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

Thrombolytic therapy has been used for treating patients suffering from a variety of clinical disorders including patients suffering from extensive venous and arterial thrombosis. This paper describes a combined approach to lytic therapy consisting of administration of small doses of streptokinase in combination with the infusion of plasminogen. The rationale for this approach is based on recent observations that additional plasminogen will be absorbed into preformed thrombi, rendering them more susceptible to lysis in the presence of activators. Forty-four patients who presented with symptoms and signs of acute or sub-acute deep vein thrombosis (DVT) confirmed by phlebography, were included in this study. Group I: 15 consecutive patients received an infusion of 600,000 units of SK dissolved in 50 ml of physiological saline over a period of half and hour. On the subsequent 4 days, a dose of 300,000 units was given twice daily. Group II: 29 consecutive patients received 60 to 90 mg of pretreated plasminogen dissolved in 50 ml of saline given intravenously over 30 min. and followed by same dosage regimen of SK. Blood samples were taken at varying intervals to assess changes in the haemostatic parameters. These were analysed for levels of alpha 2-antiplasmin, antithrombin III, fibrinogen, plasminogen, fibrinogen and degradation products, fibrinolytic activity and levels of activator complex. Findings observed will be presented. Phlebograms were performed before starting treatment and were repeated at the end of 5 days when the treatment had finished. In Group I--(15 patients)--thrombi remained virtually unchanged in 12 out of 15 patients receiving streptokinase infusion; in 3 (20%) there was partial but extensive lysis. In contrast, in Group II--(29 patients)--in 16 (55%) of 29 patients receiving plasminogen and streptokinase infusion, complete lysis of thrombi was obtained. Seven (24%) showed extensive clearance of venous tree while in remaining 6, thrombi virtually remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intermittent plasminogen-streptokinase treatment of deep vein thrombosis. 335 Mar 94

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.
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PMID:Determination of human thrombin-antithrombin III complex in plasma with an enzyme-linked immunosorbent assay. 336 26

Familial hypercoagulable states are a collection of syndromes characterized by an inherited deficiency of various proteins involved in the control of coagulation and include antithrombin III, plasminogen, protein C, and protein S. Affected patients usually develop venous thrombosis as adults. During a 15-month interval, we identified five patients with venous thrombosis accompanied by protein C deficiency. Four patients presented with deep venous thrombosis, which was recurrent in two, and one patient developed mesenteric venous thrombosis. The kindred of this last patient suggested an autosomal dominant genetic transmission of protein C deficiency. Patients' ages at the time of diagnosis of disease ranged from 28 to 41 years. All patients had low levels of protein C (range, 34 to 67 U/dL; normal, 70 to 130 U/dL). All patients were treated with heparin sodium immediately and then given long-term oral anticoagulation therapy with warfarin sodium. Protein C deficiency is a predisposing factor to the development of venous thrombosis that has only recently been recognized. Treatment of symptomatic protein C deficiency requires short-term heparin therapy followed by long-term oral anticoagulation therapy with warfarin. Oral anticoagulation treatment must be initiated slowly with no loading dose to avoid warfarin-associated skin necrosis. Patients with unexplained or unusual thrombosis, especially if it occurs at an early age, and patients with recurrent episodes of lower limb venous thrombosis should have their protein C levels measured. If a deficiency is documented, long-term warfarin anticoagulation therapy is recommended.
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PMID:Protein C deficiency. A cause of unusual or unexplained thrombosis. 338 55

