Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.5 (thrombin)
 33,306 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tissue damage by extracorporeal shock wave lithotripsy (ESWL) is assumed to be attributable to ischemic changes in the treated region surrounding the particular vessel which is first ruptured by shock waves. Such changes cannot take place without being accompanied by acceleration of coagulation and fibrinolysis. In the literature on renal damage by ESWL, no parameters of the coagulation and fibrinolysis of blood were used. The present study was designed to investigate renal damage by shock waves through the quantification of sequential changes in the following parameters between before and after ESWL: thrombin antithrombin III complex (TAT), alpha 2-plasmin inhibitor-plasmin complex (PIC), fibrin and fibrinogen degradation products (FDP) and D-dimer (D-D). In ESWL for renal stones, a significant acceleration of TAT occurred on the 1st postoperative day, followed by acceleration of PIC on the 3rd postoperative day. A transient acceleration was observed for FDP and D-D after operation. The levels of these parameters, however, returned to normal by the 1st postoperative week. In ESWL for ureteral stones, unlike for renal stones, none of the parameters showed statistically significant acceleration. In the construction of percutaneous nephrostomy (PNS) cases for ureteral stones before ESWL, none of the parameters showed significant acceleration either. Changes in these parameters of coagulation and fibrinolysis due to ESWL for renal stones were greater than those of construction of PNS or ESWL for ureteral stones. The reason for the difference of the alteration in these parameters between renal stones and ureteral stones were more abundant vessels in the kidney than the ureter. All these changes in the parameters, however, disappeared within almost 1 week.
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PMID:Studies on changes in parameters of the coagulation and fibrinolysis in association with extracorporeal shock wave lithotripsy. 846 83

In April, 1991, a 61-year-old man was admitted to our hospital because of pancytopenia and disseminated intravascular coagulation (DIC). Five years prior to admission he had developed high fever, skin eruption and arthralgia which had been improved by antibiotics, but recurred. Steroid therapy was ineffective for pancytopenia and DIC. Laboratory findings were as follows: RBC count, 274 x 10(4)/microliters; WBC count, 470/microliters; Platelets, 6.4 x 10(4)/microliters; fibrinogen, 153mg/dl; FDP, 67.0 micrograms/ml; FDP-D.Dimer, 13040ng/ml; thrombin-antithrombin complex, > 60.0ng/ml; and plasmin alpha 2-plasmin inhibitor complex, 10.3 micrograms/ml. As we suspected adult onset Still's disease on the basis of clinical course, we treated him with methylprednisolone pulse therapy, which was, however, ineffective. leukocytopenia, thrombocytopenia and DIC improved after cyclosporine treatment. Since cyclosporine is known to be very effective to autoimmune diseases, we speculate that in this patient immunological mechanism may be involve in the pathogenesis of DIC.
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PMID:[Cyclosporine therapy of adult onset Still's disease with disseminated intravascular coagulation]. 849 12

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

To study the mechanism underlying the high lipoprotein (a) [Lp(a)] level in uremic patients on chronic hemodialysis, we investigated the levels of Lp(a), acute phase reactants (C-reactive protein and sialic acid), and interleukin-6 (IL-6) in 54 dialysis patients. The mean [95% CI] Lp(a) level was increased in the hemodialysis patients compared with the 30 controls (30 [25-36] vs. 18 [14-23] mg/dl, p < 0.005). Among dialysis patients, 46% had an Lp(a) level > 30 mg/dl, which was significantly higher than the percentage in the control group (17%). The levels of C-reactive protein, sialic acid, and IL-6 were also increased in dialysis subjects compared with controls (200 [134-299] vs. 37 [24-58] micrograms/dl, p < 0.0001; 63 [59-66] vs. 54 [52-56] mg/dl, p < 0.002; and 9.2 [7.8-11] vs. 5.5 [5.0-6.1] pg/ml, p < 0.0005, respectively). The Lp(a) level was positively correlated with that of C-reactive protein (r = 0.415, p < 0.002), sialic acid (r = 0.426, p < 0.002), and IL-6 (r = 0.298, p < 0.05) in the hemodialysis patients, but not in the controls or non-dialysis uremic patients. The Lp(a) level in the dialysis patients was also positively correlated with activation markers of coagulation (thrombin-antithrombin III complex and plasmin-alpha 2-plasmin inhibitor complex, p < 0.005). These results indicate that the Lp(a) level is closely related to the acute phase reaction and hypercoagulability in chronic hemodialysis patients.
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PMID:High lipoprotein (a) levels in chronic hemodialysis patients are closely related to the acute phase reaction. 856 Apr 4

