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

Ten patients affected by proximal deep venous thrombosis were treated in an open study with a low-molecular-weight dermatan sulphate (Desmin), administered at doses of 400 mg (intravenous bolus) followed by 1200 mg/day infused intravenously for 10 days, without activated partial thromboplastin adjustment. The evolution of the deep vein thrombosis and the presence of silent pulmonary embolism were evaluated by phleboscintigraphy and lung scan, performed before treatment and after 10 days of treatment, and by repeated echocolour-Doppler examination (every 2 days during treatment). The evolution of deep vein thrombosis showed a considerable improvement; similarly, lung scan showed a substantial reperfusion of lung, with regression of perfusional deficit. Repeated echocolour-Doppler examination of the deep venous system during treatment did not document further thrombus extension in any patient. Tolerance and safety were excellent. No adverse effects were observed. These preliminary results indicate that the tested dose of Desmin can be effective in treating deep vein thrombosis and silent pulmonary embolism.
 ...
PMID:Efficacy of an intravenous low-molecular-weight dermatan sulphate (Desmin) in patients with acute proximal deep venous thrombosis and silent pulmonary embolism. A pilot study. 910 Jan 65

The aim of this study was to compare the effects on fibrinogenolysis and thrombin generation of two recombinant tissue-type plasminogen activator (rt-PA) regimens in patients with pulmonary embolism entering a randomised, controlled study with a 1:2 allocation ratio to rt-PA, 100 mg over 2 h (Group A) or rt-PA, 0.6 mg/kg, maximum dose 50 mg, over 15 min (Group B). In both groups the heparin infusion was stopped 2-4 h before starting thrombolytic treatment and resumed accordingly to the activated partial thromboplastin time (aPTT) or thrombin clotting time (TcT). Seventeen patients in Group A and 30 patients in Group B were evaluated before starting thrombolytic treatment and 2, 6 and 24 h after its end for the following parameters: aPTT, TcT, fibrinogen, fibrinogen degradation products (FDP), plasmin-alpha 2 antiplasmin (PAP) and thrombin-antithrombin III (TAT) complexes. The two groups had similar coagulation parameters at baseline. Two h after starting rt-PA, the aPTT was more prolonged in Group A than in Group B patients (P = 0.01). Patients in Group B showed less reduction in plasma fibrinogen levels at all study times after rt-PA treatment (P = 0.008). The increase in plasma FDP (P = 0.037) and PAP (P = 0.001) levels was lower at 2 and 6 h samples in Group B compared with Group A. TcT was prolonged (P = 0.003) and TAT increased (P = 0.001) during treatment without differences between the two groups. AUC0-24 of fibrinogen, FDP and PAP levels confirmed the statistically significant differences (P = 0.04) between the two groups over the entire 24 h period of the study. Three patients in Group A (17.6%) and three (10.0%) in Group B suffered major or other important bleeding. Our results indicate that the administration of weight-adjusted reduced-dose rt-PA bolus produces less impairment of blood coagulation than the FDA approved regimen.
 ...
PMID:Fibrinogenolysis and thrombin generation after reduced dose bolus or conventional rt-PA for pulmonary embolism. The Coagulation Project Investigators of the Bolus Alteplase Pulmonary Embolism Group. 919 18

The effect of antiphospholipid antibodies (aPL) on the action of activated protein C (APC) was examined in 32 patients: 19 with lupus anticoagulant (LA), 6 with anticardiolipin antibodies (aCL), and 7 with LA and aCL. Eighteen patients had a ratio of activated partial thromboplastin time (APTT) with APC to APTT without APC (APTT ratio) <2.06 (cut-off level) and no factor V Leiden mutation; these patients showed APC-resistance (APC-R) phenotype. The mean prolongation of APTT after addition of APC in a control group was 45.3 seconds, with a lower limit of 31.4 seconds. Only 3 of the 18 patients with low APTT ratio had a prolongation of <31.4 seconds; they were classified as true APC-R phenotype, whereas the other 15 patients were classified as spurious APC-R. Of the 3 patients with true APC-R, 2 had deep venous thrombosis, 1 with pulmonary embolism, and the third had recurrent abortion. Of the other 15 patients, 2 had had ischemic stroke, 1 had recurrent abortion, and 12 were asymptomatic. Circulating APC level was measured in 14 of the 18 aPL patients with a low APTT ratio; it was lower than the normal lower limit in 4 patients and within the lower limit in 2. Three of the 4 patients with reduced APC levels had a history of thrombosis. We conclude that patients with aPL who show APC-R phenotype due to a low APTT ratio without the factor V Leiden mutation can be classified into two groups: true and spurious APC-R phenotype. Since those with true APC-R phenotype could have greater thrombotic risk, adequate classification of these patients is important. Moreover, aPL can sometimes interfere with the activation of protein C, thus reducing the circulating levels of APC, and this could constitute another thrombotic risk factor.
 ...
PMID:Activated protein C resistance phenotype in patients with antiphospholipid antibodies. 928 Jan 48

