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)

Six episodes of lower extremity hemorrhage occurred in five spinal cord injured patients receiving therapeutic anticoagulation. Factors contributing to hemorrhage included excessive anticoagulation in two episodes and soft tissue trauma during vigorous range of motion (ROM) exercises in three. The three episodes without clinical evidence of trauma were initially misdiagnosed as recurrent deep venous thrombosis. Ecchymoses developed in three episodes, but were delayed in appearance in two. Noninvasive vascular tests yielded false positive results in two out of three cases. Venograms performed in four episodes were negative for thrombosis. Based on this experience, the initial investigation of lower extremity swelling in this setting should include: a search for evidence of trauma, analysis of medications for coagulation-related interactions, leg x-rays, and early determination of hemoglobin, prothrombin or partial thromboplastin time, and platelet count. If there is any question of acute thrombosis, a venogram, rather than noninvasive vascular studies, must be performed. All persons involved in the care of these patients should be aware of the increased risk of bleeding and should perform ROM exercises of weak or paralyzed extremities with caution.
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PMID:Lower extremity hemorrhage in spinal cord injured patients receiving therapeutic anticoagulation. 671 54

Despite venous stasis and a hypercoagulable state during pregnancy, the reported incidences of deep venous thrombosis and pulmonary embolism are remarkably low, about 1 in 2,000 and 1 in 10,000 cases, respectively. Mortality from antepartum thromboembolism has been reported in about 15 percent of untreated patients and less than 1 percent of treated patients. Adequate anticoagulant therapy significantly reduces maternal mortality and decreases postpartum morbidity. The proper anticoagulant agent for use during pregnancy has been widely debated. Coumarin compounds pass through the placenta and into the fetus. Hemorrhagic complications in the fetus are uncommon if prothrombin times are carefully controlled and if the drug is discontinued before delivery. However, coumarin during the first trimester has the teratogenic hazard of producing chondrodysplasia punctata. Heparin, in contrast, does not cross the placental barrier and is considered more effective treatment for deep venous thrombosis; however, long-term intravenous administration during pregnancy has been considered both impractical and possibly hazardous due to the risk of osteoporosis after 6 months of therapy. In our study, a combined regimen of intravenous and subcutaneous heparin was used successfully in four women with deep venous thrombosis. One patient who had recurrent embolization while on adequate intravenous heparin underwent vena caval clipping and had an uneventful Cesarian section at term with a normal infant. Another patient also underwent Caesarian section with a normal infant, while the other two women had normal vaginal deliveries at term. Miniheparin therapy was continued for 3 months postpartum, followed by long-term aspirin and Ascriptin therapy. Carefully controlled heparin therapy in a pregnant woman with deep venous thrombosis both safe and beneficial for mother and fetus.
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PMID:Management of deep venous thrombosis and pulmonary embolism during pregnancy. 709 23

Activation of prothrombin and the subsequent reactions of thrombin with its substrates and its major inhibitors, antithrombin III (AT III) and heparin cofactor II (HC II), likely reflect both intravascular and extravascular coagulation. Several studies have reported increased in vivo coagulation in cancer. Whether the increased thrombin production in malignancy is accompanied by a corresponding increase in thrombin inhibition is unknown. This study quantified prothrombin fragment 1 + 2 (F1 + 2), thrombin-AT III (TAT), thrombin-AT III-vitronectin (TAT.V), and thrombin-HC II-vitronectin (THCII.V) in the plasmas of healthy volunteers (n = 37); patients with localized solid tumours before treatment was initiated (n = 39); and five patients with non-Hodgkin's lymphoma, both before and during weekly chemotherapy. Two of the five non-Hodgkin's lymphoma patients developed deep venous thrombosis (DVT) during chemotherapy. In normal plasma, where the concentrations of the four parameters likely reflect haemostasis, the sum of TAT, TAT.V and THCII.V was 61% that of F1 + 2, compared with 30% in cancer plasmas. In addition, the mean +/- SEM of F1 + 2 in the plasmas of cancer patients (1.56 +/- 0.09 nM) was significantly elevated (P < 0.001) when compared with healthy volunteers (0.89 +/- 0.06 nM). Eight weeks of chemotherapy increased the F1 + 2 and the binary TAT in plasmas of the non-Hodgkin's lymphoma patients by approximately 1.5- and 2.9-fold, respectively. Thus, increased prothrombin activation in cancer patients, without corresponding increases in concentrations of thrombin-inhibitor complexes, raise the possibility that a significant portion of the thrombin generated in vivo escapes inhibition in cancer and contributes to the high risk of DVT in malignancy.
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PMID:The hypercoagulable state in cancer patients: evidence for impaired thrombin inhibitions. 751 51