The authors evaluated elements of the coagulation and fibrinolytic systems in 18 male patients with intermittent claudication vs 19 men matched for risk factors who served as controls. Prothrombin time and activated partial thromboplastin time did not significantly differ in the patients and the controls. The plasminogen level in the two groups was not significantly different. The level of lipoprotein(a) was significantly higher in the patients than in the controls. The levels of antigen and the activity of protein C did not differ significantly between the two groups. The thrombomodulin level was significantly higher in the patients than in the controls. There were no significant differences between the two groups in the levels of alpha 2-macroglobulin, C1-inactivator, or antithrombin III. The levels of fibrinogen and alpha 1-antitrypsin were significantly higher in the patients vs the controls. Significantly lower levels of alpha 2-plasmin inhibitor and higher levels of alpha 2-plasmin inhibitor/plasmin complex and thrombin/antithrombin III complex were found in the patients vs the controls. These findings suggest that the levels of thrombin/antithrombin III complex, alpha 2-plasmin inhibitor/plasmin complex, and thrombomodulin may perhaps serve as indicators for injury to the peripheral endothelium and that the coagulation and fibrinolytic systems may be activated in patients with intermittent claudication.
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PMID:Evaluation of the coagulation and fibrinolytic systems in men with intermittent claudication. 867 28

Plasma levels of selected coagulation and fibrinolytic parameters (activated partial thromboplastin time, prothrombin time, fibrinogen, antithrombin III, protein C, thrombin-anti-thrombin III complexes (TAT), plasminogen activator inhibitor-1 (PAI-1), plasminogen, alpha 2-plasmin inhibitor) were evaluated in 90 patients with clinical suspicion of pulmonary embolism (PE). Plasma levels of fibrinogen, PAI-1 and TAT were significantly higher in patients than in controls (p < 0.01): evaluation of TAT displayed a sensitivity of 96.1% and specificity of 30.8%, and positive and negative predictive values of 64.5 and 85.7%, respectively. The number of nonperfused lung segments correlated directly with TAT levels (p < 0.01) and inversely with arterial pO2 values (p < 0.01). No significant difference was found in the other parameters between patients and controls. Our results suggest that the finding of normal TAT plasma levels can help to exclude PE in patients with clinically suspected PE.
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PMID:Thrombin-antithrombin III complexes as an additional diagnostic aid in pulmonary embolism. 869 74

Five patients with hereditary angioedema (HAE) were studied during attacks and remission as were healthy controls. The high levels of C1/C1-INH complexes, low C4 and high ratio C4 activation products (C4bc)/C4 also differed significantly during remission compared to controls. During attacks C4bc/C4 increased (922-2007; P = 0.022, remission versus attacks, median values throughout), C2 and CH50 dropped (111-31%; P = 0.043 and 110-36%; P = 0.016, respectively), TCC (C5b-9) increased (0.88-1.23 AU/ml; P = 0.028). Cleavage of HK increased to be almost complete during attacks (20-90%; P = 0.009). While factor XIa/serpin-complexes did not increase, a more than twofold rise in thrombin/antithrombin-complexes (0.20-0.50 microgram/l; P = 0.009) and in plasmin/alpha-2-antiplasmin-complexes (7.3-17 nmol/l; P = 0.028) was observed. For the first time cascade activation in HAE was studied simultaneously, and corroborates that attacks lead to activation of the kallikrein-kinin system, fibrinolysis and early part of the classical complement pathway. In addition, the authors present novel data of terminal complement and coagulation activation, the latter apparently not via FXIa.
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PMID:Activation of the complement, coagulation, fibrinolytic and kallikrein-kinin systems during attacks of hereditary angioedema. 871 33

