. The impact of therapeutic intervention varies from the quiet alteration of the course of deep vein thrombosis, for which non-life threatening post-phlebitic syndrome can be largely avoided, to the sometimes striking reversal of pulmonary hypertension and possible life-saving benefit in massive pulmonary embolism, the immediate alteration of clinical course in acute peripheral arterial occlusion by reducing the need for surgical intervention, cardiopulmonary complication and one year mortality, and finally to the dramatic and life-saving potential when applied in patients with acute myocardial infarction. Since the risk of serious hemorrhage, especially intracranial hemorrhage, is a constant, regardless of the underlying thrombotic problem, thrombolytic therapy will necessarily be applied variably according to the different potential therapeutic benefits. The balance of potential benefit versus the risk of intracranial hemorrhage in the situation of cerebrovascular thrombosis and stroke remains to be clarified by ongoing studies. As to the evidence for superiority of any single thrombolytic agent or regimen, direct comparative studies are still needed for patients with venous thrombosis and arterial occlusion. Available direct comparisons of two or three agents (streptokinase, urokinase, alteplase and anistreplase) in studies of pulmonary embolism and myocardial infarction show a consistent pattern that documents positive clinical benefit for all of the agents, with striking similarity in quantitative aspects despite marked differences in biochemical properties of the agents.
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PMID:Thrombolytic therapy: overview of results in major vascular occlusions. 857 40

Impaired fibrinolytic function, mainly due to an elevation of the plasma PAI-1 concentration, is a common finding in patients with thrombotic disease. Unfortunately, regarding patients with idiopathic deep vein thrombosis (DVT), no reliable prospective or genetic studies have been published. Concerning postoperative DVT, preoperatively increased PAI-1 level seems to predict a postoperative DVT in patients subjected to hip surgery. Several longitudinal cohort studies of patients with manifest coronary heart disease (CHD) have linked elevated plasma PAI-1 or tPA antigen concentrations to future cardiovascular events, particularly myocardial infarction. Before PAI-1 can be regarded as a risk factor in the conventional epidemiological sense, its relationship to myocardial infarction must be demonstrated in prospective studies of healthy populations. Regulation of the plasma concentration of PAI-1 is complex and at present not well understood. Multiple interactions with disturbances of both carbohydrate and lipoprotein metabolism are evident. Many studies have been carried out in cultured cells, but data can hardly be transformed into human pathophysiology. It seems that both environmental and genetic factors are of importance for the plasma PAI-1 concentration. Recently, knowledge of the importance of genetic factors involved in the regulation of plasma PAI-1 concentration has become available. Interestingly, preliminary data suggest that the 4G/5G polymorphism located within the PAI-1 promoter is connected to CHD. More data on larger patient groups are needed and will certainly shed new light on the importance of impaired fibrinolytic function in the etiology of CHD in the near future.
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PMID:Plasminogen activator inhibitor 1 (PAI-1) in plasma: its role in thrombotic disease. 857 29

In 53 patients with recent (< 6 hrs) acute myocardial infarction a study was undertaken to evaluate the safety of conjunctive therapy with streptokinase (1.5 mln U), aspirin (150 mg) and low molecular weight heparin (Fraxiparine). Patients were treated with Fraxiparine 250 U anti-Xa IC/kg/24 hrs iv for 2 days (with bolus 12.5 U anti-Xa IC/kg), and 125 U anti-Xa IC/kg twice a day sc for 5 subsequent days. Clinical course in one-year observation was compared regarding the time the therapy was initiated. In the group undergoing therapy 3-6 hrs after the infarct had occurred 4 (7.5%) patients died (2 during hospitalization, 2 after discharge). In 31 patients treated within 3 hrs of the myocardial infarction there were fewer cases of recurrent myocardial infarction, unstable angina or congestive heart failure necessitating rehospitalization their (9.1%) than in 22 patients included in the treatment regimen between 3 rd and 6th h of the infarction (27.3%). Earlier thrombolysis was also connected with higher left ventricular ejection fraction (55 +/- 8% vs 49 +/- 10%) and more frequent peak CK-MB values 12 hrs after thrombolysis (81% and 68% of patients respectively). Neither symptomatic deep vein thrombosis nor pulmonary embolism was detected. The left ventricular thrombosis was diagnosed by echocardiography in 4 of 20 patients (20%) with the first anterior myocardial infarction. There was neither bleeding requiring blood transfusion nor cerebrovascular stroke. The treatment with Fraxiparine did not induce the prolongation of APTT values. Conjunctive thrombolytic therapy with low molecular weight heparin was safe and followed by a favorable outcome of the acute myocardial infarction, especially if instituted within the first 3 hrs after the onset of infarction.
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PMID:[Low molecular weight heparin (Fraxiparine) as adjunctive therapy with thrombolysis for acute myocardial infarction: a pilot study with a one year follow up]. 867 95

