Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antithrombin is one of the main endogenous anticoagulants and its deficiency is associated with deep venous thrombosis. The aim of the present study was to evaluate the prevalence of antithrombin deficiency in patients with chronic lower extremity ulcers. Forty-eight patients with chronic lower limb ulcers for longer than 10 years, evaluated during 1997, were studied: 40 were female (83.3%) and eight were male (16.6%), with ages ranging from 43 to 73 years (mean, 55.2 years). Antithrombin was dosed by the coagulometric method, with evaluation of the functional activity. Measurement was repeated in those cases where deficiency was found to be present. The highest prevalence rate for antithrombin deficiency in the general population was one in every 2000 cases. Data analysis was performed by utilizing the odds ratio with a confidence interval of 95% and P < 0.05. Deficiency in antithrombin levels was recorded in two (4.1%) of the patients with chronic ulcer. These results indicate a higher prevalence rate of antithrombin deficiency in those patients with chronic leg ulcers, suggesting that an association may be present. Further studies with a larger number of patients are required to confirm this hypothesis.
 ...
PMID:Prevalence of antithrombin deficiency in patients with chronic leg ulcer. 1168 49

Venous thrombosis, whose main clinical presentations include deep vein thrombosis and pulmonary embolism, represents a major health problem worldwide. Numerous conditions are known to predispose to venous thrombosis and these conditions are commonly referred to as risk indicators or risk factors. Generally accepted or "classically" acquired risk factors for venous thromboembolism include advanced age, prolonged immobilisation, surgery, fractures, use of oral contraceptives and hormone replacement therapy, pregnancy, puerperium, cancer and antiphospholipid syndrome. In addition to these well-established risk factors for venous thrombosis, several lines of evidence that have emerged over the past few decades indicate a role of novel genetic risk factors, mainly related to the haemostatic system, in influencing thrombotic risk. The most significant breakthrough has been the confirmation of the concept that inherited hypercoagulable conditions are present in a large proportion of patients with venous thromboembolic disease. These include mutations in the genes that encode antithrombin, protein C and protein S, and the factor V Leiden and factor II G20210 A mutations. Moreover, plasmatic risk indicators, such as hyperhomocysteinemia and elevated concentrations of factors II, VIII, IX, XI and fibrinogen, have also been documented. This extensive list of genetic and acquired factors serves to illustrate that a single cause of venous thrombosis does not exist and that this condition should be considered as a complex or multifactorial trait. Complex traits can be understood by assuming an interaction between different mutations in candidate susceptibility genes. The risk that is associated with each genetic defect may be relatively low in isolation but the simultaneous presence of several mutations may dramatically increase disease susceptibility. Moreover, environmental factors may interact with one or more genetic variations to add further to the risk. The analysis of genetic risk factors and plasmatic factors, together with private life style and environmental factors, has contributed significantly to our understanding of the genetic predisposition to venous thrombosis.
 ...
PMID:Genetic risk factors of venous thrombosis. 1170 18

We report a case of heparin resistance and its management during cardiopulmonary bypass (CPB). A 63-year-old, 96 Kg female with a posterior myocardial infarction (MI) with previous deep venous thrombosis was treated with intravenous (IV) heparin infusion for 7 days before myocardial revascularization surgery. The patient required 1200 IU/Kg of beef lung heparin to extend the activated clotting time (ACT) in order to initiate CPB. A total of 1562 IU/Kg of heparin was administered throughout the procedure. This acquired heparin resistance was attributed to an antithrombin (AT III) deficiency, and was treated with fresh frozen plasma (FFP) to restore adequate anticoagulation. The patient's heparinized ACTs ranged between 368 seconds and 387 seconds before FFP administration as opposed to 626 seconds to 1329 seconds after treatment with FFP and additional heparin once on CBP. The patient experienced an uneventful postoperative course. Future treatment with AT III concentrate rather than FFP may reduce heparin requirements that will, in turn, reduce protamine reversal dose, postoperative bleeding attributable to heparin rebound, and its associated complications.
 ...
PMID:Anticoagulation management in a patient with an acquired antithrombin III deficiency. 1180 38

