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)

Two patients with familial antithrombin III deficiency developed deep venous thrombosis of the lower limb. The diagnosis of venous thrombosis was made by the indium labelled platelet technique which also allowed for the daily assessment of thrombus size. Each patient received treatment with Warfarin, subcutaneous heparin, and infusions of antithrombin III concentrates. The authors conclude that infusions of antithrombin III concentrates may be of value in limiting the extent of acute thrombosis in patients with a severe deficiency of this protein and may help prevent pulmonary embolism. The haemorrhagic risk of continuing modest doses of heparin with high dose ATIII therapy appears small. In addition to its value in the diagnosis of venous thrombosis the indium platelet technique may give an early indication of thrombus extension and may thus indicate the effectiveness of treatment.
 ...
PMID:Treatment of venous thrombosis in antithrombin III deficient patients with concentrates of antithrombin III. 711 92

The dynamic loss modulus of clotting whole blood was measured in thrombotic patients to characterize the physical properties of coagulation in the hypercoagulable state. The dynamic loss modulus was measured by a Sonoclot. Thrombotic patients consisted of 30 with deep vein thrombosis and 25 with arterial thrombosis. An accelerated increment rate of the dynamic loss modulus at the beginning of gelling was the characteristic of hypercoagulability. This characteristic occurred more frequently than other abnormalities in other tests for hypercoagulability (beta-thromboglobulin, antithrombin III and TEG). Only in deep vein thrombosis, a moderately positive correlation was noted between the increment rate of the dynamic loss modulus and the plasma fibrinogen level.
 ...
PMID:Detection of hypercoagulability by the measurement of the dynamic loss modulus of clotting blood. 713 52

Authors review the epidemiology of deep venous thrombosis and the prothrombotic state in high risk patients; particularly antithrombin III role in blood clotting is considered. A fall in antithrombin III concentration and/or activity can induce hypercoagulability and thrombosis. Moreover authors stress the need to evaluate antithrombin III as anti-Xa activity, to detect high risk patients for deep venous thrombosis.
 ...
PMID:[Epidemiological evaluation of thromboembolic risk. Critical review of the prospects offered by determination of antithrombin III]. 735 31

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.
 ...
PMID:The hypercoagulable state in cancer patients: evidence for impaired thrombin inhibitions. 751 51

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)
 ...
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.
 ...
PMID:Thrombin regulation in children differs from adults in the absence and presence of heparin. 774 Apr 51

UFH and its derivatives, LMWHs, are effective and safe in the prevention and treatment of DVT. The mechanism for this effectiveness has been difficult to explain, given that the anti-IIa activity of LMWHs is important for their antithrombotic activity and the reported half-life of the anti-IIa activity of LMWHs is very short. The standard chromogenic anti-IIa assay is performed in an artificial system consisting of highly diluted plasma to which antithrombin III is added. It is possible, therefore, that the apparently short half-life of the anti-IIa activity is dependent on the limitations of the anti-IIa assay, commonly used in the pharmacokinetic studies. We have developed an anti-IIa assay that is more sensitive than the standard one. Our assay is based on the ability of UFH or LMWHs to catalyze the formation of TAT complexes. PTNA was able to detect in vitro the anti-IIa activity produced by 0.01 anti-Xa IU/mL of UFH or 0.05 anti-Xa IU/mL of LMWHs. Ex vivo, it was able to describe the time course of plasma anti-IIa activity of very low doses of UFH (intravenous or subcutaneous) or LMWHs. To characterize better the role of the anti-IIa activity of LMWHs, the pharmacokinetic properties of two of these agents have been evaluated in humans, assessing the anti-IIa activity by PTNA. Fraxiparine, 7500 and 10,000 ICU, and Enoxaparine, 20 and 40 mg, were administered subcutaneously to six healthy volunteers.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Plasma thrombin neutralization assay: pharmacokinetic applications. 782 61