APC resistance, due to a point mutation in factor V at amino acid position Arg506, has been identified as a major cause of inherited thrombophilia. Here we report the presence of the factor V Arg506-->Gln mutation in 2 Italian families. In 1 family 3 subjects heterozygous and 2 subjects homozygous for the factor V Arg506-->Gln mutation were identified. The only subject who developed a thrombotic event was a 20-yr-old girl who was found to be homozygous for the factor V Arg506-->Gln mutation. In the second family 10 subjects were identified to be heterozygous for the factor V Arg506-->Gln mutation; among them 2 developed a thrombotic event. In the same family 2 individuals were found to be homozygous for the mutation: the first had a myocardial infarction at age 25 yr and the second suffered from multiple episodes of deep venous thrombosis and had a stroke at age 24 yr. These data show that the risk of developing deep venous thrombosis for the carriers of the factor V Arg506-->Gln mutation is high in the families investigated. Furthermore our data imply that the factor V Arg506-->Gln mutation in its homozygous form may relate to myocardial infarction and stroke.
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PMID:Arterial and venous thrombosis in two Italian families with the factor V Arg506-->Gln mutation. 869 38

Activated protein C resistance is the most prevalent cause of thrombophilia: it is found in 20% to 30% of patients with a history of deep venous thrombosis history. Activated protein C resistance is due to an arginine 506 to glutamine mutation in factor V. This mutation prevents normal inactivation of activated factor V by activated protein C. The estimated increase in relative risk of venous thrombosis is 5 to 10 fold in heterozygotes, and 50- to 100- fold in homozygotes. Activated protein C resistance does not seem to play a role in arterial thrombosis or in the occurrence of myocardial infarction.
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PMID:[Activated protein C resistance: role in venous and arterial thrombosis]. 876 Jun 61

Intravenous immune globulin (IVIg) is advocated as a safe treatment for immune-mediated neurologic disease. We reviewed the medical records of 88 patients who were given IVIg for a neurologic illness. Major complications in four patients (4.5%) included congestive heart failure in a patient with polymyositis, hypotension after a recent myocardial infarction, deep venous thrombosis in a bed-bound patient, and acute renal failure with diabetic nephropathy. Other adverse effects included vasomotor symptoms 26, headache 23, rash 5, leukopenia 4, fever 3, neutropenia 1, proteinuria (1.9 g/day) 1, viral syndrome 1, dyspnea 1, and pruritus 1. Fifty-two patients (59%) had some adverse effect of IVIg infusion, most commonly vasomotor symptoms, headaches, fever, or shortness of breath in 40 (45%), which improved with reduced infusion rate or symptomatic medications. Five (6%) had asymptomatic laboratory abnormalities and seven (8%) had other minor adverse effects. Adverse effects led to discontinuation of therapy in 16% and permanent termination of therapy in 10% of patients. There was no mortality or long-term morbidity. Although adverse effects were frequent, serious complications were rare except in patients with heart disease, renal insufficiency, and bed-bound state.
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PMID:Complications of intravenous immune globulin treatment in neurologic disease. 930 72