Thrombus formation is recognized pathologically in the affected arteries and is supposed to play a major role in the pathogenesis of Takayasu's arteritis; however, hemostatic conditions in this disorder have not been elucidated fully. We determined plasma levels of molecular markers for platelet activity (platelet factor 4; PF4, beta-thromboglobulin; beta TG), thrombotic status (thrombin-antithrombin III complex; TAT, fibrinopeptide A; FPA), fibrinolytic status (plasmin-alpha 2-plasmin inhibitor complex; PIC, D-dimer), and endothelial injury (von Willebrand factor antigen; vWF:Ag, thrombomodulin; TM) in 30 patients with Takayasu's arteritis and 20 age-matched control subjects. Plasma levels of PF4, beta TG, TAT, FPA and D-dimer, but not PIC, in patients with Takayasu's arteritis were substantially higher than those in normal control subjects. The levels of these markers were not different between the active and inactive stages of the disease. Plasma levels of vWF:Ag in patients with Takayasu's arteritis did not differ significantly from those in normal subjects, and plasma levels of TM were significantly lower than those in normal subjects. In patients with Takayasu's arteritis, platelet and coagulation activities are significantly increased, leading to hypercoagulable state and thrombus formation, although there is little, if any, endothelial damage.
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PMID:Hypercoagulable state in patients with Takayasu's arteritis. 872 10

To clarify the relationship between the results of intracoronary thrombolytic therapy (ICT) and fibrino-coagulation in patients with acute myocardial infarction (AMI), the thrombin-antithrombin III complex (TAT) and fibrinopeptide A (FPA), as indices of accelerated coagulation, and the plasmin- alpha 2-plasmin inhibitor complex (PIC), as an index of accelerated fibrinolysis in peripheral blood, were measured just before and after heparin injection (5,000 U), and immediately after ICT. Twenty-four patients with AMI were divided into 2 groups according to the results of ICT; successful ICT (group S) and unsuccessful ICT (group F). As a control group (group C), 14 age-matched normal volunteers were also studied. The levels of TAT and FPA before ICT were significantly higher in groups S and F than in group C (p < 0.01). The TAT level before ICT in group F was higher than that in group S (p = 0.07), however, the TAT, FPA and PIC levels showed no significant differences between groups S and F at each sampling time. TAT/PIC before ICT was significantly higher in group F than in group S (F: 0.026 +/- 0.020 vs S: 0.008 +/- 0.004, p < 0.05), whereas there was no remarkable difference in FPA/PIC between groups S and F. These results indicate that hyper-coagulation had occurred in the AMI cases and that coagulation had been more accelerated in group F. TAT/PIC might be an index of the equilibrium of the fibrino-coagulating system. Therefore, TAT/PIC measurement before thrombolytic therapy may be more useful than TAT measurement alone for evaluating recanalization in ICT.
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PMID:Relationship between intracoronary thrombolysis and fibrino-coagulation--special reference to TAT/PIC and FPA/PIC. 874 Dec 40

Seventy-four patients with PSS were evaluated with regard to plasma concentration of blood coagulation and fibrinolysis factors: fibrinogen (Fbg), prothrombin time (PT), active partial thromboplastin time (APTT), protein C, thrombin-antithrombin III complex (TAT), antithrombin-III (AT-III), factor XIII (XIII) fibrinopeptide A (FPA), alpha 1-antitrypsin (alpha 1-AT), plasminogen (Pmg), alpha 2-plasmin inhibitor plasmin complex (PIC), alpha 2-plasmin inhibitor (alpha 2-PI), alpha 2-macroglobulin (alpha 2-MG), fibrinopeptide B beta 15-42 (FPB beta-15-42) and soluble fibrin monomer complex (SFMC), FDP (fibrin degradation product) and D-dimer. They were also evaluated with regard to platelet-derived proteins: beta-thromboglobulin (beta-TG), platelet factor 4 (PF4), thromboxane B2 and 6-keto-prostaglandin F1 alpha (6KF). In the coagulation/fibrinolysis systems high plasma levels of TAT, AT-III, FPA, alpha 2-MG and FPB beta 15-42 could be demonstrated in more than 50% of total PSS patients. There was no statistical correlation between those of TAT and AT-III. Plasma levels of PIC, D-dimer, FDP and SFMC were not always high. There was no statistical correlation between those of TAT and PIC. These data lead us to consider that alpha 2-MG may play an important role for inhibiting PIC, which accelerates the conversion from fibrin into FDP. Subsequently, there were high plasma levels of FPB beta 15-42 converted from fibrin monomer. These data seem to be indicative of an involvement of coagulation and platelet disorder in PSS. These platelet-vessel system disorders might be closely related to the pathophysiology of PSS.
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PMID:Plasma levels of molecular markers of blood coagulation and fibrinolysis in progressive systemic sclerosis (PSS). 878 74


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