Three patients with karyotype XYY who had presented with deep vein thrombosis and leg ulcers (plus pulmonary embolism in two of them) were investigated for: (1) androgens (plasma testosterone measurement, testosterone oestradiol binding globulin (TeBG) assay, GnRH 50 micrograms test), and (2) haemostasis by fibrinolysis tests (euglobulin lysis time and area, antigenic plasminogen activator assay before and after 10 min venostasis). Full evaluation of haemostasis failed to demonstrate the presence of circulating anticoagulant or of antithrombin III, protein C and protein S deficiencies. One patient had neither hormonal nor fibrinolytic abnormality. The other two patients shared some clinical features with male hypogonadism (gynoid morphotype in both, hypotrophy of the testes in one, gynaecomastia in the other). They also had hormonal disorders ("over-response" to the GnRH test in one case, elevated TeGB in the other case) and abnormalities of fibrinolysis (poor response to venostasis, high baseline level of plasminogen activator). Response to venostasis became normal after 3 months of treatment with percutaneous dihydrosterone 125 mg per day in the two patients with initially poor response. The mechanism of venous pathology in XYY subjects is discussed. A genetic defect not involving the fibrinolysis system is possible since fibrinolysis was normal in one patient; however, abnormal fibrinolysis may have been responsible for the venous pathology in the other 2 patients. The role played by abnormalities of fibrinolysis in the pathogenesis of deep vein thrombosis and leg ulcers is recalled, and the possible implication of these abnormalities in patients with XYY karyotype is emphasized.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Post-phlebitic leg ulcers and XYY karyotype: fibrinolysis and androgenic function tests. Apropos of 3 cases]. 343 47

Oral anticoagulants are used extensively, although their risks are not always fully recognized. The prophylaxis of venous thrombosis after hip surgery, the prevention of deep venous thrombosis and pulmonary emboli after an acute episode of these, the prevention of arterial emboli from the heart in patients at risk, and the prophylaxis of thrombosis in patients with congenital deficiency of antithrombin III, protein C, or protein S are some of the indications for oral anticoagulant use. Warfarin sodium is contraindicated in pregnancy, however. The recommended prothrombin time is 1 1/2 to two times control, lower than previously. The major risk of oral anticoagulant therapy, bleeding, is treated with vitamin K or plasma, depending on its severity. Warfarin necrosis and the "purple-toe" syndrome are seen more frequently than realized.
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PMID:Current concepts of warfarin therapy. 351 25

We conducted an evaluation of the hemostatic integrity of patients with untreated cancer of the prostate. Of 60 patients analyzed retrospectively, only 1 had a mild case of disseminated intravascular coagulation, possibly associated with concomitant estrogen therapy, and in 1 patient mild deep vein thrombosis developed preoperatively, also possibly associated with multiple medications for concurrent disorders. Of 16 other patients prospectively evaluated on admission, only 1 had frankly abnormal levels of fibrinopeptide A unaccompanied by other coagulation abnormalities. Occasional individuals had minimal, negligible deviations of partial thromboplastin times, thrombin time, or antithrombin III values. In none of these patients did hemostatic complications develop during their hospital stay. These results demonstrate that although an occasional coagulation abnormality may occur in patients with cancer of the prostate (albeit with a lower incidence than in other neoplasms), this malignancy does not require increased precautions with respect to those given to the patient population at large.
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PMID:Untreated prostatic carcinoma is not associated with frequent thrombohemorrhagic disorders. 360 3

Three factors leading to the development of postoperative deep venous thrombosis (DVT) are the hypercoagulable state, stasis, and vein wall injury, which occur in patients undergoing surgical procedures. Vein wall injury is thought to occur as a smooth muscle response to surgical trauma in veins distant from the operative site. Heparin and dihydroergotamine (DHE) were combined in an attempt to decrease the hypercoagulable factor and minimize stasis. We believe that by maintaining venous smooth muscle tone, the degree of endothelial damage is also diminished. Low-dose heparin acts through its effect of factor Xa and activation of antithrombin III; DHE selectively increases venous smooth muscle tone to accelerate venous blood flow velocity and minimize venous pooling. The European experience with combination DHE-heparin prophylaxis shows that this combination is more effective than either agent alone, and studies on orthopedic patients have shown that DHE/5,000 is effective in preventing postoperative DVT in this high-risk group. In the US, the Multicenter Trial evaluated postoperative DVT in general surgical patients. The combination of DHE/5,000 was statistically more effective in the prophylaxis of postoperative DVT than placebo (p = 0.0011). The interim results of an ongoing Multicenter Trial on the prophylaxis of postoperative DVT in patients undergoing total hip replacement indicate that DHE/5000 has significant prophylactic efficacy compared to placebo. It is proposed that the mechanism of action of the DHE-heparin combination is synergistic, since all 3 limbs of Virchow's triad are potentially affected.
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PMID:The use of dihydroergotamine and heparin in the prophylaxis of deep venous thrombosis. 369 18

