Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heparin-induced thrombocytopenia develops when patients given heparin as treatment for thrombosis have an immunologic reaction to the agent. Patients may have an underlying thrombotic disorder--for example, venous thrombosis or pulmonary embolism--that requires intervention. Alternative antithrombotic therapies that have been tried include defibrinogenating agents, LMWH and heparinoids, thrombin-specific inhibitors, antiplatelet agents, oral anticoagulants, and vena cava interruption.
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PMID:Heparin-induced thrombocytopenia. Diagnosis, natural history, and treatment options. 947 14

Tissue injury during hip surgery results in the activation of the haemostatic system. The aim of this study was to detect markers of haemostatic activity, i.e. prothrombin fragment 1 and 2 (F1+2), thrombin-antithrombin (TAT) complexes, fibrin degradation products (FbDP), and soluble fibrin monomers (SF), preoperatively, and on days 1, 7 and 35 in plasma of patients undergoing total hip arthroplasty. The study was part of a multicentre study in which the patients were randomized to receive a subcutaneous injection of low molecular weight heparin (LMWH, dalteparin, Fragmin) once daily for 5 weeks or placebo following a 1-week LMWH treatment (once daily). Bilateral phlebography was performed between days 33 and 35 or before if patients had clinical symptoms of deep vein thrombosis. A lung scan was performed in patients with clinical symptoms of pulmonary embolism. Levels of the markers were significantly increased on day 35 in the patients receiving LMWH for 7 days compared to patients receiving LMWH for 35 days. In patients receiving LMWH for 5 weeks, levels of FbDP and SF were significantly higher during the entire study period, but TAT and F1+2 were normalized on day 35. The markers were increased two to five times on the 1st postoperative day in patients with diagnosed venous thromboembolism.
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PMID:Postoperative activation of the haemostatic system--influence of prolonged thromboprophylaxis in patients undergoing total hip arthroplasty. 969 Apr 80

The anticoagulant agents most commonly used in the prevention and treatment of pulmonary embolism (PE) are unfractionated heparin, oral anticoagulants, and low molecular weight heparins (LMWHs). Unfractionated heparin at low fixed dose is the prophylactic regimen of choice for PE in patients undergoing general surgery or with serious medical diseases (low to moderate risk patients). In high risk patients perioperative prophylaxis with LMWHs or oral anticoagulants should be adopted. Therapy of pulmonary embolism should start with an intravenous bolus dose of 5000 U heparin followed by an infusion of 1250 U/h. Then the dose should be adjusted to maintain the aPTTX2-2.5 pre-treatment value. Heparin is continued for 7-10 days and is followed by oral anticoagulants for at least 3 months. Unfractionated heparin has some pharmacological limitations, mainly due to the aspecific binding to plasma proteins that limits its anticoagulant effect and causes the heparin resistance observed in some patients with PE and the inter-subject variability of the anticoagulant effect. Other antithrombotic agents such as LMWHs and selective thrombin inhibitors (hirudin and its analogues) do not aspecifically bind to plasma proteins. They have recently been used with promising results in the prevention and treatment of PE. Their definitive value in this clinical setting will be defined by the ongoing clinical trials.
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PMID:Anticoagulant agents in the management of pulmonary embolism. 970 37

Heparin-induced thrombocytopenia (HIT) is an immunologic complication of drug therapy with potentially serious venous and arterial thrombotic sequelae. Recent studies have provided insight into the molecular and cellular basis of HIT underlying the diagnosis and treatment of this syndrome. Because various approaches to HIT treatment have resulted in mixed success, the use of heparin substitutes, other anticoagulant agents, and adjunctive therapy needs to be clarified. For patients with pre-existing conditions such as deep venous thrombosis or pulmonary embolism, new understanding of the clinicopathologic syndrome of HIT offers the promise of improved antithrombotic therapy. The participation of thrombin in HIT suggests that specific (hirudin and argatroban) thrombin inhibitors may be ideal agents for treating acute HIT.
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PMID:The clinical management of heparin-induced thrombocytopenia. 993 May 59