Hirudins are a group of highly homologous polypeptides from the medicinal leech, Hirudo medicinalis. They have an extremely high and specific affinity for thrombin and are consequently potent anticoagulants. They inhibit platelet aggregation induced by thrombin and efficiently inhibit thrombin when it is bound to a fibrin clot. Recombinant hirudins have now been produced and have been used to show a wide range of effects on thrombosis in animal models. They are particularly effective against venous-type thrombi and have greater effects than heparins on the platelet-rich thrombi in arteries. Recombinant hirudins are currently undergoing clinical trails in deep venous thrombosis and acute coronary syndrome and as an adjunct to thrombolysis in myocardial infarction. Results from pilot trials indicate promising advantages over the currently used antithrombotic agents. Larger clinical trails have been initiated and we await with great interest their imminent publication.
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PMID:Hirudins: from leeches to man. 880 16

There are few conditions in medicine as difficult to diagnose as pulmonary embolism. This is certainly not due to the rarity of the disease which is probably as common as myocardial infarction in France. The circumstances surrounding pulmonary embolism and the risk factors of deep venous thrombosis have been well identified. The risk of thromboembolic venous disease has been assessed for each type of surgery. The methods of treatment and prevention have progressed over a number of years. However, in practice, these advances have not "transformed" the frequency of the disease or reduced its mortality. Further progress could come from improved identification of patients at risk, especially by biological tests and new abnormalities of blood coagulation.
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PMID:[Epidemiology of pulmonary embolism]. 881 27

The low molecular weight heparin (LMWH) dalteparin sodium is notable for its improved pharmacokinetic characteristics (chiefly increased bioavailability and plasma elimination half-life) compared with unfractionated heparin (UFH). These properties enable the drug to be given subcutaneously as a single daily dose, compared with the 8- to 12-hourly regimens necessary with UFH. Dalteparin sodium also appears to exert a greater inhibitory effect than UFH on plasma activity of coagulation factor Xa relative to its effects on clotting times [usually expressed as activated partial thromboplastin time (APTT)] and activity of factor IIa. It is not associated with any clinically significant effects on the fibrinolytic system and may have less lipolytic activity than UFH. Extensive clinical studies have been conducted to compare the antithrombotic efficacy of dalteparin sodium with that of UFH in surgical thromboprophylaxis, treatment of established deep vein thrombosis (DVT) and the anticoagulation of patients undergoing haemodialysis and haemofiltration. The majority of trails of patients receiving thromboprophylactic heparin perioperatively have shown similar efficacy of dalteparin sodium and UFH in the prevention of DVT and pulmonary embolism (PE), although 2 groups of investigators reported superior antithrombotic potency for dalteparin sodium. The two types of heparin appear similarly effective in the management of established DVT and the maintenance of the extracorporeal circulation in haemodialysis circuits. Dalteparin sodium has also shown clinical benefit in the management of patients with unstable angina or non-Q-wave myocardial infarction. The overall incidence of haemorrhagic complications observed with daltparin sodium therapy is no greater than that associated with UFH, and data suggest that perioperative transfusion requirements and frequency of bleeding are lower after dalteparin sodium. The antithrombotic efficacy of dalteparin sodium is at least equivalent to that of UFH, although further clinical comparisons with other LMWHs are required. Further studies are also needed to clearly define any advantages of dalteparin sodium over UFH (and other antithrombotics) with regard to the incidence of haemorrhagic complications. The drug has also shown clinical efficacy in the prevention of myocardial infarction and death in patients with unstable coronary artery disease. In addition, there may be cost advantages attached to the once-daily subcutaneous regimen of dalteparin sodium, but this requires further examination. Thus, dalteparin sodium is an effective antithrombotic agent for perioperative thromboprophylaxis, the management of established DVT, and the anticoagulation of patients undergoing haemodialysis.
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PMID:Dalteparin sodium. A review of its pharmacology and clinical use in the prevention and treatment of thromboembolic disorders. 884 43


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