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)

Plasma levels of prothrombin fragment 1 + 2 (F 1 + 2), of thrombin-antithrombin III complexes (TAT) and of D-dimers were evaluated at several time intervals in 15 patients affected by acute proximal deep vein thrombosis, complicated or not by pulmonary embolism, and treated by conventional heparin therapy for 9 d. The mean levels of the three markers remained significantly increased throughout the period of observation, except for F 1 + 2 on day 9, when compared to normal values established in a population of normal healthy blood donors. However, whereas heparin significantly decreased the plasma levels of F 1 + 2 and of TAT complexes in less than 3 d. D-dimer levels were not significantly altered. Significant correlations were observed between the plasma levels of the three markers but they were not correlated to the actual intensity of heparin treatment evaluated as the activated partial thromboplastin time prolongation. These results indicate that heparin improves the hypercoagulable state associated with a deep vein thrombosis within the first days of treatment as indicated by TAT and F 1 + 2. They also account for the performances of D-dimer assay for the diagnosis of deep vein thrombosis in patients already receiving heparin, a common situation in routine hospital practice.
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PMID:Prothrombin fragment 1 + 2, thrombin-antithrombin III complexes and D-dimers in acute deep vein thrombosis: effects of heparin treatment. 187 25

Reported is a case of successful pulmonary thromboembolectomy and inferior caval vein interruption in a patient with subacute massive pulmonary thromboembolism (PTE). He had been complicated by the right atrial and deep vein thrombosis due to type I familial antithrombin III (ATIII) deficiency. Pulmonary embolectomy and caval interruption was performed 20 days after the initial attack and followed by anti-coagulation therapy. Thrombi weighed 50 gm were removed mainly from the left pulmonary artery. The right atrial thrombus which had got smaller by the preoperative fibrinolytic therapy could not be found with right atriotomy. Respiratory function at rest and slightly elevated pulmonary arterial pressure was normalized post-operatively. Although the PTE in this patient was considered to be subacute by the histological findings of the fibrin thrombus removed, tapering of pulmonary arteries in PAG and obstructive intimal hypertrophy of the small vessels in the lungs suggests the chronic nature of the PTE (post-thrombotic obstruction of pulmonary arteries) caused by the hyper-coagulable state. In patients with familial ATIII deficiency, 50% of normal ATIII activity can be expected because they are heterozygotes, so the cardio-pulmonary bypass should be run with special caution to the heparin dosage. Caval vein interruption and warfarin therapy are recommended for prophylaxis of recurrent PTE.
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PMID:[Pulmonary thromboembolectomy of subacute massive pulmonary thromboembolism in a patient with familial antithrombin III deficiency]. 194 May 20

This study was performed to determine the accuracy of D-Dimer fibrin derivatives, thrombin-antithrombin III (TAT) complexes and prothrombin fragments 1 + 2 (F 1 + 2) determinations for the diagnosis of deep vein thrombosis (DVT). One hundred and sixteen consecutive patients referred to the angiology unit of our hospital for a clinically suspected DVT were investigated. They were submitted to mercury strain gauge plethysmography and to ultrasonic duplex scanning examination; in cases of inconclusive results or of proximal DVT (n = 35), an ascending phlebography was performed. After these investigations were completed, the diagnosis of DVT was confirmed in 34 and excluded in 82. One half of the patients were already under anticoagulant therapy at the time of investigation. The 3 biological markers were assayed using commercially available ELISA techniques and the D-Dimer was also assayed with a fast latex method. The normal distribution of these markers was established in 40 healthy blood donors. The most accurate assay for the diagnosis of DVT was the D-Dimer ELISA which had both a high sensitivity (94%) and a high negative predictive value (95%). The D-Dimer latex, TAT complexes and F 1 + 2 were far less sensitive and provided negative predictive values which ranged between 78 and 85%. In spite of positive and significant correlations between the levels of the 3 markers, their association did not improve their overall accuracy for detecting DVT. Therefore, with the exception of the D-Dimer ELISA, these markers were of little value for the diagnosis of DVT in this specific population.
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PMID:D-Dimers, thrombin antithrombin III complexes and prothrombin fragments 1+2: diagnostic value in clinically suspected deep vein thrombosis. 202 37