We report the pharmacodynamic properties of tinzaparin (175 U/kg antifactor Xa) given as a single daily administration for 5 consecutive days to 14 healthy volunteers as a known safe, effective treatment of deep vein thrombosis and pulmonary embolism. The Cmax for antifactor Xa (0.87 +/- 0.15 U/ml) was associated with a 2.4 +/- 0.5-fold prolongation of the activated partial thromboplastin time (APTT) and a high antithrombin activity (0.38 +/- 0.1 U/ml). The Cmax value of antifactor Xa was 1.5- and twofold lower than those generated by similar doses of nadroparin and enoxaparin respectively. The clearance of antifactor Xa activity (1.29 +/- 0.2 l/h) was 1.5- and twofold greater than those reported for nadroparin and enoxaparin respectively. These results indicated that the antithrombotic and prohaemorrhagic effects of a low molecular weight heparin were independent from the absolute levels of antifactor Xa activities and from the prolongation of the APTT.
 ...
PMID:The pharmacodynamics of tinzaparin in healthy volunteers. 1184 26

Low-molecular-weight and unfractionated heparins are frequently used to treat venous thromboembolism, but it is not known whether they are equally effective in inhibiting in vivo generation of thrombin. In this multicenter trial, 1048 patients were randomized to intravenous unfractionated heparin (group A), twice daily low-molecular-weight heparin (reviparin) for 1 week (group B), or once daily reviparin for 4 weeks (group C). All patients received vitamin K antagonists. Blood samples withdrawn at the baseline and at weeks 1 and 3 were analyzed using markers of in vivo thrombin generation and other coagulation parameters. During the first 3 weeks symptomatic recurrent deep vein thrombosis-pulmonary embolism (DVT/PE) occurred in 17 (4.5%) of 375 patients in group A compared with 4 (1.0%) of 388 patients in group B, and 9 (2.4%) of 374 patients in group C. Forty percent of patients in group A, 53.4% in group B, and 53.5% in group C showed 30% or greater reduction in thrombus size assessed by venography. Patients in group B had significantly greater reduction in D-dimer, prothrombin fragments 1 and 2 (F1 + 2), endogenous thrombin potential (ETP), and thrombin-antithrombin (TAT) complexes compared to groups A and C. Greater release of tissue factor pathway inhibitor (TFPI) and reduction in levels of thrombin activatable fibrinolysis inhibitor (TAFI) and fibrinogen were significantly more pronounced in group C patients. Reviparin administered twice daily plus vitamin K antagonist is more effective in inhibiting in vivo thrombin generation compared to intravenous unfractionated heparin plus vitamin K antagonist, and reviparin once daily produced significantly higher TFPI release and greater reduction in TAFI and fibrinogen levels.
 ...
PMID:Randomized trial of different regimens of heparins and in vivo thrombin generation in acute deep vein thrombosis. 1187 67

In a prospective study, coagulation test results were compared in 137 patients with colorectal cancer (CRC) and 39 subjects with benign colorectal diseases. Prothrombin fragment 1+2 (F1+2), thrombin-antithrombin complex (TAT), and soluble fibrin (SF) were measured in plasma before and after surgery. CRC patients presented with significantly higher values of F1+2 and TAT than controls. Patients with localised CRC had elevated values of F1+2 and TAT, whereas patients with advanced CRC also had elevated SF values. TAT and SF levels correlated with tumour spread, and normal values virtually excluded advanced cancer. Postoperative deep venous thrombosis (DVT) was diagnosed by phlebography in 20% of the CRC patients. Preoperative values of the markers did not predict postoperative DVT, but postoperative values did.
 ...
PMID:Relationship of coagulation test abnormalities to tumour burden and postoperative DVT in resected colorectal cancer. 1191 70

Prothrombin fragments (F1+2), thrombin-antithrombin complexes (TAT) and D-dimers, markers of hemostatic system activation, were measured in 59 consecutive patients with deep vein thrombosis (DVT). Patients were randomly treated either with subcutaneous unfractionated heparin (UH) administered in two to three subcutaneous doses adjusted to activated partial thromboplastin time (APTT) or with low-molecular weight heparin (LMWH) (dalteparin) administered in a fixed dose of 200 IU/kg body weight in one subcutaneous injection daily. Before treatment, F1+2, TAT and D-dimer were above the cut-off level in 27/59 (46%), 34/59 (58%) and all (100%) patients, respectively. Significant associations were observed between F1+2 and TAT (r=.66, P<.001), TAT and D-dimer (r=.36, P<.005) and F1+2 and D-dimer (r=.30, P<.050). On the third day of treatment, F1+2 and TAT significantly decreased to reference values in almost all patients (in 64/66 determinations of both F1+2 and TAT) and remained low on the seventh day of treatment. Compared to pretreatment values, a nonsignificant decrease of D-dimer was noted in both groups, but all values remained above the cut-off value. When markers of hemostatic system activation in the UH and LMWH groups were compared, no significant differences were observed. It was concluded that subcutaneous UH in an APTT-adjusted dose and subcutaneous LMWH in a once-daily weight-adjusted dose controlled these markers of hemostatic system activation in a similar manner.
 ...
PMID:Markers of hemostatic system activation during treatment of deep vein thrombosis with subcutaneous unfractionated or low-molecular weight heparin. 1192 30