We report a 40-year-old Japanese woman with antiphospholipid antibody syndrome (APS) associated with myasthenia gravis (MG). She had a history of miscarriage at the age of 27 followed by pulmonary embolism 3 weeks later. At the age of 40, she developed diplopia, bilateral ptosis and easy fatigability. Serum anti-acetylcholine receptor antibody and tensilon test were positive. She was diagnosed as having MG. The laboratory test revealed mild thrombocytopenia, prolonged activated partial thromboplastin time (aPTT) and positive findings for both beta 2-glycoprotein I-dependent anticardiolipin antibody and lupus anticoagulant. She fulfilled the diagnostic criteria of APS, but did not the criteria proposed by American Rheumatism Association for SLE. An extended total thymectomy was performed after administration of oral prednisolone and low-dose aspirin. This is a patient who had APS associated with MGs: both are known to result from autoimmune abnormality. The clinical and laboratory manifestations of APS were ameliorated after removal of the thymus, suggesting that thymectomy alleviates APS symptoms.
 ...
PMID:[A case of antiphospholipid syndrome associated with myasthenia gravis]. 939 64

The authors used an antithrombotic agent (Nadroparin Calcium) with anti-Xa effect in their experiments to prevent thromboembolic complications in the model of endoprosthetic replacement of the hip joint in mongrel dogs. 10 experimental animals (Group I.) were given doses of 100 A Xa ICU/kg/bwt of Nadroparin Calcium subcutaneously 4 hours prior to the operation and also once a day until the 3rd postoperative day; between the 4th and 10th postoperative days doses of 150 A Xa ICU/kg/bwt Nadroparin Calcium were given. The 10 control animals (Group II.) did not receive anticoagulant treatment. In both groups platelet count, activated partial thromboplastin times (APTT), prothrombin and fibrinogen levels as well as activated factor X inhibition (F Xa) were measured prior to surgery and also until the 14th postoperative day. No changes in APTT and prothrombin levels were detected during the experiment, however platelet count and fibrinogen levels as well as the extent of F Xa inhibition showed significant and different changes in groups I. and II. The Group I. which had received thromboembolic prophylaxis did not develop deep venous thrombosis or pulmonary embolism, but the control group did. Based on their investigations, the authors concluded that they had been able to achieve F Xa inhibition by giving the above mentioned doses of Nadroparin Calcium which was enough to prevent thromboembolic complications in their model experiment of implanting hip endoprosthesis.
 ...
PMID:Efficacy of prevention of thromboembolic complications with LMW-heparin in experiment. 940

Venous thromboembolism (deep vein thrombosis and pulmonary embolism) continues to constitute a major clinical challenge. Effective and safe prophylactic measures against venous thromboembolism are now available for most high risk patients. In spite of this, pulmonary embolism is responsible for approximately 150,000 to 200,000 deaths per year in the United States alone. Over the past 20 years, based on a number of high quality (Level I) clinical trials, patterns of practice with respect to the treatment of venous thromboembolism have changed dramatically. The standard treatment of venous thromboembolism has been the use of unfractionated heparin by continuous intravenous infusion, with laboratory monitoring using the activated partial thromboplastin time (APTT), with warfarin starting on day 1 or 2 and continued for 3 months. Unfractionated heparin has withstood the test of time and has been shown to be safe and effective in preventing recurrent venous thromboembolism and death in numerous clinical trials. The response of individual patients to heparin is highly variable, requiring frequent laboratory monitoring. Heparin has a number of other troublesome side effects including bleeding, heparin-induced thrombocytopenia and osteoporosis. The low-molecular-weight heparins have a number of advantages over unfractionated heparin. In particular, their increased bio-availability and prolonged half-life permit once daily subcutaneous injections and their predictable antithrombotic response based on body weight permits treatment without laboratory monitoring. Low-molecular-weight heparin in therapeutic doses causes less bleeding than unfractionated heparin and evidence is accumulating that the incidence of heparin-induced thrombocytopenia and osteoporosis are decreased as well. In individual clinical trials and meta-analyses, low-molecular-weight heparin treatment results in decreased recurrent thromboembolism, major bleeding and death when compared with unfractionated heparin in the treatment of deep vein thrombosis and pulmonary embolism. These agents have also been shown to be both effective and safe for the out-of-hospital treatment of venous thrombosis. Therefore, in many countries, low-molecular-weight heparin has replaced unfractionated heparin for the treatment of venous thromboembolism.
 ...
PMID:Heparin and low-molecular-weight heparin in the treatment of venous thromboembolism. 1033 Oct 96

