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)

Some traditional coagulation assays and several new molecular markers of hemostatic activation were measured in 37 patients with spinal cord injury (SCI). Twenty one of the patients (57%) developed deep vein thrombosis (DVT). The radiofibrinogen uptake test (RFUT) was used to diagnose DVT. Thirty eight percent of quadriplegic and 88% of paraplegic patients developed DVT (p < 0.005). No significant differences were found in platelet counts, mean platelet volumes, fibrinogen levels, von Willebrand factor (Ag) levels, platelet factor 4 and beta thromboglobulin concentrations between the groups with and without DVT. Fibrinopeptide A, thrombin/antithrombin III (TAT) complexes and plasma D-dimer levels were significantly higher in the patients with thrombosis. Most patients with DVT had elevated TAT complex levels up to three days before the RFUT became positive. D-dimer levels were highest after the diagnosis had been made.
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PMID:Thrombosis in spinal cord injury. 129 Jan 64

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

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

A low molecular weight (LMW) heparin, has recently been approved for clinical use in the prevention of deep vein thrombosis in patients undergoing hip surgery. This product is enoxaprin (Lovenox, Rhone-Poulenc Rorer Pharmaceuticals, Paris, France). The purpose of this review is to examine the possible use of LMW heparin in obstetrics and gynecology. LMW heparins are fragments of standard heparin and show a similar anticoagulant effect. The risk of bleeding complications and thrombocytopenia is reduced with the use of these agents. This may be due to their lesser effects on factor II and platelet factor 4. The enhanced bioavailability of these drugs, in conjunction with their prolonged half-life, makes subcutaneous therapy, in one to two daily doses, possible. A review of the published experience of the utilization of LMW heparins in Obstetrics and Gynecology revealed that 1) LMW heparins are effective and safe in the prevention of thromboembolic complications in gynecologic surgery. 2) LMW heparins do not cross the placenta in any trimester. 3) There is no evidence of any mutagenic and teratogenic effect of these drugs. 4) The clinical experience, although limited, suggests their safety and effectiveness in thromboprophylaxis and treatment during pregnancy.
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PMID:Low molecular weight heparins and their use in obstetrics and gynecology. 809 Mar 79

Hirudin is the most potent and specific known inhibitor of thrombin, the enzyme that plays a key regulatory function in hemostasis and blood coagulation. The importance of thrombosis in cardiovascular disease has recently highlighted the limitations of existing antithrombotic drugs and the potential value of direct thrombin inhibition as an effective approach to antithrombotic therapy. Hirudin and a small peptidomimetic analog--hirulog--are being developed as alternatives to heparin for the treatment of unstable angina, for prevention of abrupt closure and restenosis following coronary angioplasty, for prevention of deep vein thrombosis after major orthopedic surgery, and as an adjunct to fibrinolytic therapy. Direct thrombin inhibitors have several potential advantages over heparin: They can inhibit thrombin bound to clots or extracellular matrices, which are relatively resistant to heparin; they do not require antithrombin III as a cofactor, which may lead to a more predictable dose response; and they are not inhibited by activated platelets, which release platelet factor 4 and other molecules that neutralize heparin. The results of early clinical studies suggest that hirudin and hirulog may be more efficacious and more predictable and may have fewer bleeding complications than heparin for several clinical indications.
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PMID:Hirudin: clinical potential of a thrombin inhibitor. 819 74

