Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.1.108 (TAT)
 2,389 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Medroxyprogesterone acetate (MPA), which is widely used clinically as an anticancer steroid preparation, is a very useful drug that seldom causes severe side effects such as bone marrow suppression, and can be dispensed at the outpatient clinic for an oral administration at home to the advantage of QOL. Recently however, there have been several reports suggesting its relationship with thrombosis. We measured t-PA, protein C, factor X, AT III, TAT, plasminogen, PIC, fibrinogen, and D-dimer in 11 patients with gynecologic malignancies who are treated with MPA (600 mg/day) and 11 controls. Then we examined the effects of the drug on blood coagulation and fibrinolytic activities. No changes in these parameters clearly suggested thrombogenesis in either group at this measurement or during the observation period (17 months at the maximum). The present study found no remarkable abnormalities in the blood coagulation and fibrinolytic activities. Thus, to avoid the use of MPA to patients at risk is considered to be the most important precaution for prevention of thrombosis.
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PMID:[Effect of high-dose medroxyprogesterone acetate on coagulative and fibrinolytic factors in patients with gynecological cancers]. 153 83

A longitudinal study has been undertaken in 125 pregnant women between 25 and 40 weeks of gestation, to provide systematic information on the changes that occur in a wide range of haemostasiological and haemorheological variables. Fibrinogen, D-Dimer, Factor VIIIR: Ag, erythrocyte aggregation and plasma viscosity rose markedly throughout pregnancy. Antithrombin III and alpha 2-antiplasmin were unchanged during pregnancy. There were no significant differences between women in the pre-eclamptic group (N = 16) and the control group. HELLP syndrome (N = 7) was associated with high D-Dimer (p less than 0.05), and TAT (p less than 0.05), low antithrombin III (p less than 0.03), protein C (p less than 0.01) and platelets (p less than 0.001). Our results demonstrate that during pregnancy (also, however, in pre-eclamptic women) alterations of the coagulation system occur, but these changes do not affect the overall haemostatic balance. Findings in patients with "true" HELLP syndrome are consistent with an increased tendency for intravascular coagulation.
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PMID:[Hemostasis and pre-eclampsia]. 205 97

Patients who had undergone prosthetic valve replacement were treated with warfarin (anticoagulant) alone or in combination of ticlopidine (200 mg/day) or aspirin (81 mg/day) (anti-platelet agents). The study of blood coagulation factors and platelet aggregation were carried out with these cases. 1) The patients (n = 24) receiving warfarin for 21 days after prosthetic valve replacement revealed marked increases in PIVKA-II and vitamin K1-epoxide. The protein C activity was significantly lower than that before the operation. High levels of more than 5 ng/ml of TAT were found before operation and after warfarin administration for 21 days. 2) Warfarin did not affect platelet aggregation, whereas ticlopidine inhibited ADP-induced platelet aggregation and aspirin inhibited both collagen-induced and arachidonic acid-induced aggregation. In conclusion, combined use of anticoagulants and antiplatelet agents after prosthetic valve replacement will suppress not only the blood coagulation but also the platelet aggregation systems.
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PMID:[Significance of combined use of anticoagulants and antiplatelet agents in the early stage after prosthetic valve replacement]. 756 36

We studied 37 hemodialysis patients, treated with erythropoietin (EPO), prior to and upon reaching target Hb and after 3 months at steady state Hb levels. Our aim was to analyze the effects of EPO on markers of all stages of coagulation and anticoagulation during a standardized hemodialysis procedure upon reaching target Hb as well as long term effects of a stable Hb. The Hb rose from 82 +/- 9 to 111 +/- 12 g/L at target Hb (p < 0.0001) and was 108 +/- 15 g/L after 3 months of steady state. The heparin dose was individually titrated, using a whole blood activated coagulation time method (WBACT) and kept constant during the first phase of the study. The titrated heparin dose increased significantly at target Hb and this increase persisted after 3 months at steady state. Accordingly the increase in WBACT decreased significantly. There was a significant increase in platelets at target Hb and this increase persisted at steady state. beta-thromboglobulin increased significantly at target Hb and this increase persisted after 3 months at steady state. Platelet factor 4 was unchanged throughout the study period. Inhibitors of plasma coagulation: AT III, protein C and total and free protein S were unchanged throughout the study period. There was no changes in indicators of intravascular coagulation: TAT, fibrin monomers or FPA throughout the study period. There was no FPA generation during dialysis. The residual blood volume in the dialyzer was unaffected throughout the study period. There was a significant decrease in D-dimers at target Hb and after 3 months at steady state.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term effects of erythropoietin treatment on the coagulation system during standardized hemodialysis. 760 81