Venous thromboembolism is a rare but threatening complication of pregnancy. Little conclusive information is available on the actual risk of venous thromboembolism during pregnancy or puerperium in women with inherited thrombophilia, particularly in carriers of factor V Leiden and of the G20210A prothrombin gene mutation. To determine the pregnancy-related and puerperium-related risk of venous thromboembolism in women with inherited thrombophilia, we performed a case-control study on 119 women who had a first episode of deep vein thrombosis and/or pulmonary embolism during pregnancy or puerperium and 232 healthy women who had at least one pregnancy without thrombosis. Inherited thrombophilia was diagnosed in 47 patients (39.5%) and 15 controls (6.5%). The relative risk of venous thromboembolism was 10.6 (95% CI, 5.6-20.4) for heterozygous carriers of factor V Leiden, 2.9 (95% CI, 1.0-8.6) for heterozygous carriers of the prothrombin mutation and 13.1 (95% CI, 5.0-34.2) for those with antithrombin, protein C or protein S deficiency taken together. Sixty-eight of the 119 women (57%) had thrombosis after delivery, confirming the puerperium as a particularly high-risk period. When women were divided into two groups of those with antenatal or postnatal thrombosis. the relative risks associated with each type of inherited thrombophilia were of similar magnitude. In conclusion, women with inherited thrombophilia have an increased risk of venous thromboembolism during pregnancy. Among thrombophilic abnormalities, the prothrombin mutation was the weakest risk factor. Thrombosis occurred more frequently in puerperium than in pregnancy, whether or not thrombophilia was diagnosed.
 ...
PMID:Inherited thrombophilia and first venous thromboembolism during pregnancy and puerperium. 1266 37

Antithrombotic therapy with unfractionated heparin (UFH) and warfarin for the treatment of deep venous thrombosis (DVT) and pulmonary embolism (PE) became widely accepted in the early 1960s. Subsequent clinical trials have focused on the importance of early intravenous UFH in the treatment of venous thromboembolic events, the method of heparin administration, the importance of rapid anticoagulation to prevent recurrent venous thromboembolism (VTE), and the optimal duration of UFH administration. Low-molecular-weight heparin (LMWH) represents a significant advance over UFH therapy for VTE. Developed in the late 1980s, LMWH has become an excellent alternative to UFH because it offers superior efficacy and safety, improved pharmacokinetics, longer half-life, and once- or twice-daily subcutaneous administration without the need for laboratory monitoring. Fondaparinux is the first of a new class of antithrombotic agents that targets factor Xa. Based on studies of the heparin binding site of antithrombin, this novel pentasaccharide has superior pharmacokinetics and bioavailability when compared with LMWH and can be administered once daily. Studies in patients undergoing major orthopedic surgery and in those with proximal DVT indicate that the efficacy and safety of fondaparinux may represent an improvement over those of LMWH.
 ...
PMID:Treatment of symptomatic venous thromboembolism: improving outcomes. 1207 79

The aim of the following study was to evaluate the diagnostic value of selective hemostasis activation markers, prothrombin activation fragment 1 + 2 (F1 + 2), thrombin-antithrombin complex (TAT), plasmin-alpha 2-antiplasmin complex (PAP) and D-dimer in patients with acute deep venous thrombosis (DVT). The study was performed on 56 patients with freshly diagnosed acute DVT confirmed by venography. The study indicated that patients with acute venous thrombosis have increased concentrations of F1 + 2, TAT complex, PAP complex and D-dimer in blood plasma. The statistical analysis showed that F1 + 2 is the most sensitive test while the D-dimer measurement proved to be the most specific in diagnosing DVT. The conducted logistic regression showed that the most reliable parameter that confirms the existence of acute venous thrombosis is the D-dimer test. The measurement of both F1 + 2 and the D-dimer concentrations rises the reliability of the DVT up to 97%.
 ...
PMID:[Diagnostic value of hemostasis activation markers in acute deep vein thrombosis]. 1210 82


<< Previous 1 2 3 4 5 6 7 8 9 10