Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.5 (thrombin)
33,306 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lacunar infarcts are related to occlusion of penetrating arteries. Lipohyalinosis affects the smaller arteries 40-200 microns in diameter, and atherosclerosis involves larger arteries 200-850 microns in diameter. We hypothesized that the processes of thrombus formation might be different among these two kinds of lacuner infarcts, including those caused by lipohyalinosis and atherosclerosis. We studied acute coagulation and fibrinolytic activation in lacunar infarct patients which were divided into two groups according to their size: smaller lacunar group and larger lacunar group. Then we divided lacunar infarct patients into two groups in terms of the progression of motor deficits: those who showed the progression and those did not. And coagulation and fibrinolytic activation were compared each other. One hundred and twenty four patients were enrolled in this study, including 34 control subjects, 39 patients with smaller lacune (3 mm-10 mm in diameter), 28 patients with large lacune (10 mm-20 mm), and 23 patients with atherothrombotic infarcts confirmed by angiography. The levels of TAT activity in large lacune and atherothrombotic infarcts were significantly higher than those in control subjects (p = 0.009, p < 0.0001, respectively), whereas those in small lacune were not. Also, the levels of D-dimer activity in large lacune and atherothrombotic infarcts were significantly higher than those in control subjects (p = 0.0003, p < 0.0001, respectively), whereas those in small lacune were not. The progression of motor deficits were more frequently recognized in large lacune than in small lacune: three patients out of 39 small lacune patients and 22 patients out of 28 large lacune patients (difference was significant, p = 0.001). The level of TAT activity in patients who showed progression of motor deficits was significantly higher than that in those who did not (p = 0.0002), whereas the difference of the levels of D-dimer activity in two groups did not reach significant differencial levels. The process of thrombin and fibrin formation in large lacunar infarcts which are related to microatheroma and atheroscrelosis appears to be different from that in small lacunar infarcts. Antiplatelet and anticoagulation therapy should be tailored to large lacunar infarct patients.
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PMID:[Coagulation and fibrinolytic activation in lacunar infarct patients]. 1068 30

Hemostatic abnormalities were examined in 55 patients during maintenance hemodialysis (HD). Before HD, plasma protein C and protein S antigens were almost within the normal range, while plasma thrombin-antithrombin III complex (TAT III) and plasmin-plasmin inhibitor complex (PPIC) levels in HD patients were increased slightly, and plasminogen activator inhibitor 1 level was significantly increased, compared to that in normal volunteers. Plasma activated protein C (APC) and protein C inhibitor (PCI) complex and APC alpha 1 antitrypsin (alpha 1AT) complex were not detected in normal volunteers; however, plasma APC-PCI complex was increased in 36 of the patients and plasma APC-alpha 1AT complex was increased in 25 patients. Plasma PCI levels in these patients before HD were significantly decreased. Plasma TAT, PPIC, and tissue type plasminogen activator levels were significantly higher before HD than after 1 hour HD and at the end of HD, while the changes in plasma protein C antigen, protein S antigen, PCI antigen, APC-PCI complex, and APC-alpha 1AT complex were not significant after 1 hour of HD or at the end of HD compared to levels before HD. Plasma PCI levels were correlated with APC-PCI complex, suggesting that decreased PCI levels might be caused by the activation of protein C.
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PMID:Increased activated protein C: protein C inhibitor complex and decreased protein C inhibitor levels in patients with chronic renal failure on maintenance hemodialysis. 1072 91

Patients with active Cushing's syndrome have an increased thrombotic tendency. We chose to reassess the mechanism underlying the thrombophilic state associated with this clinical condition using sensitive markers of coagulation and fibrinolysis activation in 17 patients with active disease. The results were compared with those obtained in 12 Cushing's patients successfully treated by surgery and in 20 normal individuals. The general pattern of results in patients with active disease was the finding of increased levels of von Willebrand factor (VWF: Ag), a marker of enhanced metabolic function of endothelial cells (VWF:Ag 181 +/- 42 vs 110 +/- 43, p<0.001 in normal subjects), accompanied by signs of heightened thrombin and plasmin generation, expressed by high levels of thrombin-antithrombin (TAT 5.59+/-3.6 vs 3.06+/-0.92 ng/ml in controls, p<0.01) and plasmin-antiplasmin complexes (PAP 407+/-176 vs 245+/-67 ng/ml in controls, p<0.01). VWF:Ag and TAT values were significantly higher in hypertensive than in normotensive patients with active disease (205+/-40 vs 155+/-26 U/dl, p<0.05 and 7.49+/-3.7 vs 3.45+/-1.8, p<0.01, respectively). Plasma levels of plasminogen activator inhibitor type 1 were higher, though not to a statistically significant extent, in patients with active disease compared to controls (12.8+/-12.3 vs 5.6+/-7.4 IU/ml, NS) and positively correlated with body mass index (r=0.66, p<0.01). After surgical control of Cushing's syndrome, there was a partial or complete reversal of the abnormalities to values similar to those found in normal individuals. Our data suggest that the thrombophilic state present in patients with active Cushing's syndrome is related to an enhanced metabolic function of endothelial cells; this in turn may be caused by an heightened production of thrombin with secondary hyperfibrinolysis. Primary prophylaxis with anticoagulants is recommended in these patients when they are exposed to a thrombophilic condition such as surgery.
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PMID:Markers of activation of coagulation and fibrinolysis in patients with Cushing's syndrome. 1080 70