Abnormal antithrombin III (AT III) was found in a 30-year-old woman who suffered from recurrent thrombosis during pregnancy and the postpartum period. Among her family members, only her father had recurrent episodes of deep vein thrombosis of the lower extremities, from his youth. The antithrombin and antifactor Xa heparin cofactor activities of the proposita's plasma were 61% and 42% of normal, respectively. The progressive antithrombin and antifactor Xa activities were also decreased to 55% and 58% of normal, respectively. The immunoreactive level of AT III was within the normal range (23.1 mg/dl). Analysis of the proposita's plasma by crossed immunoelectrophoresis in the presence or absence of heparin and by affinity chromatography on heparin-Sepharose revealed that the proposita's AT III had apparently normal affinity for heparin. Nucleotide sequencing of 7 exons of the proposita's AT III gene amplified by polymerase chain reaction (PCR) disclosed that the second base of codon 393 comprised both G and A, indicating Arg393-His conversion. The base sequences of exons 1, 2, 3a, 3b, 4, and 5 were normal, excluding any other mutation. These findings indicated that the proposita's AT III was a variant of AT III at the thrombin binding site and that the proposita was a heterozygote for the abnormality. Heparin affinity of purified abnormal AT III from the proposita's plasma was demonstrated to be increased upon affinity chromatography using heparin-Sepharose, suggesting that the mutation (Arg393-His) per se could possibly increase the affinity of antithrombin III for heparin. For this variant AT III (Arg393-His), the name AT III Kumamoto II is proposed.
 ...
PMID:Antithrombin III Kumamoto II; a single mutation at Arg393-His increased the affinity of antithrombin III for heparin. 783 87

In order to evaluate the usefulness of determining D-dimer and thrombin-antithrombin III complex (TAT) in the diagnosis of deep venous thrombosis (DVT), three D-dimer assays were tried: one ELISA and one latex test from Diagnostica Stago and one new latex method from Biopool. TAT was assessed using an ELISA (Behringwerke). We studied 96 consecutive outpatients with suspected DVT, of whom 36 had phlebographically confirmed DVT. Statistical calculations showed high sensitivity and a negative predictive value for the D-dimer ELISA (97% for both), confirming the results obtained by others. The new latex method (Biopool) showed similar figures (96% for both). The latex method from Diagnostica Stago and TAT showed lower sensitivity and negative predictive values. No differences in the D-dimer results were found with or without antifibrinolytics in the tubes for blood sampling. Our data suggest that negative results when using the new simple and cheap latex method (Biopool) may reduce the number of phlebographic examinations.
 ...
PMID:D-dimer and thrombin/antithrombin III complex--diagnostic tools in deep venous thrombosis? 784 46

A young man with a history of deep vein thrombosis and pulmonary embolism 11 years ago presented again with acute pulmonary embolism and was treated initially with intravenous heparin at our institution. Five days later he had another massive bout of pulmonary embolism causing hypotension. Pulmonary angiography confirmed the presence of thrombi in both pulmonary arteries, with complete obstruction of the left pulmonary artery. He was treated successfully by emergency pulmonary embolectomy. Blood investigations later confirmed the diagnosis of protein S deficiency and he was started on warfarin therapy for life. Massive pulmonary embolism should be treated aggressively. Thrombolytic therapy accelerates clot lysis, reduces pulmonary pressures, restores pulmonary capillary volume and reverses right heart failure faster than heparin alone. There is also a trend towards decreased mortality with thrombolysis. In the presence of shock, the patient should be resuscitated and if facilities for emergency embolectomy are available, surgery is a viable alternative to thrombolysis, especially if the clot burden is massive. In young patients with recurrent venous thromboembolism in the absence of obvious predisposing factors, it is important to exclude inherited plasma protein deficiencies of protein S, protein C, antithrombin III, plasminogen and fibrinogen.
 ...
PMID:Massive acute pulmonary embolism in protein S deficiency--a case report. 794 58


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