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)

The assay of fibrinopeptide A (FPA) has stimulated particular interest because of its high sensitivity and unique specificity for the action of thrombin. It has proved to be an extremely useful tool in research studies concerning the pathophysiology of thrombotic disease. Use of FPA in the diagnosis and treatment of deep venous thrombosis and pulmonary embolism is reviewed, and the potential usefulness of measuring FPA in the monitoring of the effectiveness of anticoagulant therapy is discussed.
 ...
PMID:Fibrinopeptide A in the diagnosis and treatment of deep venous thrombosis and pulmonary embolism. 649 99

Urokinase (average 1670 IU/kg X h) and heparin (average 17 IU/kg X h) was infused over several days into the main pulmonary artery of 12 patients with acute massive pulmonary embolism, after diagnostic pulmonary angiography. Pulmonary artery pressures and blood clotting values were serially recorded. There was convincing improvement in the clinical condition of all patients: none died or had a recurrence of embolism. The heart rate and pulmonary vascular obstruction decreased, mean pulmonary artery pressure fell and arterial pO2 rose. There were other, also statistically significant, changes in a decrease of fibrinogen, rise in thrombin time and decrease in haemoglobin concentration. Pulmonary artery pressure after 24 hours had fallen slightly, after 5.8 days significantly. In two patients a haemoglobin fall of more than 3 g/dl required blood transfusion. The findings indicate that after massive pulmonary embolism local continuous infusion of urokinase can, after 5-6 days, normalize pulmonary haemodynamics; the pulmonary angiogram shows almost complete disappearance of the pulmonary vascular obstruction.
 ...
PMID:[Local thrombolysis with urokinase in acute massive pulmonary embolism]. 669 63

Six patients are described in whom disseminated intravascular coagulation of uncertain cause was found to be due to occult pulmonary embolism. The peripheral blood smear showed thrombocytopenia in all patients and schistocytes in four. Coagulation studies revealed increased levels of fibrinogen/fibrin degradation products (six of six patients), positive results for fibrin monomer (five patients), prolonged thrombin times (four patients), hypofibrinogenemia (three patients), prolonged prothrombin times (two patients), and decreased plasma coagulation factors (two patients). Pulmonary embolism was confirmed by lung scanning or pulmonary angiography. Institution of full-dose heparin therapy was associated with hemostatic and clinical improvement in all patients. The association of disseminated intravascular coagulation with occult pulmonary embolism merits recognition since full-dose heparinization is required for successful therapy.
 ...
PMID:Unrecognized pulmonary embolism presenting as disseminated intravascular coagulation. 672 Jul 24

A 33 year old woman presented with dyspnea and dizziness. These symptoms had recurred several times during the months preceding. At initial investigation we palpated a tumor in the upper abdomen corresponding to the sonographic finding of a 10 X 10 cm sized cystic tumor in the liver. Because of reduction of fibrinogen, prolonged thrombin time and thrombocytopenia a malignant disease involving the liver and producing pulmonary embolism and disseminated intravascular coagulation was suspected. However, during routine echocardiography a right atrial mass prolapsing in the right ventricle was detected. After normalization of fibrinogen and thrombin-time following a low dose heparin therapy a myxoma sized 6 X 5 cm was removed from the right atrium. The patient did not recover and died 20 days following surgery. At autopsy the liver tumor proved to be a benign cholangioendothelial cyst.
 ...
PMID:[Recurring pulmonary artery embolisms and disseminated intravascular coagulation in right atrial myxoma]. 672 75