The significance of acquired antithrombin III (AT III) deficiency must be interpreted in close relation to the underlying disease process. In patients with acute or chronic liver impairment, the AT III activity is related to a decrease of procoagulatory factors, whereas, in protein loss syndromes such as nephrotic syndrome, the AT III indicates an increased risk of thromboembolic events. The effect of oral contraceptives (OC) on AT III levels in young healthy females (n = 30) was determined prospectively. AT III decreases during OC usage could not be related to the estrogen content of the examined oral contraceptives, and there was no parallel decrease of AT III activity and concentration in each type of OC. In a prospective study, the extent of AT III decrease was determined in patients undergoing cardiopulmonary bypass operations (CPB) receiving different anticoagulant schedules during extracorporeal circulation (n = 49). There was no significant influence on the effectiveness of anticoagulation by the observed AT III decreases. AT III deficiency during CPB was primarily the result of hemodilution. However, the AT III kinetics were significantly influenced by the different protamin dosages and were not affected by the different heparin dosages. Correction of diminished AT III levels by substitution of AT III concentrates is beneficial in cases, in which an interruption of an enhanced coagulatory process such as disseminated intravascular coagulation is necessary or in patients requiring high dosage heparinization as in deep vein thrombosis. In those cases the quality of AT III correction correlates to the course of the disease. However, the potency of concentrates as well as the individual AT III recovery and half-life must be considered for an appropriate treatment with AT III substitution.
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PMID:[Clinical aspects of acquired antithrombin III deficiency]. 371 7

Ever since 1961, there has been discussion on possible thromboembolic effects from the use of oral contraceptives. The purpose of this Danish study was to determine if birth-control pill users did have an increased risk of venous thromboembolic disease (VTD), including deep venous thrombosis and pulmonary embolism. In previous research, morbidity from VTD has been found to show a great variance, as high as 1/330 woman years in 1 study to as low as 1/5,000 woman years in another. In these studies no significant difference was found between users and non-users of oral contraceptives. Only in 1 study was there found to be increased morbidity from VTD among pill users: 1/5,200 woman years, compared with 1/35,000 woman years for non-pill users. As a possible explanation of the pill's effect, several studies have demonstrated a rise in certain coagulation factors, increased fibrinogen and lowered antithrombin III. In the present study, medical records of all women aged 34 or under who had been referred to a Copenhagen hospital between 1981 and 1983 for treatment of phlebographic-or lungescintographic-confirmed VTD were investigated. After controlling for exclusion factors, there remained 35 test subjects between the ages of 16 and 34 (median age 22). Of the 22 cases of known etiology, 16 suffered from iatrogenic VTD. Of 13 women who suffered from VTD of unknown etiology, 69% were pill users, compared with only 29% (a significant difference) in a background-population interview study conducted in Denmark during 1983. With a known disposition to VTD, oral-contraceptive usage meant a relative risk of 0.9 for developing the disease, which figure conforms well with other cited research (in which the risk factor varied from 0.4 to 3.8).
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PMID:[Venous thromboembolic disease and oral contraceptives]. 377 22

Plasminogen, fibrinogen, antithrombin III, euglobulin lysis time, tissue plasminogen activator (t-PA) and fast-acting t-PA inhibitor were measured in 21 patients receiving either stanozolol (10 mg orally given for 14 days preoperatively) or subcutaneous heparin, during a continuing comparative trial in the prevention of postoperative deep vein thrombosis. Stanozolol treatment resulted in significant (p less than 0.01) increases between the 14th and 1st preoperative days in the plasma concentrations of plasminogen (3.4 to 4.9 Cu/ml) and antithrombin III (107% to 132%); t-PA levels did not increase significantly (6.0 to 16.0 mU/ml; p greater than 0.1). There were significant (p less than 0.02) falls in fast-acting t-PA inhibitor (132% to 75%) and fibrinogen (2.4 to 1.8 g/l). Surgery reversed the changes in fibrinolytic activity seen preoperatively in the stanozolol-treated patients, and similar changes were seen in the heparin-treated group. In this dosage, stanozolol does not appear to prevent the fibrinolytic shutdown which occurs after elective major surgery.
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PMID:Effects of oral stanozolol used in the prevention of postoperative deep vein thrombosis on fibrinolytic activity. 387 18


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