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)

The plasma concentration of the platelet-specific protein beta-thromboglobulin was measured in fourteen patients who had been investigated for deep venous thrombosis by venography or 125I-fibrinogen scanning. All six patients with a proven thrombus had a raised plasma concentration of beta-thromboglobulin. Eight patients in whom no thrombus could be demonstrated had plasma concentrations of beta-thromboglobulin similar to a control group of thirty-five normal individuals. These results indicate that the measurement of plasma beta-thromboglobulin concentrations may be of use in the diagnosis of deep venous thrombosis.
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PMID:New rapid method for diagnosis of deep venous thrombosis. 4 2

The measurement of plasma beta-thromboglobulin as a potential diagnostic test for venous thrombosis has been investigated in 16 normal volunteers, 24 patients presenting with deep vein thrombosis (DVT) or pulmonary embolism and 46 patients screened by 125I fibrinogen test (IFT) for post-operative DVT. The normal mean was 33 ng/ml (range 15-117 ng/ml). Of the 24 patients with clinical thrombotic disease 22 presented with DVT confirmed by phlebogram or IFT and 2 presented with embolism confirmed by lung scan. At the time of first presentation 12 out of 24 had betaTG values greater than 70 ng/ml. All except 3 of this group of 24 patients had values of greater than 70 ng/ml at some stage during a subsequent week of daily sampling. DVT was detected in 13 out of 46 screened post-operative patients. There was a rise om betaTG observed within 24 hr of the IFT becoming positive but the mean rise did not reach significance at the 5% level. An association between DVT and high betaTG values has been confirmed. However, its clinical value cannot yet be fully elucidated until factors, probably related to blood sampling and clearance, are further investigated.
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PMID:beta-thromboglobulin and deep vein thrombosis. 7 29

Plasma beta-thromboglobulin (beta TG) levels were measured in 103 healthy controls and 112 patients suffering from either peripheral vascular disease (PVD), or cerebrovascular disease (CVD) or deep vein thrombosis (DVT). Plasma beta TG was significantly elevated in 46 PVD patients and 24 recent DVT patients compared to controls, but did not differ significantly in 18 chronic DVT and 24 old CVD patients. In addition, heparin neutralizing activity (HNA) and platelet aggregation induced by adenosine diphosphate, 1-epinephrine and thrombin were compared in 33 out of the 46 PVD patients to 33 controls. The mean HNA was significantly shorter in the PVD patients than in controls. The rate and extent of platelet aggregation were increased in PVD patients compared to controls, but the difference was not statistically significant. Platelet production time (PPT) was measured in 20 controls, 35 PVD patients, nine chronic DVT and 12 chronic CVD patients; significantly shorter PPT was only observed in 14 patients with advanced PVD compared to controls, suggesting increased platelet consumption in these patients. All four assays (plasma beta TG, HNA, platelet aggregation and PPT) were performed in 25 patients; no correlation between the four tests was found in these patients suggesting that the tests were measuring various aspects of platelet function. These results suggest that in vivo platelet consumption as well as platelet aggregation and 'release reaction' are presumably enhanced in PVD and recent DVT patients and that plasma beta TG and PPT assays may be better and more specific indicators of in vivo platelet activation than in vitro platelet aggregation test.
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PMID:beta-Thromboglobulin, platelet production time and pletelet function in vascular disease. 9 36

A method for labelling of platelets with technetium-99m (Tc-99m) is presented. In principle, aminobenzoic acid and tartaric acid are used as reagents, allowing Tc-99m complexes of intermediate chemical stability to be formed. These complexes react rapidly with proteins, such as platelet proteins, when added. We have examined the isolation procedure for the platelets and the labelling procedure using residual aggregational ability and residual content of beta-thromboglobulin (beta-TG) as indicators of damage to the platelets. In its final version the method allowed a 32.6 +/- 2.7% (mean +/- SD) incorporation of Tc-99m into platelets which again showed a 66 +/- 15% residual aggregational ability, tested by 50 mumol/l of ADP, and a 79 +/- 17% residual content of beta-TG releasable by 10 IU/ml of thrombin. In a pilot clinical study involving 28 patients we found labelled autologous platelets useful in detecting lung embolism and deep vein thrombosis.
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PMID:Radiolabelling of platelets with technetium-99m. 214 Feb 7

