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)

In a randomized doubled-blind placebo-controlled study, plasma levels of thrombin-antithrombin-III (TAT) and factor VIII activity (VIII:C) were measured pre-operatively and on days 1, 3, 5 and 7 post-operatively in 70 consecutive patients undergoing total hip replacement. Patients received either a subcutaneous injection of low-molecular-weight heparin (LMWH) or placebo once daily. Post-operative deep vein thrombosis (DVT) was diagnosed by bilateral phlebography. The levels of TAT and VIII:C both increased significantly after operation and were not significantly influenced by LMWH. Thirty-three patients in whom post-operative DVT developed had a significantly lower level of VIII:C on day 7, compared with patients without DVT.
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PMID:Levels of thrombin--antithrombin-III complex and factor VIII activity in relation to post-operative deep vein thrombosis and influence of prophylaxis with a low-molecular-weight heparin. 196 94

Antithrombotic activity, necessary doses and effects on coagulation and lipid variables of the low molecular weight heparin derivative Fragmin were compared to unfractionated (UF) heparin in long-term multicentre trials. Results of more than 10,000 dialyses are reported. On the basis of preliminary studies, UF heparin and Fragmin doses were used that lead to anti-Xa activities of more than 0.5 U/ml. With this dose, sufficient antithrombotic activity was achieved with both heparins. Bleeding complications were not noticed. Partial thromboplastin time (PTT) and thrombin time were only marginally increased by Fragmin (5-8 s) in contrast to UF heparin (PTT 90-120 s, thrombin time 230-260 s). Surprisingly, the elevated levels of factor VIII strongly decreased during the 6-month treatment period with Fragmin and increased again during the following 6-month treatment period with UF heparin. Creatinine, urea, haemoglobin and transaminases did not change in both heparin groups: this excluded reduced dialysis efficiency or occult blood loss. Additionally, 15 patients with acute renal failure and high bleeding risk were dialysed with low doses of Fragmin (anti-FXa: 0.2-0.3 U/ml). No severe bleeding occurred. A continuous ambulant peritoneal dialysis patient with deep vein thrombosis was treated effectively with intraperitoneal application of Fragmin for 6 months without any problems.
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PMID:Comparison of unfractionated heparin and low molecular weight heparin during long-term use in chronic haemodialysis and haemofiltration patients. 309 59

The efficacy and the safety of a new urokinase dosage regimen (loading dose 250,000 IU, initial maintenance dosage 2,000 IU/kg/h in combination with heparin) was studied in ten cases of deep vein thrombosis with regard to the changes of the blood coagulation and fibrinolytic enzyme system. The coagulation analyses demonstrated a pronounced activation of the fibrinolytic system with a statistically significant (p less than 0.05) shortening of the euglobulin clot lysis time and increase of the FDP. The fibrinogen concentration ranged from 50-100 mg/dl already after 12-36 hours. Plasminogen was reduced by 63%, alpha 2-macroglobulin by 32% and factor VIII:C by 42% (p less than 0.05 each). The decrease of fibrinogen (Clauss method) related well to the method of Ratnoff and Menzie, the reduction of plasminogen and the shortening of the euglobulin clot lysis time. According to our data, a sufficient plasma fibrinogenolytic activity may permit on its own an assessment of an adequate therapy with urokinase and the requirements of dose adjustment. The dosage regimen applied here proved effective and readily controllable. Relevant side reactions were not observed.
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PMID:Blood coagulation changes during effective thrombolysis using urokinase and heparin. 617 40

