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)

A congenitally abnormal fibrinogen (Vlissingen) was isolated from the blood of a young woman suffering from massive pulmonary embolism. Fibrinogen Vlissingen showed an abnormal clotting time with both thrombin and Reptilase. The release of the fibrino-peptides A and B by thrombin was normal, but fibrin polymerization was impaired both in the presence and absence of Ca2+ ions. On sodium dodecyl sulfate-polyacrylamide gel electrophoresis performed according to Laemmli the gamma-chain of fibrinogen Vlissingen showed two bands, one normal and one having an apparently lower molecular mass of about 1,500 daltons. The previously described protective effect of Ca2+ ions on plasmin degradation of the carboxyl terminus of the gamma-chain of normal fibrinogen was only partially detectable in fibrinogen Vlissingen. In addition the binding of Ca2+ ions was decreased. Fibrinogen Vlissingen bound 2.4 Ca2+ ions per fibrinogen molecule at pH 7.4, whereas normal fibrinogen bound 3.1 Ca2+ ions. At pH 5.8 fibrinogen Vlissingen bound 1.1 Ca2+ ions, whereas normal fibrinogen bound 2.0 Ca2+ ions per molecule fibrinogen in the D-domains, again indicating a structural change in the carboxyl terminus of fibrinogen. The structural defect was determined by sequence analysis of DNA amplified by use of the polymerase chain reaction. Exons VIII, IX, and X of the gamma-chain gene were amplified and the DNA sequence of the amplified fragments was determined. A 6-base deletion was found in 50% of the fragments corresponding to exon VIII, indicating that the patient was heterozygous for the mutation. This deletion codes for amino acids Asn-319 and Asp-320 in the normal fibrinogen gamma-chain. The data indicate that Asn-319 and Asp-320 are crucial for maintaining the integrity of the carboxyl-terminal polymerization sites, the protective effect of Ca2+ ions on plasmin degradation of the carboxyl terminus of the gamma-chain, and the calcium binding domain at the carboxyl terminus of fibrinogen.
 ...
PMID:A congenitally abnormal fibrinogen (Vlissingen) with a 6-base deletion in the gamma-chain gene, causing defective calcium binding and impaired fibrin polymerization. 207 11

The authors report the case of a Bothrops lanceolatus snake bite complicated by severe pulmonary embolism a few hours after admission. This thromboembolic complication developed despite heparin therapy and was followed by disseminated intravascular coagulation (DIC). Vascular thrombosis and pulmonary embolism are rare after Bothrops lanceolatus snake bite as patients are usually hypocoagulable due to DIC. In this case, the thromboembolism was probably caused by the procoagulant effect of the thrombin-like enzymes of the snake venom which may have been injected directly into the vein of a young woman taking a contraceptive pill. A specific antivenin which has recently become available fort treatment may decrease the complications of Bothrops lanceolatus snake bite.
 ...
PMID:[Pulmonary embolism and disseminated intravascular coagulation after being bitten by a Bothrops lanceolatus snake. Apropos of a case]. 251 45

Post-operative thrombo-embolic disease remains a frequent occurrence in spite of advances in their prophylaxis. Evaluation of 60 case-reports of this disease which often includes peripheral manifestations and always pulmonary manifestations, enables to specify the role of the procedure itself (mostly orthopaedic surgery 60%), pelvic surgery 20%, the chronology of events (possibility of early embolism between D1 and D3 and usual occurrence of manifestations between D8 and D18, and the importance of the background, whether investigated or not: deficiencies in anti-thrombin III, protein C and S: 4 cases. The diagnosis is based on clinical signs (non-specific) and the laboratory tests, especially scintigraphy (screening) and angiography, absolutely necessary for the diagnosis and evaluation of the amputation coefficient (Miller index). With a diagnosis of pulmonary embolism, it is always necessary to look for a proximal venous thrombosis. The treatment, calls for heparin (quite seldom), thrombolytics (Urokinase, Plasminogen in our experience), the indication of which must take into consideration the delays and the nature of the previous procedure, and finally surgery (massive forms where thrombolytics are contraindicated). The thrombo-embolic manifestations with thrombogenic thrombopenia secondary to heparin are quite frequent, in a surgical environment (10 cases) and difficult to treat.
 ...
PMID:[Postoperative pulmonary embolism]. 266 1

