Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coagulation and fibrinolytic studies have been performed in patients who were undergoing major gynaecological surgery and randomised to either fixed minidose warfarin (1 mg daily) or matched placebo. With warfarin, a prolongation of the prothrombin time was observed on day 2 which persisted for at least 5 days and was greater than with placebo. The maximal postoperative mean INR was, however, only 1.2 which is considerably less than the target value for prophylaxis of deep vein thrombosis with full dose warfarin. The warfarin group showed two unexpected findings: significantly elevated fibrin specific degradation products throughout the postoperative period compared with placebo and absence of the expected rise of PAI, the major fibrinolytic inhibitor, on the first day after surgery. Levels of fibrinogen degradation products and F1 + 2 prothrombin fragments rose significantly and progressively in both groups in the postoperative period. With placebo, F1 + 2 showed an apparent higher percentage increase on each post-operative day but the differences between the groups were not significant. Increased fibrinolysis may be one of the mechanisms for the protective action of minidose warfarin in prophylaxis of DVT after major surgery.
 ...
PMID:Effects of fixed minidose warfarin on coagulation and fibrinolysis following major gynaecological surgery. 208 36

We have identified an inhibitor of the protein C anticoagulant pathway in the plasma of a patient with systemic lupus erythematosus and a history of recurrent deep vein thrombosis, fetal wastage, and seizures. The patient's plasma contained anticardiolipin antibodies as well as a weak lupus anticoagulant. Examination of this patient's plasma revealed normal levels of protein C and protein S antigen, normal levels of functional protein C, as well as essentially normal levels of every blood coagulation factor. In a modified prothrombin time assay, the activated protein C-mediated prolongation of the clotting time observed in normal plasma was not observed in this patient's plasma. Gel permeation chromatography of the patient's plasma revealed that the inhibitory material was a high molecular weight protein that coeluted with the IgM peak. The inhibitor did not appear to circulate as a complex with protein C, since the inhibitor could easily be separated from protein C during fractionation procedures, and did not interfere with the activation of protein C in plasma as assessed by a functional amidolytic assay. Our findings suggest that the recurrent thrombotic episodes observed in this patient may have occurred as a result of the patient's antiphospholipid antibody neutralizing specific phospholipids essential for the full expression of the anticoagulant activity of activated protein C.
 ...
PMID:Impairment of the protein C anticoagulant pathway in a patient with systemic lupus erythematosus, anticardiolipin antibodies and thrombosis. 210 91

Broad spectrum assays which measure a range of fibrinogen/fibrin derivatives (FDPs) in serum have become an established means of identifying activation of blood coagulation and/or fibrinolysis, such as occurs in disseminated intravascular coagulation (DIC). There is considerable interest in the application of these assays to the diagnosis of other hypercoagulable states, such as recurrent deep venous thrombosis and myocardial infarction. In recent years, more sensitive and specific FDP assays (e.g. for fragment E, fragment E neoantigen, D-dimer, fragment D neoantigen, fibrinopeptide A and fibrin fragment beta 15-42) have been devised, some of which allow measurement in plasma of FDPs without interference from fibrinogen or certain of its derivatives. It was predicted that these assays would both avoid the possibility of artifacts introduced as a consequence of serum preparation and improve detection of hypercoagulable states. In the light of these expectations we have reviewed data published on the use of assays to detect clinical hypercoagulability, giving prominence to assays of crosslinked fibrin derivatives and nothing particularly certain studies that have compared the performance of different assays on the same samples. The accumulating evidence indicates that all of the assays are adequate for detection of DIC. The same cannot be said for other hypercoagulable states. Here much variation is evident between different studies of similar patients in the ability of a particular marker to discriminate between a normal control group and patients determined to be hypercoagulable by an independent method. This variability would seem to be a function of patient group heterogeneity and selection, as assays that detect different antigenic determinants produce results on the same plasma samples that are well correlated. It appears that the precise antigenic determinant does not critically affect detection of hypercoagulability. Additionally, some studies have indicated that use of serum need not introduce artifacts. Despite there being no other obvious advantage, the convenience of some of the plasma assays may well encourage their widespread use. Assays have also been developed for measuring activation fragments of coagulation proteins (e.g. prothrombin fragment F1 + 2 and protein C activation peptide) and for proteinase inhibitor complexes (e.g. thrombin-antithrombin complex) generated during activation of coagulation. The latter assays have been useful in providing a biochemical definition of a 'prethrombotic state'.
 ...
PMID:Assessment of hypercoagulable states by measurement of activation fragments and peptides. 218 46

Twenty-three patients with malignant glial neoplasms were treated with anticoagulant therapy for thromboembolic complications. Fifteen patients had deep vein thrombosis alone, and 8 patients had both deep vein thrombosis and pulmonary embolism. Serum prothrombin times were maintained at 1.25 times control for an average of 5.8 months per patient, for a total patient exposure to warfarin therapy of 132 patient-months (11 patient-years). Only 1 patient suffered a recurrent pulmonary embolism, and this occurred during an episode of gastrointestinal bleeding, when anticoagulant therapy had to be discontinued prematurely. All patients were followed with serial computed tomographic or magnetic resonance imaging scans, and no patient showed radiographic evidence of intratumoral hemorrhage either during or after warfarin therapy. One patient, who died from a large recurrent glioblastoma, was found at autopsy to have scattered foci of intratumoral hemorrhage. This series, together with a review of the available literature, suggests that oral anticoagulant therapy is both a safe and effective means of treating thromboembolic complications in patients with residual malignant glial tumors.
 ...
PMID:The risk and efficacy of anticoagulant therapy in the treatment of thromboembolic complications in patients with primary malignant brain tumors. 206 23