The relationships between factor VIII associated activities, platelet function, and venous thrombosis were studied in 18 patients with lower limb paralysis following acute spinal cord injury (SCI). Deep vein thrombosis (DVT) was detected in 13 patients (72%). Eight of the 13 thromboses were documented between 6 and 8 d following injury while the other five episodes were noted on days 11 (two), 13, 18 and 22. The detection of thrombosis was preceded by marked increases in VIIIR:Ag and VIII:RCoF whereas VIII:C was only marginally increased. The platelet aggregation response to collagen was hyperactive by the sixth day while the platelet aggregate ratio (PAR) did not become abnormal until after DVT was detected. These studies suggest a chronology in the series of events leading to DVT in patients with lower limb paralysis following SCI. Initial elevations in VIII:Ag and VIII:RCoF are followed in sequence by increased platelet responsiveness to collagen, the occurrence of DVT, and the appearance of circulating platelet aggregates. Conceivably, VIIIR:Ag elaborated by endothelial cells alters platelet reactivity and provides an important determinant for venous thrombosis.
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PMID:Sequential changes in factor VIII and platelets preceding deep vein thrombosis in patients with spinal cord injury. 676 66

Sixty consecutive patients with phlebographically verified deep venous thrombosis of the upper arm were studied for disorders of coagulation and fibrinolysis. No appreciable increase in abnormalities of the factor VIII complex, antithrombin III, or inhibitors of activators of fibrinolysis were found. A decreased fibrinolytic defence mechanism, evident either as a deficient release capacity of fibrinolytic activators from the vein during stasis or as decreased fibrinolytic activity in the vein wall as determined histochemically, was found in 26 out of 53 patients studied (49%). It is concluded that deep venous thrombosis of the upper arm is a multifactorial disease. An impaired fibrinolytic defence mechanism is one of the factors that may be of pathogenetic importance.
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PMID:Deep venous thrombosis of the arm: a study of coagulation and fibrinolysis. 678 81

Intermittent pneumatic compression (IPC) or graduated static compression stockings, both effective mechanical methods in the prophylaxis of postoperative deep venous thrombosis, have been investigated in 50 patients regarding the effect of compression on the fibrinolytic system and factor VIII activators. All the patients were subjected to one of the two methods before operation upon varicose veins. In 38 patients IPC with a pressure of 40 mmHg was applied on one leg or arm for at least two hours. In 23 of these patients the compression pattern was slow, two minutes' inflation and two minutes' deflation period. In the remaining 15 patients the compression pattern was quick, three seconds' inflation, followed by 20 seconds' deflation, three cycles a minute. Twelve patients were treated with a compression stocking on one leg for about 24 hours before the operation. Blood samples for determination of fibrinolytic activity and factor VIII in plasma were obtained before and immediately after the end of compression and application of a stocking, respectively. Also the level of plasminogen activator activity (PA) in the vein wall was determined. Neither IPC nor the application of an elastic stocking had any demonstrable effect on the variables studied. In addition, the results did not vary with the rate (slow or quick) or with the duration of IPC, sex or site of application (arm or leg) of IPC. Blood samples from the compressed leg were also uninfluenced.
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PMID:Effect of intermittent pneumatic and graduated static compression on factor VIII and the fibrinolytic system. 680 41

Twenty-eight consecutive patients with acute spinal cord injury were randomised to one of two regimens for the prevention of deep vein thrombosis (DVT): external pneumatic calf compression (EPCC, 15), or EPCC combined with aspirin, 300 mg bid, and dipyridamole, 75 mg tid (ASA/dip, 13). DVT, detected by the 125I-fibrinogen test and impedence plethysmography, was confirmed by contrast venography. The incidence of DVT in the total group was 33 per cent, significantly less than the 78 per cent observed in 37 untreated patients studied previously (p less than 0.001). DVT developed in six of 15 patients receiving only EPCC, and three of 12 on ASA/dip as well as EPCC (p less than 0.1). The untreated patients studied earlier had significantly increased circulating platelet aggregates, increased platelet affinity for collagen, and elevated factor VIII activities, which generally coincided with the development of DVT (usually 7-9 days after injury). Prophylaxis partially prevented these coagulation abnormalities and delayed the onset of thrombosis. While the differences in the haemostatic parameters between those not treated with ASA/dip and those receiving these agents were not statistically significant (except for the platelet-collagen affinity), there was a trend toward less elevated values in the drug-treated patients. We conclude that spinal cord injury patients are at extreme risk for DVT, and have abnormal platelet and factor VIII activities. Prophylaxis with EPCC significantly and safely reduces the risk of DVT in these patients.
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PMID:Deep vein thrombosis in spinal cord injury: effect of prophylaxis with calf compression, aspirin, and dipyridamole. 681 14