The activation of the clotting cascade leading to deep venous thrombosis begins during total hip arthroplasty, but few studies have assessed changes in coagulation during surgery. A better understanding of thrombogenesis during total hip arthroplasty may provide a more rational basis for treatment. In 3 separate studies, the following observations were made. Circulating indices of thrombosis and fibrinolysis: prothrombin F1.2, thrombin-antithrombin complexes, fibrinopeptide A, and D-dimer, did not increase during osteotomy of the neck of the femur or during insertion of the acetabular component, but rose significantly during insertion of the femoral component. Thrombin-antithrombin complexes, fibrinopeptide A, and D-dimer were higher after insertion of a cemented component than insertion of a noncemented femoral component. A significant decline in central venous oxygen tension was observed after relocation of the hip joint and after insertions of cemented and noncemented femoral components, providing evidence of femoral venous occlusion during insertion of the femoral component. In patients receiving a cemented femoral component, mean pulmonary artery pressure increased after relocation of the hip joint, indicating intraoperative pulmonary embolism. No changes in mean pulmonary artery pressure were noted with noncemented total hip arthroplasty. Administration of 1000 units of unfractionated heparin before insertion of a cemented femoral component blunted the rise of fibrinopeptide A. The results of these studies suggest that (1) the greatest risk of activation of the clotting cascade during total hip arthroplasty occurs during insertion of the femoral component; (2) femoral venous occlusion and use of cemented components are factors in thrombogenesis during total hip arthroplasty; and (3) measures to prevent deep venous thrombosis during total hip arthroplasty (such as intraoperative anticoagulation) should begin during surgery rather than during the postoperative period and be applied during insertion of the femoral component.
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PMID:The John Charnley Award. Thrombogenesis during total hip arthroplasty. 755 26

A 70-year-old woman on maintenance hemodialysis for 3 years was admitted to our hospital because of deep vein thrombosis (DVT) in the right femoral vein. Seven days before admission, she suddenly noticed severe pain in her right inguinal region while she was walking on the street. A wide range of stenosis from the iliac to the distal femoral region was detected by both CT scanning and venography. Her hematocrit reading was 30% and her serum erythropoietin level was 10.5 MU/ml, which was within the normal range, on the day of admission. The results of routine coagulation tests, including prothrombin time, activated partial thrombin time and plasma fibrinogen values, were normal. Plasma anti-thrombin III and plasminogen were also normal. In contrast, beta-thromboglobulin, platelet factor IV, fibrinogen degradation product, D-dimer, thrombin-antithrombin III complex (TAT) and fibrinopeptide A were abnormally elevated. In the venous occlusion test which was performed in the forearm of the opposite side of the arterio-venous shunt, plasma tissue type plas-minogen activator values showed little response to occlusion indicating that the vessel endothelium may have been partially damaged. These data suggest that the DVT had been induced by imbalance of increased blood coagulation and decreased fibrinolytic activity. Damaged vascular wall may also have contributed to the production of DVT. Furthermore, it is surprising that the patient had elevated values of D-dimer and TAT for many years without recurrence of the DVT. Spontaneous DVT in an apparently healthy individual on maintenance hemodialysis seems to be rare, compared with arterial thrombosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A long-term hemodialysis patient with spontaneous deep vein thrombosis, showing high levels of coagulo-fibrinolytic markers]. 760 31

The physiologic mechanisms that protect children from thromboembolic complications are not known. We investigated the regulation of thrombin in children because of its central importance to thrombosis. The capacity to generate thrombin in vitro (chromogenic assay) was decreased by 26% in plasmas from children (1-16 yrs; n = 102) compared to adults ([20-45 yrs; n = 20; p < 0.001]). The addition of purified prothrombin to plasmas from children increased thrombin generation to adult values. The capacity of plasmas to inhibit 125I-alpha-thrombin was increased by 21% in children compared to adults (p = 0.020), with significantly more thrombin complexed to alpha 2-macroglobulin (alpha 2M) in children. When DVT occur in children, adult guidelines for heparin therapy are used. At low heparin concentrations (0.1 and 0.2 U/ml), thrombin generation was decreased by 30% in children compared to adults (p < 0.001). At high heparin levels (0.4 U/ml), thrombin generation was negligible in all plasmas. ATIII inhibited over 95% of thrombin in all plasmas in the presence of heparin. In summary, thrombin regulation differs in children from adults and may protect children from thromboembolic complications. When DVT do occur, heparin requirements may differ in children compared to adults.
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PMID:Thrombin regulation in children differs from adults in the absence and presence of heparin. 774 Apr 51