Plasma D-dimer (DD) and thrombin--antithrombin III complex (TAT) were measured with ELISAs in 99 patients investigated by 102 ventilation--perfusion lung scintigraphy because of suspected pulmonary embolism. High-probability lung scan was associated with increased DD (more than 500 ng/ml) and TAT (more than 4.1 ng/ml) levels (sensitivity of 100 and 70%, respectively). The corresponding figures of specificity were 81 and 42%. In the 56 patients with low-probability or indeterminate probability scans, 31 (55%) had DD concentrations of less than 500 ng/ml. These preliminary data suggest that a plasma DD concentration of less than 500 ng/ml might rule out the diagnosis of pulmonary embolism in suspected patients with an inconclusive lung scanning.
 ...
PMID:Laboratory diagnosis of pulmonary embolism: value of increased levels of plasma D-dimer and thrombin--antithrombin III complexes. 267 5

Adequate anticoagulation treatment in patients with deep vein thrombosis reduces the risk of thrombus extension or embolization to less than 5%. Thrombolytic treatment may possibly prevent subsequent postthrombotic syndrome. Heparin is the initial treatment of choice for most patients with deep vein thrombosis. The dose is adjusted according to the results of tests such as the whole blood clotting time, thrombin clotting time, activated partial thromboplastin time or plasma heparin concentration. The most commonly used test is the activated partial thromboplastin time which should be maintained at 1 1/2 to two times the control level. Initially the test should be performed two to three times daily and when optimal adjustment has been established, clotting studies are required only at 24-hour intervals. In general, treatment with intravenous heparin should be continued for seven to ten days. Thereafter, for secondary prophylaxis, treatment with oral anticoagulants is carried out for six to eight weeks for symptomatic lower leg thrombosis, for twelve weeks in the case of proximal venous thrombosis and pulmonary embolism. Oral anticoagulant therapy with warfarin should be given overlapping the last few days of heparin with the dose adjusted to prolong the prothrombin time to 1.3 to 1.5 times control. Initially, the prothrombin time should be monitored weekly, thereafter at intervals of two to three weeks. If oral anticoagulant therapy is contraindicated, secondary prophylaxis with subcutaneous heparin given twice daily in doses sufficient to prolong the activated partial thromboplastin time to 1 1/2 times control is an effective and safe alternative. The major side effect of oral anticoagulant therapy, as well as that of heparin, is bleeding.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Therapy of deep vein thrombosis. 269 42

A series of 80 patients operated for total hip prosthesis under epidural anesthesia was randomly allocated to treatment with Kabi 2165 (n = 40): 2,500 U anti-Xa preoperatively and evening of operation and 2,500 U anti-Xa morning and evening daily up to the 9th or 10th day postoperatively, or standard heparin (n = 40): 3,750 U preoperatively and then 8 hourly, at a dose adjusted with thrombin time and cephalin + activator time, daily up to the 9th or 10th day. Phlebography was performed routinely on the 9th or 10th day. Venous thrombosis occurred in 7 patients (17.5%) in the Kabi 2165 group, including two high, potentially emboligenic, localizations (5%), and in 4 patients (10%) in the standard heparin group, including 2 potentially emboligenic clots (5%). The difference is not statistically significant (total number: p = 0.5; potentially emboligenic: p = 0.33). Pulmonary embolism did not occur. Overall tolerance, evaluated from hemoglobin and hematocrit values, intra- and post-operative bleeding and operation wound hematoma and at injection site was comparable in the two groups.
 ...
PMID:[Comparison of the efficacy and tolerance of Kabi 2165 and standard heparin in the prevention of deep venous thrombosis in total hip prosthesis]. 283

In 22 patients with suspected pulmonary embolism and 19 patients with suspected deep vein thrombosis, thrombin-antithrombin III complex (TAT) as an indicator of thrombin activation was measured using a newly developed ELISA. For comparison fibrinopeptide A (FPA), as a marker of an activated coagulation, as well as platelet factor 4 (PF4), and beta-thromboglobulin (beta-TG), as markers of platelet activation, were determined. In all patients in whom pulmonary embolism was confirmed by perfusion lung scan and in 15 of 16 patients in whom deep vein thrombosis was confirmed by phlebography, TAT exceeded the upper limit of normal (3.0 ng/ml). FPA was increased in 71% of the pulmonary embolism patients, PF4 in 53%, and beta-TG in 59%. The data for the patients with deep vein thrombosis were comparable. PF4 and beta-TG were increased in more than 25% of the normal controls, FPA in 17%, and TAT in 9%. TAT is very sensitive in detecting an activation of the coagulation system in patients with suspected thromboembolic events. The test, however, is not specific for thromboembolism; it only indicates an activation of the coagulation system. Acute pulmonary embolism or deep vein thrombosis would appear to be unlikely if TAT is normal. The measurement of TAT is easier and less susceptible to disturbances than that of FPA, PF4, and beta-TG.
 ...
PMID:[Significance of the thrombin-antithrombin III complex in the diagnosis of pulmonary embolism and deep venous thrombosis--comparison with fibrinopeptide A, platelet factor 4 and beta-thromboglobulin]. 295 57