Streptokinase was infused for 103 +/- 25 hrs. in 27 patients (6 with deep vein thrombosis of the leg, 7 with thrombosis of Vv. axillaris and subclavia, 9 with acute massive pulmonary embolism, 3 with chronic artery occlusion, 2 with thrombosis of the retinal vein). Blood coagulation studies were performed repeatedly. Anticoagulation (prolongation of thrombin time to 1 1/2-2 1/2 of normal) could be achieved without additional heparin by reduction of streptokinase to doses as low as 20 000 U/h. Reptilase time correlated significantly with thrombin times. Following 24 hrs. of infusion, PTT was less than 50 sec. and Quick test less than 50% of normal in most instances. No correlation was found between PTT or Quick test and factor II, V, VI, X activities during streptokinase infusion. Bleeding was observed in 18 patients. The infusion was stopped because of bleeding in 3 cases. None of the coagulation tests performed in this study correlated with the incidence of bleeding. Hemoglobin concentration decreased 2,6 +/- 1,6 gr% and this decrease could no be explained by blood lesses.
 ...
PMID:[Control of blood coagulation and complications in long-term streptokinase therapy]. 719 87

Incorporation of indium-111-labeled platelets (In-111-P) into venous thrombi and pulmonary emboli may permit rapid detection of these thromboemboli by gamma imaging. In a series of dogs in which femoral-vein thromboses and/or pulmonary embolism were induced experimentally by stasis and small amounts of thrombin, we addressed several questions pertinent to the sensitivity, specificity, and potential applicability of this approach. We found that when In-111-P were injected intravenously before thrombus induction or embolus release, femoral-thrombus images were consistently detectable within 15 min, whereas control femoral-vein images were unremarkable. Pulmonary emboli were also promptly imaged, and such In-111-P images agreed well with defects on Tc-99m MAA perfusion scans. When thrombi were aged in vivo for up to 10 hr after formation, they could still be imaged within 20-90 min after In-111-P injection. Administration of heparin, as an initial bolus followed by constant infusion, blocked platelet deposition on femoral-vein thrombi as assessed by both thrombus-to-blood ratios and failure to image. Injection of protamine at 6 hr, however, resulted in prompt thrombus imaging. These data indicate that this approach may well have applicability to the detection of thromboemboli in humans, since imaging remains possible in canine thrombi aged in vivo for 10 hr so long as heparin therapy has not been instituted. The dose of heparin required to inhibit imaging is not known. However, if these data prove comparable in humans, they suggest that imaging of thromboemboli could be achieved so promptly that only modest delay in the institution of heparin therapy would be required.
 ...
PMID:Study of factors that may condition scintigraphic detection of venous thrombi and pulmonary emboli with indium-111-labeled platelets. 743 Nov 4

Activated protein C (APC)-protein C inhibitor (PCI) complex level was examined in 35 patients with acute pulmonary embolism (PE) and in 20 healthy volunteers. Thrombin-antithrombin III complex, plasmin alpha 2 plasmin inhibitor complex, and fibrin-D-dimer levels were significantly increased in the patients with PE compared to levels in healthy volunteers. Levels of plasminogen activator inhibitor-I, tissue type plasminogen activator, and von Willebrand factor antigens were also significantly increased in patients with PE. Plasma level of APC-PCI complex was increased in most patients with PE and APC-alpha 1 antitrypsin complex level was increased in 13 patients. These complexes were not detected in healthy volunteers. These findings suggested that plasma protein C was activated in patients with PE, and that PCI was the major inhibitor of APC generated in this condition. Thus, regulation of the protein C pathway might play an important role in the pathogenesis of PE.
 ...
PMID:Increased activated protein C-protein C inhibitor complex levels in patients with pulmonary embolism. 751 16