The diagnostic efficacy of D-dimer, fibrin degradation products (FbDP) and prothrombin fragment 1+2 (F1+2) in patients with clinically suspected deep venous thrombosis (DVT) was investigated. 161 patients suspected of DVT were investigated. The diagnosis DVT was made in 58 patients using isotope leg scanning and ultrasonic duplex scanning. In all patients D-dimer, FbDP and F1+2 levels were determined using a latex method for D-dimer and enzyme-linked immunosorbent assays (EIA) for FbDP and F1+2. For the D-dimer latex assay sensitivity was 69% and specificity 92% (cut-off level 500 ng/ml). For the FbDP assay sensitivity was 100% and specificity 8% (cut-off level 250 ng/ml). For the F1+2 assay sensitivity was 100% and specificity 17% (cut-off level 0.3 nM). Specificity could not be improved by the combination of FbDP and F1+2. We conclude that in our population the use of the latex D-dimer assay, FbDP and F1+2 EIA's have no value as screening tests to rule out the diagnosis DVT in clinically suspected patients.
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PMID:Comparison of the efficacy of D-dimer, fibrin degradation products and prothrombin fragment 1+2 in clinically suspected deep venous thrombosis. 774 May 15

Twenty patients having routine laboratory control of oral anticoagulation after total hip or knee arthroplasty were consecutively included in the study and were anticoagulated at an International Normalized Ratio (INR) between 2.5 and 3.5. Patients with mechanical heart valve prostheses (n = 20), deep venous thrombosis or pulmonary embolism (n = 20), at the same level of oral anticoagulation, served as control groups. Plasma concentrations of prothrombin fragment 1 + 2 and D-dimer were measured and compared. In the mechanical heart valve prosthesis and deep venous thrombosis groups the median prothrombin fragment 1 + 2 concentrations were significantly lower than in the orthopaedic patient group (0.15 and 0.17 nmol/l versus 0.29 nmol/l). The D-dimer concentrations displayed a similar picture (150 and 200 micrograms/l versus 840 micrograms/l). The D-dimer/prothrombin fragment 1 + 2 ratios in the patients after total hip or knee arthroplasty were significantly higher (12.4) than in the control groups (5.3 and 6.0). These data show that the fibrinolysis/coagulation balance is enhanced, mainly due to a disproportional rise in D-dimer. After assessing when the D-dimer concentration returns to normal in this anticoagulated group, this parameter may indicate the appropriate duration of oral anticoagulant treatment after surgery for total knee or hip replacement.
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PMID:Coagulation activation and reactive fibrinolysis in patients receiving oral anticoagulation after total hip or knee replacement. 784 18

One hundred and fifty six consecutive cemented total knee arthroplasties (TKA) in 147 patients (39 males, 108 females, mean age: 67) received preoperatively low-dose-warfarin for thromboembolic prophylaxis. Warfarin 10 mg was given the night before surgery and warfarin 5 mg the night of surgery. Thereafter, the dosage was adjusted to maintain a prothrombin time between 1.2-1.5 times control (INR = 2.0-3.0). The screening for any deep vein thrombosis (DVT) in the operated limb was by ascending venography. The reported incidence of DVT after TKA without prophylaxis is superior to 50%, more than 10% of those are proximal DVT. In this study, the overall incidence of DVT is down to 22.4%. Only five patients (3.4%) had a proximal DVT. There were no deaths and no clinical pulmonary embolisms. Patients with venous insufficiency had a significantly higher incidence of DVT (36.7%, p = 0.05). The average blood loss was 406 ml. Three major local bleedings occurred (2.0%). At one year follow-up, there were no infections. Low dose warfarin is efficacious in reducing DVT formation with TKA. It is safe and does not create excessive bleeding in cemented TKA.
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PMID:[Efficacy and safety of prophylactic preoperative administration of low-dose warfarin in cemented total knee prostheses]. 787 20

Prothrombin fragments (F1+2) can be used to monitor oral anticoagulation; their generation is also suppressed by heparin. We studied the course of F1+2, aPTT, heparin doses administered and heparin concentrations, as well as prothrombin time, during the first 7 days of heparin therapy (target aPTT 70 s) and overlapping oral anticoagulation (target INR 2-3) in 26 patients routinely treated for deep venous thrombosis (deep venous thrombosis +/- pulmonary embolism, 23 patients) or pulmonary embolism with a history of recurring deep venous thrombosis (3 patients). Although we found significant suppression of F1+2 between all pre- and post-treatment values, a transient, significant increase was seen on days 2-4. The amount of heparin given was stable from day 1-5; the fact of a transient increase in F1+2 might thus indicate that heparin doses routinely used are too low for the treatment of hypercoagulability in deep venous thrombosis in patients. We also found a decrease in heparin concentration on day 2, which may be explicable by changed pharmacokinetics of heparin in individuals with deep venous thrombosis. In conclusion, F1+2 may be useful for monitoring heparin treatment and oral anticoagulation in deep venous thrombosis patients from a laboratory point of view. However, larger studies are necessary to confirm these results. It remains to be clarified whether monitoring of anticoagulation by molecular markers might improve therapy of deep venous thrombosis. Such studies are in progress.
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PMID:[Is the assessment of prothrombin fragment F1+2 for monitoring of heparin therapy in patients with deep vein thrombosis useful?]. 789 70


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