The aim of this retrospective study was to evaluate the adequacy of heparin treatment in deep venous thrombosis and the rate of symptomatic complications under the everyday conditions of a hospital. The investigation was carried out in 200 consecutive patients, 117 women and 83 men (mean age 61 +/- 17 years) with verified deep venous thrombosis. Na-heparin was given over 12 +/- 7 days; the initial daily dosage amounting to 31700 IU followed by a maintenance dosage of 36150 IU. 153 patients were treated exclusively or predominantly by the subcutaneous route (3 times daily) and 47 by continuous i.v. infusion. In the i.v. group 47% of thrombin times (TT) were prolonged to values exceeding 48 seconds in comparison with only 39% in the subcutaneous group (p less than 0.001). 34 patients developed thromboembolic complications (pulmonary embolism in 33), causing death in 13 cases. Patients with thromboembolic complications differed from those without in respect to the rate of a therapeutically prolonged TT (10% vs 44%, p less than 0.001) and signs of pulmonary embolism on admission (44% vs 8%, p less than 0.001), but not with respect to heparin dosage. Thromboembolic complications appeared in only 3 patients receiving i.v. therapy. Patients with thrombosis of the iliac or femoral veins appeared twice as likely to develop pulmonary embolism than patients with calf vein thrombosis (n.s.). Bleeding was registered in 11 patients. One patient died from retroperitoneal haemorrhage. At the time of bleeding 10 patients were on subcutaneous heparin and in 9 patients the TT was prolonged to over 2 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Heparin in deep venous thrombosis of the leg--effectiveness and safety]. 318 35

An enzyme-linked immunosorbent assay (ELISA) was developed for the determination of thrombin-antithrombin III complex (TAT) in human plasma. The test system follows the sandwich principle and uses two different antibodies directed against human thrombin and human antithrombin III, respectively. The antibodies bind selectively to the corresponding antigen moieties of TAT. The assay was calibrated with definite concentrations of preformed purified TAT added to TAT-poor plasma. The lower limit of sensitivity of the assay was 0.5 microgram/l. Mean coefficients of variation of 4.2% (intraassay) and 3.5% (interassay) were found for TAT concentrations between 2 and 60 micrograms/l. A reference range from 0.85 to 3.2 micrograms/l was calculated from TAT concentration in plasma samples from 88 healthy donors (mean value +/- SD: 1.45 +/- 0.4 micrograms/l). In plasma samples from patients with pulmonary embolism (n = 17), TAT concentrations between 3 and 25 micrograms/l were measured. In 15 patients with deep vein thrombosis, TAT was found up to 3 to 25 micrograms/l. From these data we conclude that measurement of TAT can be a sensitive parameter for specific detection of a latent activation of the clotting pathway.
 ...
PMID:Determination of human thrombin-antithrombin III complex in plasma with an enzyme-linked immunosorbent assay. 336 26

Protein C is, after activation by thrombin, a potent inhibitor of blood coagulation. An isolated deficiency of protein C increases the risk of thrombosis. The two forms of protein C deficiency, the heterozygous and the homozygous deficiency state, have different clinical features. Patients with heterozygous protein C deficiency are at a high risk to develop venous thrombosis and pulmonary embolism. In newborns with homozygous protein C deficiency with very low protein C levels (1%) a purpura fulminans like syndrome was observed. Heparin and coumarin derivatives are effective drugs in heterozygous protein C deficiency, homozygous patients may be treated either by replacement of protein C or coumarin derivatives. Decreased protein C levels were observed in various other diseases: Chronic and acute liver disease, disseminated intravascular coagulation, malignancy, postoperatively and during treatment with asparaginase. The role of protein C in these diseases to trigger thrombosis is not yet established.
 ...
PMID:Clinical relevance of protein C. 352 11


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