Postpartum deep vein thrombosis is believed to be related to increased activation of the hemostasis system at the time of delivery. To date, studies designed to test this hypothesis have had relatively small sample sizes or used the measurement of specific coagulation factors and functional tests reflecting hemostasis activity in vitro. With the use of recent technologic advances we determined the effect of delivery on hemostasis in vivo by measuring 11 hemostatic indices simultaneously in 70 healthy pregnant women. Significant increases were found in fibrinopeptide A (p less than 0.001), beta-thromboglobulin (p less than 0.001), and platelet factor 4 (p less than 0.001), suggesting maximum platelet activation and fibrin formation at the time of delivery. In addition to continued clotting activity at 3 hours post partum, increased D-dimer, fibrin-fibrinogen degradation products, and decreased alpha 2-antiplasmin levels suggest maximum fibrinolysis. These changes reflect a peak in hemostatic activity at delivery and in the immediate postpartum period that may predispose the development of deep vein thrombosis.
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PMID:Changes in hemostasis activity during delivery and the immediate postpartum period. 214 Feb 36

The euglobulin lysis time (ELT) in antecubital vein and femoral vein was investigated in 35 patients before and after bilateral intermittent sequential leg compression for one hour. After compression, ELT in antecubital vein was shortened, and that in femoral vein was significantly shortened (p less than 0.05). beta-thromboglobulin, fibrinopeptide B beta 15-42 and alpha 2-plasmin inhibitor were also investigated, but no significant change was found after compression. The mean and peak blood velocity of the femoral vein before and during compression was measured using Doppler ultrasound in 20 patients. The mean blood velocity increased about 183% (p less than 0.001), and the peak blood velocity also increased 178% (p less than 0.001). ELT was measured pre- and post-operatively in 31 patients who had intermittent sequential compression during operation and succeeding two days and in 31 controls which had no compression. Both in antecubiltal vein and in femoral vein, ELT in the compression group was significantly shorter than that of control group in the first postoperative day. This study demonstrates that intermittent sequential compression of the legs increased fibrinolytic activity, and this effect may contribute to the prevention of deep venous thrombosis.
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PMID:[Postoperative deep venous thrombosis prevention with intermittent sequential compression]. 293 32

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.
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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

A prospective study involving 120 consecutive patients undergoing total hip replacement was performed to compare the effectiveness of aspirin (high and low dose) or a combination of heparin plus dihydroergotamine (heparin-DHE) in preventing isotopic and phlebographic deep vein thrombosis (DVT), and to evaluate their effect on postoperative platelet changes. Phlebographic DVT was demonstrated in 9 cases (30%) in control group, in 1 (3.3%) in aspirin (high-dose) group (p less than 0.01), in 1 (3.3%) in aspirin (low-dose) group (p less than 0.01) and in 5 (16.6%) in heparin-DHE group (p = NS). Aspirin was able to reduce the postoperative increase in circulating platelet aggregates, platelet factor 4 and beta-thromboglobulin observed in control group. This study shows that aspirin is effective in the prevention of DVT for patients undergoing total hip replacement. Small aspirin dose (250 mg/day) represents an effective form of prophylaxis in these patients.
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PMID:Prophylaxis of thromboembolic disease and platelet-related changes following total hip replacement: a comparative study of aspirin and heparin-dihydroergotamine. 353 58

Postoperative changes related to platelets and their correlation with the incidence of deep venous thrombosis (DVT) were studied in 30 patients undergoing total hip replacement. Levels of platelet count, platelet-crit, mean platelet volume, spontaneous platelet aggregation, platelet factor 4 (PF4) and beta-thromboglobulin (beta-TG) were measured before operation and on the 1st, 3rd and 7th postoperative days. DVT was detected by 125I-fibrinogen leg scanning in 11 of the patients. After the operation there was a significant and progressive increase (p less than 0.01) in PF4 and beta-TG, and the presence of circulating platelet aggregates was demonstrated. Platelet count levels and platelet-crit were decreased on the 1st and 3rd postoperative days followed by recovery on the 7th day. The changes observed following total hip replacement were not related to the development of postoperative DVT.
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PMID:Deep vein thrombosis and related platelet changes after total hip replacement. 407 46

Platelets may be useful as markers of thromboembolic disease. When labeled with indium 111 they allow external imaging of localized clots. Indium 111 is much superior to chromium 51 for this procedure. Detection of circulating platelet aggregates also appears to be a simple means of determining the presence of thromboembolic disorders. In response to injury or involvement in clotting, platelets release several unique proteins not normally found in the plasma. Therefore, elevated levels of these proteins suggest the presence of such damage. Platelet factor 4 and beta-thromboglobulin are the most widely studied of these proteins, and both can be quantitated by radioimmunoassay. Such assays are now commercially available. Elevated levels have been demonstrated in such diverse disorders as deep venous thrombosis, atherosclerosis and diabetes. However, blood must be drawn with great care to avoid in vitro damage to platelets and false elevation of these markers. All of these procedures are promising at present, but their precise role and value await further study.
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PMID:Platelet markers of thromboembolic disease. 616 74


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