Fibrin formation is a multistep process initiated by thrombin. At first thrombin converts fibrinogen to fibrin molecules which in vivo form soluble complexes with fibrinogen. Soluble fibrin is considered to be an early biochemical marker for intravascular fibrin formation and impending thrombotic events, such as deep venous thrombosis (DVT), pulmonary embolism (PE) and disseminated intravascular coagulopathy (DIC). A new enzyme immunoassay (EIA) was developed on the basis of a monoclonal antibody directed against a fibrin specific neo-epitope located on the gamma-chain of fibrinogen; gamma-(312-324). In addition, it was possible to prepare a lyophilized reference material of thrombin-generated soluble fibrin, that allowed for full antigen recovery after reconstitution with buffer. Assay conditions, e.g. solid phase-Ig concentration and buffer composition, sample and conjugate dilution, and incubation times were optimised. The present assay was found to be specific (no interference of homologous antigens) and reproducible (intra-assay CV 4-8%, interassay CV 4-9%), and therefore highly suited for measuring soluble fibrin levels in a plasma milieu. The median normal value for soluble fibrin was determined in plasma samples obtained from apparently healthy volunteers (n = 81) and found to be 0.040 microg/ml, with a range (10-90 percentiles) of 0.026-0.059 microg/ml. A retrospective study showed that soluble fibrin levels were highly significantly increased in patients with a confirmed diagnosis of DIC (median 1.042 microg FEU/ml, range 0.160-2.319 microg/ml, n = 21, P<0.0001 vs. normal). PE (median 0.527 microg FEU/ml, range 0.084-1.234 microg/ml, n = 29, P<0.0001 vs normal) and DVT (median 0.126 microg FEU/ml, range 0.059-0.878 microg/ml, n = 36, P<0.0001 vs. normal), as determined by the Mann-Whitney U-Test.
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PMID:A new enzyme immunoassay for soluble fibrin in plasma, with a high discriminating power for thrombotic disorders. 997 75

Total hip arthroplasty (THA) is a major orthopaedic procedure with a high risk of postoperative thromboembolism. Increasing demand for this type of surgery, together with its high cost, has led to examination of means by which the cost of THA may be minimised. Current clinical opinion favours the use of suitable pharmacological thromboprophylaxis in patients undergoing THA; such prophylaxis may be provided with subcutaneous standard unfractionated heparin (UFH), oral warfarin or subcutaneous low molecular weight heparin (LMWH). Traditionally, LMWHs have been perceived as being more expensive to use than UFH or warfarin because of their relatively high acquisition cost. However, recent pharmacoeconomic data have shown that cost savings are possible when LMWHs are used. This is attributed mainly to reduced frequency of administration, reductions in costs associated with diagnosis and treatment of deep vein thrombosis (DVT) and pulmonary embolism (PE), and the lack of need for laboratory monitoring of blood coagulation parameters. LMWHs have proportionally less anti-factor IIa (antithrombin) activity relative to anti-factor Xa activity than UFH. Enoxaparin, a LMWH with a mean molecular weight of 4 to 5kD, is reported to have approximately 5 times less activity against thrombin than UFH, for equivalent anti-factor Xa activity. Randomised clinical trials in patients undergoing THA have shown enoxaparin to be at least as effective as UFH in the prevention of DVT and PE, with consistent trends towards a lower incidence of DVT with enoxaparin than with UFH. Similar rates of haemorrhagic complications were reported for enoxaparin and UFH in most trials, although a significantly higher total transfusion requirement was reported for UFH than for enoxaparin in a double-blind study. A significantly higher incidence of bleeding was observed with UFH than with enoxaparin in another study, with similar transfusion requirements for both treatment groups. Cost comparisons in which costs were assigned retrospectively to clinical data have shown cost advantages for LMWHs in general over UFH when costs of administration, hospital bed occupancy and laboratory/radiology procedures are calculated. Cost savings with LMWHs were attributed mainly to reductions in the cost of managing thromboembolic complications in patients receiving these drugs. One meta-analysis showed a saving of $US50 000 (1993 figures) for LMWH over UFH (both subcutaneously twice daily) for every 1000 patients. Subcutaneous enoxaparin at a dosage of 30mg twice daily was shown to be more cost effective than oral warfarin in the prophylaxis of DVT and PE in 2 North American studies in which costs were related to outcomes. One study comprised the application of a decision analysis to a hypothetical group of 10 000 patients; an incremental cost effectiveness of $US12 288 (1993 figures) per death averted was reported for enoxaparin. Enoxaparin was also associated with an overall incremental cost effectiveness of $Can29 140 (1992 figures) per year of life saved (YLS) in the other study, in which costs were applied to clinical data obtained retrospectively from 10 randomised trials. Although no cost-effectiveness analyses have been carried out to compare enoxaparin with UFH, a UK cost comparison reported an overall cost saving of pounds 20 per patient (figures from 1989 to 1990) with enoxaparin 40mg once daily subcutaneously over subcutaneous UFH 5000IU 3 times daily. It has also been suggested that the use of once- or twice-daily enoxaparin in preference to UFH may reduce the overall length of hospital stay; a significant difference emerged in 1 analysis (9.9 or 9.5 vs 11.3 days). Pharmacoeconomic data therefore support the use of enoxaparin as an effective thromboprophylactic treatment with potential cost advantages over warfarin and UFH. Cost-effecti
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PMID:Enoxaparin. A pharmacoeconomic appraisal of its use in thromboembolic prophylaxis after total hip arthroplasty. 1016 20