The activation of the clotting cascade leading to deep venous thrombosis begins during total hip arthroplasty, but few studies have assessed changes in coagulation during surgery. A better understanding of thrombogenesis during total hip arthroplasty may provide a more rational basis for treatment. In 3 separate studies, the following observations were made. Circulating indices of thrombosis and fibrinolysis: prothrombin F1.2, thrombin-antithrombin complexes, fibrinopeptide A, and D-dimer, did not increase during osteotomy of the neck of the femur or during insertion of the acetabular component, but rose significantly during insertion of the femoral component. Thrombin-antithrombin complexes, fibrinopeptide A, and D-dimer were higher after insertion of a cemented component than insertion of a noncemented femoral component. A significant decline in central venous oxygen tension was observed after relocation of the hip joint and after insertions of cemented and noncemented femoral components, providing evidence of femoral venous occlusion during insertion of the femoral component. In patients receiving a cemented femoral component, mean pulmonary artery pressure increased after relocation of the hip joint, indicating intraoperative pulmonary embolism. No changes in mean pulmonary artery pressure were noted with noncemented total hip arthroplasty. Administration of 1000 units of unfractionated heparin before insertion of a cemented femoral component blunted the rise of fibrinopeptide A. The results of these studies suggest that (1) the greatest risk of activation of the clotting cascade during total hip arthroplasty occurs during insertion of the femoral component; (2) femoral venous occlusion and use of cemented components are factors in thrombogenesis during total hip arthroplasty; and (3) measures to prevent deep venous thrombosis during total hip arthroplasty (such as intraoperative anticoagulation) should begin during surgery rather than during the postoperative period and be applied during insertion of the femoral component.
 ...
PMID:The John Charnley Award. Thrombogenesis during total hip arthroplasty. 755 26

Dermatan sulphate catalyses thrombin inhibition by heparin cofactor II; it has a lower haemorrhagic to antithrombotic ratio than that of heparin in animal models. Consecutive patients aged forty years or more, electively undergoing total hip replacement under general anaesthesia, were randomly allocated to one of three dosage regimens of dermatan sulphate (MF701, Mediolanum Farmaceutici) given intramuscularly. These were 200 mg once daily (n = 50), 200 mg twice daily (n = 52) and 300 mg twice daily (n = 51), administered from twenty-four hours pre-operatively until the tenth postoperative day. The overall incidence of DVT assessed by bilateral venography was 53%, 51% and 34% respectively (Chi-square test for trend p = 0.06). The incidence of major proximal DVT was 10.6%, 8.5% and 2.1% respectively. Pulmonary embolism (PE) and bleeding were assessed in all 153 patients. There was one case of PE in each dose group. The incidence of bleeding episodes, volume of blood lost and blood transfusion requirements were low and showed no increase with increasing dose. The patients were followed up 4-8 weeks after discharge. We conclude that the two lower doses were subtherapeutic in this population, however dermatan sulphate given 300 mg twice daily, proved to be efficacious with an incidence of proximal major DVT of 2.1% and a low incidence of bleeding complications. A trial of dermatan sulphate 300 mg twice daily compared to standard prophylactic agents is needed.
 ...
PMID:A dose ranging study to evaluate dermatan sulphate in preventing deep vein thrombosis following total hip arthroplasty. 774 Apr 43

Thrombomodulin (TM) is the anticoagulant endothelial cell membrane-bound protein cofactor in the thrombin-mediated activation of protein C (PC). It has been clearly demonstrated that the anticoagulant and profibrinolytic functions of the PC system are important for the prevention of a thromboembolic disease. Patients with PC, protein S, or PC "'cofactor"' deficiency and/or dysfunction develop thromboembolic diseases. However, the molecular abnormality in at least 20% to 30% of thrombophilic patients cannot be identified by hitherto recognized defects. A putative pathologic lesion in the TM gene could be one of several candidates for these prothrombotic mutations. A directed search strategy for deletions, insertions, or point mutations in the TM gene has not been performed. Therefore, in the present study, we have analyzed the entire TM gene, including the promoter region, by polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) in normal healthy volunteers and in patients presenting with a thromboembolic disease. We have identified a patient with a thromboembolic disease and a TM point mutation. In a 45-year-old Hispanic man with a documented pulmonary embolism, PCR-SSCP showed an aberrant band pattern and subsequent DNA sequence analysis showed a heterozygous substitution for G1456 to T. This substitution predicts an Asp468 to a Tyr change in the amino acid sequence that is located between the transmembrane domain and the sixth epidermal growth factor-like domain. The Asp468 to Tyr change would probably lead to significant structural changes not allowing the expression of the TM protein or to a conformational change that is not functional.
 ...
PMID:The first mutation identified in the thrombomodulin gene in a 45-year-old man presenting with thromboembolic disease. 781 89


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