We have developed a specific and sensitive ELISA for the measurement of the TAT in human plasma. The assay follows the sandwich principle and uses two different antibodies directed against human thrombin and human antithrombin III, respectively. The anti-thrombin antibody population used for coating was purified by immunoadsorption on immobilized prothrombin and thrombin, respectively. Antithrombin III antibodies were conjugated with peroxidase. Plasma samples containing TAT were incubated in polystyrene tubes coated with anti-thrombin antibodies; after washing, peroxidase-conjugated antithrombin III antibodies were added and bound enzyme activity was subsequently measured using o-phenylenediamine. The assay was calibrated with definite concentrations (2.0 to 60 micrograms/l) of preformed purified TAT added to TAT-poor plasma. Plots of absorbance at 492 nm against TAT concentrations revealed a linear correlation (r = 0.98). A reference range from 0.85 to 3.0 micrograms/l was calculated from TAT concentration in plasma samples from 88 healthy donors (mean value +/- SD: 1.45 +/- 0.4 micrograms/l). In patients with deep vein thrombosis confirmed by phlebography (n = 15), TAT was found up to 7-13 micrograms/l. Patients with septicemia associated with a consumption coagulopathy (n = 10) showed markedly increased TAT values (greater than or equal to 10 micrograms/l). From these data it can be concluded that measurement of TAT might be a parameter for detection of a latent clotting pathway activation.
 ...
PMID:Determination of human thrombin-antithrombin III complex by enzyme immunoassay. 246 14

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

Deep venous thrombosis and pulmonary embolism are frequently diagnosed in patients encountered in a primary-care practice. Poor prognosis is related to acute sudden death and to recurrent thromboembolic disease. Anticoagulant therapy with heparin followed by coumarin derivatives is highly effective in preventing such recurrences, but the intensity of anticoagulation must be strictly monitored. Treatment with heparin, sufficient to prolong the activated partial prothrombin time to 1.5 to 2.0 times the control, should be continued for five to ten days, and oral anticoagulation should be overlapped with heparin for four to five days. The recommended therapeutic range for the prothrombin time during coumarin therapy is an INR of 2.0 to 3.0. The duration of anticoagulant treatment must be tailored to the individual patient. Patients with slowly resolving risk factors must be treated for at least three months after an acute deep vein thrombosis and for six months after a pulmonary embolism. Patients with tumors, antithrombin III, protein C or S deficiency should be treated indefinitely.
 ...
PMID:[Prevention of recurrence of thromboembolic disease: maintenance of anticoagulant therapy]. 281 10

The aim of our work was to study in a population of high risk patients with hemorrhagic and or thrombotic disease, the preventive or therapeutic effect of a low molecular weight heparin fraction, CY 216 (Choay, France), particularly in surgery. CY 216 was given to 9 patients for the treatment of a thrombosis (pulmonary embolism, acute ischemia, deep venous thrombosis) and to 40 patients in prevention of thrombosis. In this second group, 28 had a high thromboembolic risk such as valvular prosthesis, cardiac arrythmia, coronary artery bypass, etc. For all the patients, CY 216 was injected sub-cutaneously twice or three times a day at the mean dose of 1.5 mg/kg/d, equivalent to 300 U anti-Xa Choay/24 h, and always injected 24 hours before surgery. The biological tests used were: blood cells count, platelet count, prothrombin time, activated partial thromboplastin time, heparinemia levels by two technics: anti-factor-Xa activity and anti-factor IIa activity. None thrombotic complication was observed in the 40 patients prophylactically treated and a constant improvement of thrombosis was noted for the 9 patients with thrombo-embolic disease. In 3 patients, bleeding complications were observed: for 2 patients, all the coagulation tests were normal and anti-Xa activities were less than 0.55 U/ml; in one patient, the bleeding time was prolonged (15 minutes Ivy Incision) and returned to normal when the CY 216 was stopped. Concerning the biology, there was no modification except for anti-Xa activity which mean was 0.30 U/ml (01-07). However, this test is unable to predict either thrombotic or hemorrhagic events.
 ...
PMID:[Prophylactic and therapeutic use of a low molecular weight heparin fraction, CY 216]. 283 83

The various therapeutic modalities in deep venous thrombosis of the lower limbs (surgical thrombectomy, thrombolysis, anticoagulation, bed rest) are discussed with special reference to developments in the last ten years (new generation of thrombolytics, introduction of INR to express prothrombin time). Tentative therapeutic guidelines are proposed.
 ...
PMID:[The treatment of deep venous thrombosis of the lower limbs]. 305 66

In Western countries, hepatic vein thrombosis (Budd-Chiari syndrome) is, as a rule, an uncommon though well-known complication of acquired or hereditary thrombophilia. It may be complicated by overt defibrination when secondary to deep venous thrombosis ascending to the vena cava. To be effective treatment should consist of early initial intensive thrombolysis for up to one week, followed without interruption by an APTT-controlled heparin infusion. Oral anticoagulant therapy is started together with the heparin, which should not be discontinued until the prothrombin times, expressed as international normalized ratios (INR), lie within a therapeutic range of 3-5 INR for 2 days, the target being 4 INR. After this intensity of anticoagulation has been maintained for three weeks, the range may be lowered to 2.5-4 INR, the target being 3 INR. Oral anticoagulation should be continued for as long as thrombophilia persists.
 ...
PMID:[Fibrinolytic and anticoagulation therapy in Budd-Chiari syndrome. Review and recommendations]. 312 3


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