Venous thromboembolism is a common medical condition in both out-patients and in-patients. Despite the development of non-invasive tests, the diagnosis of deep vein thrombosis and pulmonary embolism remains a clinical challenge. In an effort to improve diagnostic accuracy and to reduce the necessity of serial testing, laboratory markers of thrombin generation and fibrinolysis have been investigated as first-line screening tests. Although the majority of markers are elevated in acute thrombosis, D-dimer, a specific derivative of cross-linked fibrin, appears to have the most potential clinical utility. Accuracy studies and preliminary management trials suggest that rapid D-dimer enzyme-linked immunosorbent assays and the whole blood agglutination assay, SimpliRED D-dimer (Agen Biomedical, Brisbane, Australia), have strong potential as exclusionary tests in patients with suspected venous thrombosis.
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PMID:Laboratory diagnosis of venous thromboembolism. 1033 Oct 94

Heparin cofactor II (HCII) is a specific inhibitor of thrombin in the presence of heparin or dermatan sulphate. Although there have been reports on families in which a heterozygous HCII deficiency is associated with thromboembolic events, several epidemiological studies revealed that heterozygous HCII deficiency is as prevalent among healthy subjects as it is among patients with deep venous thrombosis (DVT). It is therefore not yet clear whether HCII is or is not a thrombotic risk factor. We analyze and describe in an extended family the biochemical and genetic thrombophilic risk factors and evaluate the potential thrombotic risk involved in homozygous and heterozygous HCII deficiency, either alone or associated with other thrombotic or circumstantial risk factors. The propositus has had three episodes of DVT and a pulmonary embolism. During the first episode of DVT the patient was diagnosed as having AT deficiency. Later, a functional and antigenic HCII deficiency, compatible with the homozygous form, was detected. The family study shows that both the propositus and her sister have homozygous HCII deficiency and that 12 of the 27 family members have heterozygous HCII deficiency. This is possibly the first case report on a homozygous phenotype for the HCII deficiency with. in addition, partial AT deficiency. The propositus has suffered several thrombotic events, unlike the other 12 family members with heterozygous HCII deficiency and her sister, who is also homozygous for this disorder. We suggest that HCII deficiency may play a limited in vivo role as a thrombotic risk factor unless associated with AT deficiency or another congenital thrombotic risk factor.
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PMID:Hereditary homozygous heparin cofactor II deficiency and the risk of developing venous thrombosis. 1049 55

Pregnancy has been widely recognized as a predisposing risk factor for deep vein thrombosis (DVT). However, it still remains unclear why pregnant women without a history of familial thrombophilia or antiphospholipid syndrome (APS) have a higher incidence of DVT and pulmonary embolism (PE) during pregnancy and puerperium. We examined the activated protein C (APC) system in healthy pregnant women and in patients with the onset of DVT during puerperium. Sixty unselected Japanese pregnant women without a past or family history of thrombosis or APS and 3 Japanese women with DVT during puerperium were evaluated. Endogenous thrombin potential-ratio (ETP-r) was measured by determination of thrombin-alpha2-macroglobulin complexes in thromboplastin-activated patient plasma. APC sensitivity ratio (APC-sr) was calculated by the determination of ETP-r in patient plasma in the presence and absence of APC (final concentration [conc.] 5.9 nM) to evaluate the functional APC anticoagulant activity. Mean APC-sr was significantly increased at 30 weeks' gestation (2.35 +/- 0.72) and remained high during puerperium compared with the mean APC-sr in nonpregnant women (1.15 +/- 0.63). Mean APC-sr in patients with DVT at the onset was significantly higher (3.57 +/- 0.54) than mean APC-sr during puerperium was, indicating that the sensitivity to APC was reduced in the ETP-based assay. These data suggest a significant reduction in the functional sensitivity to APC associated with an increased risk of venous thrombosis during pregnancy.
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PMID:Detection of decreased response to activated protein C during pregnancy by an endogenous thrombin potential-based assay. 1062 9

During and following significant surgical intervention, deep venous thrombosis prophylaxis by application of anticoagulants is routinely used. However, patients with malignant disorders are subject to an especially high risk of deep venous thrombosis progressing in severe cases to subsequent pulmonary embolism. The present study focuses on appraising modern markers of deep vein thrombosis in 34 patients undergoing major maxillofacial surgery, with some malignant disorders. No significant differences between the two patient groups were noted using the markers of the kallikrein-kinin-system. From the first postoperative day plasma levels of the coagulation indicator thrombin-antithrombin-III complexes were significantly higher in the group of tumour patients. Markers of fibrinolysis indicated corresponding results: on the first postoperative day tissue-plasminogen activator values rose to 18.9 +/- 3.2 micrograms/l in the group of malignant patients, but only to 7.4 +/- 1.1 micrograms/l (P < 0.05) in the control group. Also postoperative D-dimer concentrations in the malignancy group were significantly above those of the control group. In the present study it could be demonstrated that patients with malignant neoplasia undergoing major maxillofacial surgery are exposed postoperatively to a particularly high risk of developing thromboembolic complications. All in all, the status of anti-thrombotic therapy requires reappraisal with respect to the current treatment approach adopted in tumour patients.
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PMID:Evaluation of markers of deep vein thrombosis in patients undergoing surgery for maxillofacial malignancies. 1062 61


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