The diagnosis of thromboembolic diseases is still difficult to establish before the occurrence of the pathological event, although it is now known that they are the result of a progressive alteration of the cardiovascular system. Introduction of new diagnostic tools for the evaluation of the thromboresistance capacity of the body or for the measurement of molecular markers allows the testing of the body defenses against thrombosis which is becoming a routine clinical diagnosis. Antithrombin III (AT III), protein C, protein S, and parameters of fibrinolysis have been recognized to be very important anticoagulant proteins and regulators of thrombin formation and thrombus extension. Furthermore, a normal factor V is necessary for the normal function of the protein C pathway. The presence of a factor V mutation leads to the activated protein C resistance syndrome. However, the major incidence of thrombotic events concerns the overall population. It has been epidemiologically related to the existence of risk factors producing blood activation, which progressively saturates the body's thromboresistance. This period is clinically silent for a long time. The new molecular markers recently introduced can show the existence of a preclinical state of blood activation at the plasma level (fibrinopeptide A, thrombin-antithrombin complexes, modified antithrombin III, fragments 1 + 2 of prothrombin, D-dimer) or at the platelet level (B-thromboglobulin, platelet factor 4, and thrombospondin), and promising developments concern the endothelial level (soluble thrombomodulin). The most universally used blood activation test is the D-dimer assay. This analyte has become very popular in past years for its high sensitivity, its long half-life, and its easy detection directly on citrated plasma. Its negative predictive value (in deep venous thrombosis or pulmonary embolism) as well as its use for monitoring of thrombotic risk in the post-operative period have been well documented clinically. New investigations are initiated to find analytes reflecting endothelial damage, an early platelet activation, or the involvement of blood cells (mainly monocytes and neutrophils) in abnormal processes. It also becomes possible to evaluate directly pathological causes inducing blood activation, such as the presence of antiphospholipid antibodies or other autoimmune antibodies.
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PMID:Thromboembolic diseases: biochemical mechanisms and new possibilities of biological diagnosis. 880 28

Heparin-induced thrombocytopenia (HIT) is an immunoglobulin-mediated adverse drug reaction associated with a high risk of thrombotic complications. The pathogenic antibody, usually immunoglobulin (Ig) G (HIT-IgG), recognises a multimolecular complex of heparin and platelet factor 4, resulting in platelet activation via platelet Fc receptors. In addition to in vivo platelet activation, it is now recognised that there is a concomitant activation of coagulation, as shown by marked elevations in thrombin-antithrombin complex levels. It is possible that this increased thrombin generation predisposes HIT patients to a newly recognised complication: warfarin-induced venous limb gangrene. This syndrome is characterised clinically by necrosis complicating deep venous thrombosis in the absence of large-vessel arterial occlusion, and appears to result from acquired protein C deficiency during warfarin therapy for deep vein thrombosis and HIT. The recommended treatment for HIT is an agent that reduces thrombin generation, either indirectly via factor Xa inhibition [e.g. danaparoid sodium (a mixture of anticoagulant glycosaminoglycans)] or directly using a specific thrombin inhibitor (e.g. recombinant hirudin; argatroban). HIT is potentially preventable: there is a lower frequency of HIT, associated thrombosis and HIT-IgG seroconversion in patients treated with low-molecular-weight heparins, compared with unfractionated heparin.
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PMID:Heparin-induced thrombocytopenia. Pathogenesis, frequency, avoidance and management. 939 76

Skin necrosis is a rare but debilitating complication of treatment with vitamin K antagonist anticoagulants such as warfarin. A clinically similar syndrome has been reported less frequently with heparin therapy. We recently managed a thirty-year-old female patient who developed skin necrosis on her left lower extremity while on warfarin for postpartum DVT. The lesions started to develop 48 hr after stopping heparin therapy. Discontinuation of warfarin and reinstitution of heparin was complicated by a rapid decrease in platelet count consistent with heparin-induced thrombocytopenia (HIT) and its associated risk of platelet activation and thrombosis. The diagnosis was supported by the identification of antibodies against heparin/platelet factor 4 complexes in the patient's serum. The platelet count recovered and the patient improved after switching to therapy with the heparinoid danaparoid. Evaluation for a hypercoagulable state revealed a partial deficiency of protein S, a condition that previously was identified in two of her family members. It is not clear if this patient suffered from warfarin-induced skin necrosis, a manifestation of heparin-mediated platelet activation, or a complex condition in which both drugs contributed. HIT may affect 1-3% of patients who receive unfractionated heparin, and this case raises the possibility that heparin may contribute to, or cause, some episodes of skin necrosis attributed to warfarin. Because many patients who develop warfarin-induced skin necrosis have been treated initially with heparin, it would seem prudent to consider HIT in these situations.
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PMID:Anticoagulant-induced skin necrosis in a patient with hereditary deficiency of protein S. 1007 17


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