The plasma levels of thrombin-antithrombin III-complexes (TAT) and the fibrin split product D-Dimer were measured in 39 patients with phlebographically proven acute DVT: 34 patients had proximal DVT, 5 had calf DVT. The sensitivity of D-Dimer and TAT measurements in the diagnosis of proximal DVT was found to be dependent on the duration of symptoms: 0 to 7 days (n = 27): elevated D-Dimer levels (greater than 120 ng/ml) = 1, D-Dimer Latex test positive (greater than 500 ng/ml) = 1, elevated TAT levels (greater than 6 ng/ml) = 0.88. Eight to 14 days (n = 7): elevated D-Dimer levels = 1, D-Dimer Latex test positive = 0.33, elevated TAT levels = 0.66; specificity: elevated D-Dimer: 0.48, D-Dimer Latex test: 1, elevated TAT: 0.76. Calf DVT patients (n = 5) had elevated D-Dimer levels, negative Latex tests and 3 of them had normal TAT values. Hemostatic and fibrinolytic parameters were also determined in 13 patients during heparin treatment of proximal DVT. Elevated D-Dimer and TAT levels rapidly decreased after initiation of anticoagulant therapy. In 2 of 13 patients a marked increase in D-Dimer and TAT levels was observed in periods of ineffective heparinization, documented by normal or only slightly prolonged thrombin clotting times. We conclude from our results that 1) D-Dimer EIA measurement, in contrast to TAT measurement, shows a very high sensitivity in the diagnosis of DVT, 2) due to low specificity this test can only be used to exclude thrombosis in patients with suspected DVT, and 3) the determination of the plasma levels of D-Dimer and TAT may be useful for judging the effect of anticoagulant treatment on thrombotic processes.
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PMID:D-dimer and TAT measurement in patients with deep venous thrombosis: utility in diagnosis and judgement of anticoagulant treatment effectiveness. 212 71

Inherited deficiencies of protein S, an inhibitor of the coagulation system, are now recognized as occurring at least twice as frequently as antithrombin III deficiency in patients with venous thrombosis. Protein S is present in plasma in a complexed form, which is inactive, and in a free or functional form. Free protein S combines with activated protein C to inhibit factors V and VIII. This report describes the evaluation of a family with recurrent deep venous thrombosis and superficial thrombophlebitis. Levels of antithrombin III and protein C as well as plasminogen were normal. The levels of total protein S, which includes the value for the free and complexed forms of protein S, were also normal. However, the free protein S levels were greatly reduced in all symptomatic members who were studied. This report illustrates the importance of obtaining measurement of free protein S levels in patients who are suspected of having inherited venous thrombotic disorders.
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PMID:Free protein S deficiency in a family with venous thrombosis. 214 6

The protein C inhibitor (PCI) concentration and other parameters of the protein C pathway were studied in 19 patients with symptomatic acute deep vein thrombosis before and during the first 5 days of heparin treatment. The mean levels of PCI antigen and activity decreased rapidly and significantly during the first day of heparin therapy from 83 and 84% to 60 and 59% of the pooled normal human plasma (p less than 0.01), respectively, and to 56 and 54% after 5 days of treatment (p less than 0.01). In contrast, antithrombin III decreased progressively 25% during 5 days of heparin treatment. Protein C antigen and activity and total protein S remained unchanged during heparin treatment. Free protein S was decreased before heparin treatment (83%, p less than 0.05) and increased to normal values after 5 days of treatment. C4b-binding protein was significantly increased before and during heparin treatment (p less than 0.01). Activated protein C (APC) complexed to its two major plasma inhibitors, PCI and alpha 1-antitrypsin (alpha 1AT) were measured by specific ELISA's. Before treatment, 18 of the 19 patients studied had increased levels of APC:alpha 1AT complexes with a mean value of 27 +/- 22 ng/ml (range, 6-86 ng/ml) compared to normal values (8 +/- 2 ng/ml) and 12 of the patients also had detectable APC:PCI complex levels with a mean value of 11 +/- 17 ng/ml (range, 5-68 ng/ml). Both APC:inhibitor complexes decreased significantly during heparin treatment.
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PMID:Protein C inhibitor and other components of the protein C pathway in patients with acute deep vein thrombosis during heparin treatment. 216 56

D-dimer and thrombin-antithrombin III complex (TAT) were assayed in 11 patients at various times pre- and post-operatively in order to determine the possible value of these parameters in screening for thromboembolic complications. Phlebography revealed distal thrombosis in 6 of the 11 patients. The D-dimer level, already elevated before surgery, increased at day 1 and remained high at days 5 and 10. Two methods were used for the assays and showed strongly correlated results. The TAT level increased at day 1 and then progressively returned toward basal values. No difference was observed at any time between patients with or without thrombosis. The results in surgical patients undergoing knee replacement suggest that neither D-dimer nor TAT assays are valid screening procedures for post-operative DVT. Nevertheless, in view of the small number of patient studied, further work is required to confirm these results.
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PMID:D-dimer and thrombin-antithrombin III complex levels uncorrelated with phlebographic findings in 11 total knee replacement patients. 219 59