Pulmonary embolism occurs in more than 175,000 patients each year in the United States. The objectives of treatment are to prevent death from the existing embolus, to prevent death and morbidity from recurrent pulmonary embolism, and to prevent morbidity from recurrent deep-vein thrombosis. For patients with adequate cardiorespiratory reserve, the primary objective is to prevent recurrent pulmonary embolism. Anticoagulant therapy with intravenous unfractionated heparin or subcutaneous low molecular weight heparin followed by oral anticoagulant treatment for at least 3 months is the treatment of choice for most of these patients. Clinical trials indicate that the effectiveness of intravenous heparin depends on achieving an adequate heparin effect (activated partial thromboplastin time above lower limit) during the initial 24 hours. A validated protocol for intravenous heparin should be used to lessen the likelihood of delayed heparinization. Low molecular weight heparin given subcutaneously either once or twice daily is as effective as intravenous heparin for the treatment of patients with deep-vein thrombosis and submassive pulmonary embolism. Low molecular weight heparin enables many patients with uncomplicated deep-vein thrombosis to be treated in an outpatient setting.
 ...
PMID:Heparin and low molecular weight heparin for treatment of acute pulmonary embolism. 1040 88

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.
 ...
PMID:Detection of decreased response to activated protein C during pregnancy by an endogenous thrombin potential-based assay. 1062 9

Physicians face a therapeutic dilemma in patients with acute hemorrhagic stroke requiring long-term, high-intensity anticoagulants because this treatment increases the risk of intracranial hemorrhage (ICH) 8- to 11-fold. We retrospectively studied 15 patients with ICH which occurred under anticoagulation with phenprocoumon, with an international norrmalized ratio (INR) of 2.5-6.5 on admission. Hemispheric, thalamic, cerebellar, intraventricular, or subarachnoid hemorrhage without aneurysm occurred. Absolute indications for anticoagulation were double, mitral, or aortic valve replacement, combined mitral valve failure with atrial fibrillation and atrial enlargement, internal carotid artery-jugular vein graft, frequently recurring deep vein thrombosis with risk of pulmonary embolism, and severe nontreatable ischemic heart disease. As soon as the diagnosis of ICH was established, INR normalization was attempted in all patients by administration of prothrombin complex, fresh frozen plasma, or vitamin K. After giving phenprocoumon antagonists (and neurosurgical therapy in four patients) heparin administration was started. Nine patients received full-dose intravenous and six low-dose subcutaneous heparin. The following observations were made: (a) All patients with effective, full-dose heparin treatment with a 1.5- to 2-fold elevation in partial thromboplastin time after normalization of the INR were discharged without complication. (b) Three of four of the patients with only incomplete correction of the INR (> 1.35) experienced relevant rebleeding within 3 days (all patients with an INR higher than 1.5), two of whom were on full-dose heparin. (c) Three of seven of the patients with normalized INR and without significant PTT elevation developed severe cerebral embolism. Although our data are based on a retrospective analysis, they support treatment with intravenous heparin (partial thromboplastin time 1.5-2 times baseline value) after normalization of the INR in patients with an ICH and an urgent need for anticoagulation.
 ...
PMID:Managing the therapeutic dilemma: patients with spontaneous intracerebral hemorrhage and urgent need for anticoagulation. 1078 17

Patients in intensive care may be at high risk of in vivo platelet activation because comorbid conditions, such as infections, septicemia, shock, disseminated intravascular coagulation, and cancer represent procoagulant states. Hyperreactivity of platelets with or without a decline of cell count may result in thromboembolic complications potentially associated with the phenomenon of heparin-induced thrombocytopenia. We analyzed the data of 10 patients highly suspected of having heparin-induced thrombocytopenia during their intensive care treatment of 29 plus or minus 22 days. In seven patients, thrombocytopenia coincided with thromboembolic complications. Six patients had additionally undergone fibrinolytic therapy before starting activated partial thromboplastin time-adapted alternative anticoagulation with r-hirudin. In three patients, the platelet count decreased without a clinical manifestation, of heparin-induced thrombocytopenia. R-Hirudin treatment monitored by activated partial thromboplastin time and prothrombin time (PT) was effective and safe. The target value for activated partial thromboplastin time was a twofold prolongation. In four of five patients with deep venous thrombosis, a partial recanalization of the lower extremity could be achieved. Three patients with pulmonary embolism associated with deep venous thrombosis in two cases and in one additional case with an acute myocardial infarction did clinically profit from fibrinolysis with recombinant tissue plasminogen activator (rtPA) and r-hirudin treatment. Two lethal events probably caused by the underlying multimorbidity could not be prevented. No recurrence of thrombosis occurred, and there were no severe bleeding complications attributed to r-hirudin treatment. Platelet counts were significantly reduced on day 9.4 plus or minus 6.4 of heparin administration in all cases (>50% decrease related to the initial values) from 224,000 plus or minus 126,000/microL to 96,000 plus or minus 61,000/microL, and increased during rhirudin treatment to mean values of 224,000 plus or minus 126,000/microL. The heparin-induced platelet activation assay (HIPAA) assay was positive in 8/10 cases, whereas the PF4 enzyme-linked immunosorbent assay showed a positive result in four of eight analyzed cases. In four cases, the assays were concordantly positive. The PF4 enzyme-linked immunosorbent assay was not performed in two cases.
 ...
PMID:Heparin-induced thrombocytopenia: a critical risk/benefit analysis of patients in intensive care treated with R-hirudin. 1089 75


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>