New markers of intravascular activation of coagulation have been developed, based on advance in our understanding of the biochemistry of the haemostatic mechanism. These are sensitive methods for measuring of peptides liberated with the generation of thrombin (factor IX activation peptide, factor X activation peptide, peptide F1 + 2), for measuring concentration of enzyme-inhibitor complexes (eg. thrombin-antithrombin III-TAT complexes), as well as for investigating the effect of thrombin on fibrinogen (fibrinopeptide A-FPA) or on protein C (protein C activation peptide). Studies employing these markers indicate that a state of hypercoagulability can be detected in the blood of humans prior to the appearance of thrombotic phenomena. However, further studies will be required to determine whether these methods can identify individuals who are entering a clinically relevant hypercoagulable state as well as to monitor an antithrombotic treatment.
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PMID:[Markers of intravascular activation of coagulation]. 799 71

In this study, we evaluated the effects of anticoagulants used in blood sampling on the measurements of coagulation activation markers F1 + 2, TAT, D-Dimers by Elisa methods. The study was carried out on normal subjects and patients with inherited deficiency of coagulation inhibitors, antithrombin III (ATIII) protein C (PC) and protein S (PS). Three different anticoagulant solutions were compared: 1) ACD/EDTA/adenosine/heparin, 2) EDTA/aprotinin/a synthetic thrombin inhibitor and 3) sodium citrate. The results showed that sodium citrate, commonly used in coagulation laboratories, is a suitable anticoagulant for the study of coagulation activation markers. In addition, the type of tubes (plastic tubes vs glass Vacutainer R tubes) used for blood sampling as well as the order of sampling (early or late after the phlebotomy procedure) did not influence the results. We concluded that assays of coagulation activation markers F1 + 2 and D-Dimers can be performed in samples collected routinely by haemostasis laboratory staff using Vacutainer R tubes with sodium citrate. Further investigations are needed to understand why TAT measurements gave a pattern of results quite different from F1 + 2 or D-Di measurements.
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PMID:Influence of conditions of blood sampling on coagulation activation markers (prothrombin fragment 1 + 2, thrombin-antithrombin complexes and D-dimers) measurements. 808 41

Pediatric patients with acute lymphoblastic leukemia (ALL) are at an increased risk of thromboembolic events. Potential responsible mechanisms include the disease process itself, treatment with chemotherapeutic agents (particularly L-Asparaginase [ASP]), or a combination of the disease and treatment. We studied thrombin regulation in 26 consecutive children with ALL and 14 healthy age-matched controls by: (1) plasma concentrations of prothrombin; (2) plasma inhibition of 125I-alpha-thrombin; and (3) four biochemical markers of in vivo thrombin activation (thrombin complexed to its inhibitor antithrombin III [ATIII; TAT], prothrombin fragment 1.2 (F1.2), activated protein C complexed to the inhibitors alpha 1 antitrypsin [APCAT]), and protein C inhibitor (APC-PCI). Measurements were made at presentation before treatment, after treatment with ASP alone, and during combination chemotherapy with and without ASP. At presentation, the capacity to generate thrombin (reflected by plasma prothrombin concentrations) and the capacity to inhibit thrombin (125I-alpha-thrombin--inhibitor complex formation) were similar in children with ALL compared with that for healthy children. After ASP alone or as part of combination chemotherapy, prothrombin levels were preserved, whereas plasma inhibition of 125I-alpha-thrombin decreased significantly because of a decrease in plasma concentrations of inhibitors, most importantly ATIII. After combination chemotherapy without ASP, plasma concentrations of ATIII and the capacity to inhibit 125I-alpha-thrombin returned to normal values, whereas prothrombin levels increased above control values. Thrombin generation in vivo also differed from healthy controls. At presentation, plasma concentrations of three of four markers of in vivo thrombin activity (TAT, F1.2, APCAT, but not APC-PCI) were increased in children with ALL. Neither ASP alone nor combination chemotherapy with or without ASP significantly altered values of these three markers. In summary, although the in vitro capacity to generate thrombin was preserved, the in vitro capacity to inhibit 125I-alpha-thrombin decreased after ASP therapy. Evidence for increased endogenous thrombin generation was documented in children with ALL at presentation and throughout treatment. We speculate that poor regulation of this thrombin may contribute to thrombotic complications in children with ALL.
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PMID:Increased endogenous thrombin generation in children with acute lymphoblastic leukemia: risk of thrombotic complications in L'Asparaginase-induced antithrombin III deficiency. 828 39

