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)

Heparin (Lipo-Hepin, Liquaemin Sodium) and warfarin sodium (Coumadin, Panwarfin) are the classic anticoagulants in use for venous thromboembolic disease. They work by modifying the coagulation mechanism, heparin having an immediate effect and warfarin having a more delayed effect. The most common adverse effects of anticoagulation therapy are hemorrhagic complications. Thrombolytic therapy should be considered in all patients with massive pulmonary embolism with hypotension and in patients with deep venous thrombosis in the popliteal area or higher. Such therapy has been shown to help preserve the pulmonary microcirculation after pulmonary embolism and to decrease the incidence of the postthrombotic syndrome following deep venous thrombosis. If certain clinical guidelines are followed rigidly, the incidence of significant bleeding complications is low. Although the use of tissue plasminogen activator in venoocclusive disease has been limited to isolated cases, results have been very promising.
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PMID:Treatment of venous thromboembolic disease. A pragmatic approach to anticoagulation and thrombolysis. 370 54

A patient with methicillin-resistant Staphylococcus aureus bacteremia received vancomycin (MIC = 0.8 microgram/ml, MBC = 15 micrograms/ml) and heparin simultaneously through the same intravenous line to treat a septic deep venous thrombosis. Bacteremia persisted for 7 days. Bacteremia terminated when the simultaneous infusion of heparin and vancomycin through the same line was stopped. This suggested that an interaction between vancomycin and heparin may have occurred, which resulted in a reduction in vancomycin activity. To test for such an interaction, mixtures of heparin and vancomycin in various concentrations were made and tested for antimicrobial activity against the organisms in the patient. A precipitate formed at the concentrations achieved in the intravenous lines, and when the vancomycin concentrations were measured by bioassay, a 50 to 60% reduction in activity was noted. In contrast, when these solutions were prepared and mixed at microgram concentrations, a precipitate was no longer observed, and antimicrobial activity was not reduced. Heparin appeared to interact unfavorably with vancomycin at the concentrations in the intravenous lines when these drugs were administered simultaneously to patients. This may be the cause of poor therapeutic responses to vancomycin in some patients, especially those infected with tolerant organisms.
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PMID:Persistent staphylococcal bacteremia in an intravenous drug abuser. 371 29

Hereditary protein C deficiency, which is inherited as an autosomal-dominant trait, predisposes to venous thrombotic disease. Heterozygotes are at risk for superficial thrombophlebitis, deep venous thrombosis and/or pulmonary embolism, which may occur without apparent cause at a young age. Other manifestations are cerebral venous thrombosis and mesenteric vein thrombosis. In severe, often homozygous, protein C deficiency, a purpura fulminans syndrome may occur shortly after birth, resulting in death due to extensive thrombosis, if it is not adequately treated. The thrombotic manifestations in heterozygotes are effectively prevented by coumarin therapy. However, in the initial phase of oral anticoagulant therapy, the patients have an increased risk for the development of coumarin-induced haemorrhagic skin necrosis. The purpura fulminans syndrome can be treated with either replacement therapy or with coumarin therapy. Heparin appears to be ineffective in the prevention of both the purpura fulminans syndrome and the coumarin-induced skin necrosis.
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PMID:Hereditary protein C deficiency. 384 Jan 12

The sensitivity of impedance plethysmography (IPG) for diagnosing deep vein thrombosis was evaluated in the presence of dihydroergotamine, an agent with significant venoconstrictor activity. In a prospective, randomized, controlled clinical trial, 105 patients undergoing total hip replacement surgery were investigated to evaluate the thromboprophylactic efficacy of DHE-Heparin using IPG and 125I-Fibrinogen Leg Scanning to monitor the incidence of DVT. Retrospective analysis of the IPG data indicated that DHE-Heparin impaired the sensitivity of impedance plethysmography by decreasing venous capacitance and venous outflow. Although the patient sample size was relatively small, the results showed trends which suggested that the utility of impedance plethysmography for diagnosing DVT was limited in the presence of a vasoactive agent. Alternate noninvasive diagnostic methods may need to be considered in select patients receiving concomitant medications possessing venoconstrictor activity.
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PMID:Limitation of impedance plethysmography in assessing efficacy of dihydroergotamine-heparin prophylaxis of deep vein thrombosis. 388 36

The cause of postoperative DVT is considered to be changes in blood coagulation, stasis of blood within the veins, and injury to the vein wall. The coagulation changes have been investigated and documented and involve platelet activation, stimulation of the coagulation cascade, and blunting of endogenous fibrinolytic activity. Stasis has been objectively identified by retention of contrast material in soleal sinuses and marked changes in venous flow velocity in patients in the supine position and in those under general anesthesia. Vein wall injury is more controversial, but has been shown to be directly related to venodilation. Such dilation of veins occurs in response to operative trauma, hence venous endothelial damage most likely plays a part in the milieu responsible for postoperative DVT. The prophylaxis provided by the combination of dihydroergotamine and heparin appears to affect each of the three limbs of Virchow's triad. Heparin achieves its prophylactic benefit by activating antithrombin III. Activated antithrombin III affects numerous sites in the coagulation cascade. It has been shown that 1 micrograms of antithrombin III inhibits the formation of 1 unit of thrombin; however, in the presence of heparin, 1 micrograms of activated antithrombin III inhibits 750 units of thrombin. Dihydroergotamine increases venous smooth muscle tone without affecting arteriolar smooth muscle. Hence, it has the effect of preventing stasis without increasing blood pressure. It also affects the platelet membrane, prostaglandin synthesis, and blood distribution, although these findings need to be elucidated. The combination of dihydroergotamine and heparin seems to have a synergistic prophylactic effect in preventing postoperative DVT. Heparin modifies the coagulation changes, whereas dihydroergotamine minimizes stasis and potentially prevents the endothelial damage caused by excessive operative venodilation. Such a combination of effects can explain the synergistic prophylactic efficacy found when dihydroergotamine and heparin were employed in combination in the multicenter trial [42].
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PMID:Combined dihydroergotamine and heparin prophylaxis of postoperative deep vein thrombosis: proposed mechanism of action. 390 91