Pulmonary embolism (PE) is a devastating complication in patients with traumatic spinal cord injury (SCI). Prophylactic measures such as venous compression hose or low-dose heparin are only partially protective in reducing the risk of venous thromboembolism and are contraindicated in some patients. Because of extended perturbations in fibrinolytic activity, catecholamine effects on platelet aggregation, increased activity of complement and acute phase reactants, abnormally high factor VIII concentrations, and persistent venous stasis with ongoing endothelial damage, the patient with an SCI remains at prolonged risk for venous thromboembolism. A retrospective 5-year review at the Medical Center Hospital of Vermont revealed seven patients with eight documented PEs (three fatal; 2.7%) in 111 SCI patients (6.3%). Six PEs (75%) occurred after discharge from the acute care facility. Median time to PE after injury was 78 days (range, 9-5993). Although comprising only 4% of all trauma admissions, SCI accounted for 31% of all PEs in the total trauma population (2525 patients). Beginning in July 1991, a new prophylaxis protocol was instituted, which included the percutaneous insertion of vena cava filters under local anesthesia in all SCI patients with paraplegia or quadriplegia. Fifteen patients have undergone the insertion of titanium filters. Impedance plethysmography was performed weekly to detect deep venous thrombosis. No complications were associated with vena cava filter insertion. No patients developed deep venous thrombosis during their acute hospitalization (median, 22 d), and no patients have developed PE after filter insertion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prophylactic vena cava filter insertion in patients with traumatic spinal cord injury: preliminary results. 796 30

The important roles of thrombin in the development and propagation of thrombosis are well recognized. In addition to being the enzyme for clotting fibrinogen (the major protein component of blood clots), thrombin accelerates its own generation by activating factor V, factor VIII, factor XI and platelets. It accelerates the stabilization of clots by activating factor XIII to factor XIIIa, the enzyme which crosslinks fibrin. There are probably two major pathways for regulating the availability of thrombin in vivo: inactivation of thrombin (by antithrombin III/vessel wall heparan sulfate and perhaps by other endogenous antithrombins) and the inactivation of factor Va and factor VIIIa by activated protein C. Factor Va and factor VIIIa accelerate the production of thrombin. However, when thrombin becomes bound to fibrin (in clots or possibly on cell surfaces), the ability of antithrombin III/heparin to inactivate thrombin is then reduced significantly. Impairment by fibrin of thrombin inhibition by antithrombin III may account in part for the inability of unfractionated heparin to prevent post-operative deep vein thrombosis in up to 20% of patients who undergo major elective orthopaedic surgery, and may also explain the need for oral anticoagulants after unfractionated and low molecular weight heparins are used to initiate the treatment of established deep vein thrombi. The ineffectiveness of the antithrombin III/heparin pathway for inhibiting thrombin under some circumstances has been a contributory factor for the development, evaluation and identification of other inhibitors of thrombin which are more able than antithrombin III/heparin to inactivate thrombin when the enzyme is bound to fibrin. The focus of this review is to detail how these synthetic agents, by directly or indirectly inactivating thrombin, can also effectively inhibit prothrombin activation in vitro.
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PMID:Mechanisms for the anticoagulant effects of synthetic antithrombins. 815 38

Acquired haemophilia is a rare disorder that it is associated with several diseases. Patients may present with spontaneous haematomas in different places which can sometimes be fatal. We present a 69-year-old woman with breast carcinoma who developed a factor VIII inhibitor. The initial haemorrhagic event was a spontaneous deep muscular haematoma in the right leg mimicking a deep venous thrombosis. She was successfully treated with prednisone.
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PMID:Presentation of an acquired factor VIII inhibitor with a muscular haematoma mimicking a deep venous thrombosis in a patient with breast cancer. 856 41


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