A 26-year-old pregnant woman was diagnosed as having both lupus anticoagulant (LA) and anticardiolipin antibody (ACA). Her previous pregnancy ended in intrauterine fetal death at 27 weeks' gestation. During the present pregnancy she was treated with aspirin, dipiridamole, predonisolone, and heparin. At 24 weeks, fetal growth became retarded, accompanied by markedly decreased activities of AT-III, protein C, plasminogen and alpha 2-plasmin inhibitor. Supplement of human AT-III led both to prolongation of the gestational period and improvement of fetal growth. The pregnancy ended in cesarean section because of signs of fetal distress at 30 weeks. The infant was a 1025-g male with Apgar scores of 5 and 9 at one and five minutes, respectively, and is healthy. The mother developed DIC after surgery, but recovered after therapy. In this case, TAT, alpha 2PI-plasmin complex, FDP Ddimer, FPB beta 15-42, L-FDP showed little correlation with the clinical course.
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PMID:[Administration of human AT-III in a case of lupus anticoagulant positive pregnancy]. 831 36

In order to predict a hypercoagulable state in patients with advanced breast cancer receiving medical treatment, the effects of chemoendocrine therapy on the coagulation-fibrinolytic systems were investigated prospectively. The patients were randomly divided into two groups. The ACT group had 38 patients, who received 20 mg/m2 adriamycin (ADM) i.v. on days 1 and 8, 100 mg cyclophosphamide (CPA) p.o. on days 1-14, and 20 mg tamoxifen (TAM) p.o. daily. The ACM group had 44 patients, who received 20 mg/m2 ADM i.v. on days 1 and 8, 100 mg CPA p.o. on days 1-14 and 1200 mg medroxyprogesterone acetate (MPA) p.o. daily. The treatment was repeated every 28 days until there was evidence of progressive disease or until the full ADM dose (550 mg/m2) had been given. The following 9 hematologic parameters were measured every 4 weeks: alpha 2-plasmin inhibitor plasmin complex (PIC), anti-thrombin-III (AT-III), D-dimer (Dd), fibrinogen (Fg), plasminogen (Pg), protein C (PC), thrombin-antithrombin-III complex (TAT-III), tissue plasminogen activator (t-PA), and factor X (FX). Compared to the ACT group, patients in the ACM group showed significantly higher values of AT-III and PC, which exceeded the normal ranges. The levels of Pg, t-PA and FX were significantly higher in the ACM group than in the ACT group, but were still within the normal ranges. The levels of TAT-III, Dd and PIC decreased in the ACT group and were unchanged in the ACM group after the start of treatment. Fg remained unchanged in both groups after the start of treatment. One patient in the ACM group had thrombophlebitis of the lower extremities with high levels of TAT-III, Dd and PIC and a decrease of Fg, but her condition returned to normal after reduction of the MPA dose. Although these data are not directly indicative of a hypercoagulable state in patients receiving chemoendocrine therapy, changes in AT-III, TAT-III, Dd and PIC should be monitored carefully when this type of treatment is given.
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PMID:Effects of chemoendocrine therapy on the coagulation-fibrinolytic systems in patients with advanced breast cancer. Japan Advanced Breast Cancer Study Group and Japan Clinical Oncology Group. 851 13

Underlying disorders of the coagulation system such as inhibitor deficiencies or decreased fibrinolysis are common in patients suffering from venous thrombosis. They may lead to the necessity of a lifelong prophylaxis. Prompt diagnosis is obviously to the patients benefit. We investigated 22 patients suffering from venous thromboses for the inhibitors antithrombin III (ATIII), protein C, and protein S during the first 8 to 12 days after admission to hospital and in addition after withdrawal from anticoagulant treatment after several months. At the day of admission ATIII and protein C levels were comparable to those several months later, but after 2 days they shifted downward or upward, respectively. Protein S did not shift during the period of hospitalisation, but was initially slightly lower than several months later. For inhibitors the day of admission to hospital is most suitable to take the samples. About 50% of the patients still had elevated activation markers (prothrombin fragments F1+2, thrombin-antithrombin complex TAT, and D-dimers) after several months.
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PMID:Parameters of haemostasis during acute venous thrombosis. 858 90


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