It has been suggested that early heparin requirements are greater in patients with acute deep venous thrombosis (DVT) and pulmonary embolism (PE). Heparin requirements were recorded for 73 patients with suspected DVT and PE. The maintenance dosage (days 1 through 4) of heparin sodium required to achieve therapeutic partial thromboplastin times (PTTs) was significantly higher in patients with DVT (n = 54; mean +/- SD dosage, 1,151 +/- 246 units/hr) compared with patients with no DVT (n = 19; mean +/- SD dosage, 952 +/- 190 units/hr). The first posttreatment PTT was significantly lower in patients with DVT (mean +/- SD PTT, 68.74 +/- 27.96 s) compared with control patients (mean +/- SD PTT, 89.41 +/- 23.25 s). This study supports the clinical impression that initial heparin requirements are greater and heparin clearance is more rapid in patients with acute DVT and PE.
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PMID:Prediction of heparin requirements in acute thromboplastic venous disease. 398 88

Bleeding complications occurred in 30 (11%) out of 280 patients who received continuous heparin infusion for deep venous thrombosis (DVT). 22 (8%) had minor while 8 patients (3%) had major bleeding complications (1 intrathoracic [fatal], 2 gastrointestinal and 5 retroperitoneal). Heparin activity, in daily drawn blood samples, was determined by four assays (chromogenic substrate [CS] assay, activated partial thromboplastin time [APTT], thrombin time with citrated plasma [CiTT] and thrombin time with recalcified plasma [CaTT]). The differences in median heparin activity between patients with minor bleeding and patients with no bleeding did not reach significance for any of the tests. In patients with major bleeding, the differences were significant with the CS (p = .011) and the CaTT (p = .030) assays. Patients with retroperitoneal bleeding had significantly increased median activity judged by all four assays: CS (p = .002), CaTT (p = .003), APTT (p = .010), CiTT (p = .029). The difference was most pronounced after four days of heparin treatment, but there was a considerable overlap with patients without bleeding.
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PMID:Heparin assays and bleeding complications in treatment of deep venous thrombosis with particular reference to retroperitoneal bleeding. 402 37

We have outlined our treatment for acute DVT with thrombolytic agents. We prefer to use thrombolytic agents unless a specific contraindication is present. Both heparin and thrombolytic agents carry the risk of bleeding. In our opinion, the long-term results of restoring the deep venous system anatomically and physiologically are more likely if thrombolysis is the chosen therapy. Heparin therapy simply arrests the problem and relies on the development of sufficient venous collateral pathways, recanalization, or both to improve venous return. The short-term results (the first 6 months) of thrombolytic therapy and heparin are similar. The results of prospective, randomized studies comparing standard anticoagulation versus lytic therapy have documented improved long-term venous function in patients receiving thrombolytic therapy.
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PMID:Thrombolytic therapy for deep vein thrombosis. 405 Nov 21

The efficacy of intravenous infusion of dextran 70 or subcutaneous administration of low-dose heparin in preventing postoperative thromboembolic complications has been investigated in a prospective randomized trial. During part 1 of the study, 232 patients over the age of 40 years who were undergoing major gynecologic surgery underwent a complete test protocol. The 125I fibrinogen uptake test (FUT) was used for the diagnosis of deep vein thrombosis (DVT) in 117 patients in the dextran and 115 patients in the heparin group. Heparin was significantly more effective than dextran for reducing DVT (P less than .001). During part 2 of the study no FUT was done but the incidence of clinical and fatal pulmonary embolism (PE) and the number of complications were studied. Of 444 patients (parts 1 and 2) 1 fatal and 2 nonfatal pulmonary emboli were diagnosed. All the emboli occurred in the dextran group. The benefit: hazard ratio appeared to favor heparin for the prophylaxis of DVT.
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PMID:Prevention of postoperative thromboembolism by dextran 70 or low-dose heparin. 615 72

In order to investigate whether a more intensive initial oral anticoagulation still would be safe and effective, we performed a prospective randomized study in patients with deep vein thrombosis. They received either the conventional regimen of oral anticoagulation ("low-dose") and heparin or a more intense oral anticoagulation ("high-dose") with a shorter period of heparin treatment. In the first part of the study 129 patients were randomized. The "low-dose" group reached a stable therapeutic prothrombin complex (PT)-level after 4.3 and the "high-dose" group after 3.3 days. Heparin was discontinued after 6.0 and 5.0 days respectively. There was no difference in significant hemorrhage between the groups, and no clinical signs of progression of the thrombosis. In the second part of the study another 40 patients were randomized, followed with coagulation factor II, VII, IX and X and with repeated venograms. A stable therapeutic PT-level was achieved after 4.4 ("low-dose") and 3.7 ("high-dose") days, and heparin was discontinued after 5.4 and 4.4 days respectively. There were no clinical hemorrhages, the activity of the coagulation factors had dropped to the same level in both groups at the time when heparin was discontinued and no thromboembolic complications occurred. Our oral anticoagulation regimen with heparin treatment for an average of 4.4-5 days seems safe and reduces in-patient costs.
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PMID:Intensive initial oral anticoagulation and shorter heparin treatment in deep vein thrombosis. 639 71


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