Deep venous thrombosis and its complication pulmonary embolism are responsible for more than 50,000 deaths annually in the US, 2/3 of which occur postoperatively. Nearly 75% of such deaths could be avoided by adequate prophylaxis. All forms of surgery entail some risk of deep venous thrombosis, ranging from 10% after endoscopic prostate resection to over 50% for total hip replacement. 1.6 of thromboses will embolize and 1/4 of pulmonary emboli are fatal. The goal of prevention is to decrease the incidence of fatal pulmonary emboli while limiting the risks related to prevention. A secondary goal is to reduce the frequency of postthrombotic syndrome, a late complication of deep venous thrombosis which frequently causes invalidism. A preoperative evaluation of risks of deep venous thrombosis and of the likelihood of bleeding problems should be followed by selection of appropriate preventive measures. The evaluation should be repeated postoperatively, taking into account such factors as the duration of the intervention, the diagnosis, and the predicted duration of bed rest. Evaluation of the risk of deep venous thrombosis requires knowledge of its etiopathogenesis. Deep venous thrombosis results from a multifactorial process involving venous stasis, lesion of the vascular wall, and anomalies of blood composition. All the clinical risk factors for deep venous thrombosis are related to 1 or more of these elements. Risk factors related to stasis include immobilization, postoperative or postpartum status, pregnancy, and Cockett's syndrome. Risk factors related to lesions of the vascular wall include hip surgery, trauma, age, sepsis, varices and obesity, and postthrombotic syndrome. Risk factors related to blood anomaly include postoperative status, pregnancy, oral contraceptive use, cancer, nephrotic syndrome, hypercoagulability, trauma, and heredity. The most common clinical risk factors for deep venous thrombosis are age, surgical intervention, trauma, burns, cancer, pregnancy and delivery, oral contraceptive use, varices, obesity, and postthrombotic syndrome. The relative risk of deep venous thrombosis among OC users is 4.0 overall and higher for those with type A blood. The pathogenic mechanisms are similar to those of pregnancy except that the fibrinolytic capacity is not change. The principal mechanism is perhaps the declining level of antithrombin III, observed with estrogens and some progestins. Among methods of prevention are different forms of compression, use of heparin alone or in combination with other drugs, and oral anticoagulants.
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PMID:[Epidemiology and etiopathogenesis of deep venous thrombosis of the lower limbs]. 224 Apr 6

The study was carried out of 53 patients with acute myocardial infarction receiving no anticoagulant treatment. Changes were traced in certain indices of the blood clotting system and fibrinolysis in plasma in the first 14 days of the disease, with particular attention given to patients in whom during the hospitalization signs of deep vein thrombosis in the lower extremities appeared or a positive result was obtained of the test with 125I-fibrinogen. In a group of 9 patients with deep vein thrombosis developing during the observation, on the first day of myocardial infarction shortening of the kaolin-cephalin clotting time and considerable rise of the level of fibrinogen-fibrin (FDP) degradation products were noted in serum, and on the 14th day raised fibrinogen level and reduced exogenous fibrinolytic activity of the plasma were noted. Increased level of fibrinogen and FDP and exogenous and endogenous plasma fibrinolytic activity observed on the 7th day of the disease were not related to the development of thrombotic complications. The thrombin clotting time, platelet count, factor X level, protein C concentration and antithrombin III activity in the plasma were not significantly changed during myocardial infarction. The obtained results suggest a limited usefulness of the basic tests of the clotting and fibrinolytic systems for early diagnosis of deep vein thrombosis in acute myocardial infarction.
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PMID:[Assessment of hemostasis in patients with myocardial infarction complicated by deep venous thrombosis]. 227 86

The pre-surgery identification of patients at risk for the development of post-operative venous thromboembolism has not yet been achieved. It is a well recognized fact that major surgery without prophylaxis encompasses a high risk for thrombosis, in particular orthopaedic operations (hip/knee surgery approximately 50%) and abdominal surgery (approximately 20%). Other well-defined risk factors, though rarely occurring, are deficiencies of the major inhibitors of blood coagulation (i.e. protein C, protein S and antithrombin III). Less well-defined risk factors are a history of previous thrombosis, obesity, varicosis, cancer etc. In an attempt to identify patients at risk for thrombosis prior to surgery, several investigators have developed complicated risk predictors, i.e. formulae comprising combinations of coagulation test results and physical characteristics such as body weight. However, the clinical usefulness has only been demonstrated in two small studies evaluating gynaecological surgery patients. These prognostic indices have not, however, found general acceptance and are not used routinely. The importance of all these risk factors for patient management with regard to thrombosis prevention is relatively small. Irrespective of the absence or presence of identified risk factors, currently the majority of patients will receive some formal thrombosis prophylaxis. The major problem at present is the development of proximal vein thrombosis despite the best possible thrombosis prophylaxis (approximately 10% after hip surgery). Identification of these patients pre-operatively or in an early stage in the post-operative phase by single screening tests should be a major research issue. Furthermore, the development of a prophylactic regimen which eliminates proximal deep vein thrombosis is still desperately needed.
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PMID:Pre-surgical identification of the patient at risk for developing venous thromboembolism post-operatively. 228 76


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