Thrombopoietin is produced at a constant rate by the liver and kidney and is removed from the circulation upon binding and subsequent uptake via the Tpo receptor, c-Mpl, expressed by platelets and mega-karyocytes. Apart from uptake, this study shows that platelets can also function as a storage pool for Tpo. Upon stimulation with various platelet agonists, full-length biologically active Tpo was released by platelets. Platelet fractionation experiments indicated that this Tpo most likely is contained in the granules. When platelets were preincubated with Tpo-peptide mimetic or truncated Tpo prior to maximal activation, a three- to fivefold increment in Tpo release was seen. whereas, the release of other granule proteins such as vWF-propeptide or serotonin remained unchanged. Therefore, the Mpl agonists might compete with Mpl-bound Tpo, thereby releasing Tpo into the platelet supernatant. Intravascular release of Tpo by platelets might occur in patients with massive platelet activation, as occurs in patients with disseminated intravascular coagulation. The Tpo concentration in these patients is elevated (p <0.01) and correlates with markers for thrombin generation, TAT complexes and F1+2(r(p)= 0.8 and 0.9; p <0.01). This suggests that the increment in Tpo concentration was attributed to Tpo release by activated platelets in vivo, which might be instrumental in subsequent stimulation of thrombocytopoiesis.
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PMID:Platelets release thrombopoietin (Tpo) upon activation: another regulatory loop in thrombocytopoiesis? 1089 50

Monocyte tissue factor expression is supposed to play an important role in the hypercoagulability of blood in cancer patients. The relation between coagulation parameters and the expression of monocyte membrane proteins involved in hemostasis or monocyte activation was studied in 21 patients with a disseminated malignancy and 21 age- and sex-matched healthy controls. In the cancer patient group no increase of monocyte tissue factor expression was found (8. 4% vs. 7.8%; P = 0.83), but a significant increase of monocyte-bound activated protein C (APC) (28.8% vs. 13.4%; P = 0.009) and monocyte CD16 expression (34.5% vs. 27.0%; P = 0.007) was observed. There was also a significant increase of D-dimers (2.0 vs. 0.2 microg/ml; P = 0.001), a decrease of antithrombin (83.5% vs. 102.0%; P = 0.004), but no increase of TAT complexes (1.7 vs. 1.5 microg/l; P = 0.38) or factor VII(a) (68.5% vs. 75.0%; P = 0.52). The increase of D-dimers was significantly correlated with the monocyte APC (R = 0.60; P = 0. 005), but not with monocyte tissue factor levels (R = -0.22; P = 0. 35) or TAT complexes (R = 0.12; P = 0.60). These results reflect a local rather than systemic thrombin and fibrin formation. It is suggested that the APC formed locally enters the circulation and binds to peripheral blood monocytes. APC bound on monocytes is known to inhibit monocyte cytokine production and might therefore be involved in regulatory responses of monocytes in cancer patients.
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PMID:Increased D-dimer levels correlate with binding of activated protein C, but not tissue factor expression, on peripheral blood monocytes in cancer patients. 1091 81

In vitro testing of blood contacting materials before clinical application is generally advisable. Four heparin coatings from different manufacturers were tested for adsorbed proteins and soluble activation markers. The surface with the highest antithrombin, thrombin, high-molecular-weight-kininogen (HMWK) and the lowest fibrinogen binding capacity (Carmeda, Medtronic) showed significantly lower levels of granulocytes and platelet activation (beta-TG, PMN-elastase release). No statistically significant differences in soluble markers of the coagulation system could be detected (F1 + 2, TAT). Interestingly, complement activation (TCC) was significantly reduced within the group of the lowest adsorption of the complement factor C3. Our data demonstrate that there is a relation between the binding affinity of proteins (C1-inhibitor, C3-complement) and the consecutive changes in complement activation (TCC). Therefore, measuring adsorbed proteins on artificial surfaces is a suitable, sensitive and very reproducible method for assessing the thrombogenicity of biomaterials.
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PMID:Quality assessment of heparin coatings by their binding capacities of coagulation and complement enzymes. 1097 57

This study was conducted to assess right and left atrial hemostatic function in patients with mitral stenosis (MS) and to investigate the immediate effect of balloon mitral valvuloplasty (BMV) on hemostatic function. BMV was performed in 28 patients with MS (age 29 +/- 8 years) who had sinus rhythm and no left atrial (LA) thrombus. Right and left atrial biochemical markers of platelet activity (platelet factor 4 [PF4] and B thromboglobulin [BTG]), coagulation (thrombin-antithrombin III complex [TAT]), and fibrinolytic activity (D-dimer) were measured before and 30 minutes after BMV. Right atrial levels of these markers were also measured in 20 control subjects. Compared with control subjects, patients with MS had higher right atrial levels of PF4 (30 +/- 15 vs 5 +/- 2 IU/ml), BTG (231 +/- 53 vs 30 +/- 8 IU/ml), TAT (7 +/- 4 vs 2 +/- 0.3 microg/L), and D-dimer (380 +/- 145 vs 160 +/- 35 ng/ml, p < 0.0001 in all). TAT levels were higher in the left atrium than in the right atrium of patients before BMV (8 +/- 4 vs 7 +/- 4 microg/L, p < 0.0001). BMV was successful (final mitral valve area > or = 1.5 cm2 and > or = 50% increase of the initial valve area) in all patients. There was a significant reduction of LA levels of PF4 (35 +/- 8 to 26 +/- 9 IU/ml, p < 0.0001), BTG (225 +/- 41 to 196 +/- 28 IU/ml, p < 0.001), and TAT (10 +/- 5 to 7 +/- 1 microg/L, p < 0.05) in the 16 patients with LA pressure < 10 mm Hg after BMV, whereas these markers were not reduced in the 12 patients with left atrial pressure > or = 10 mm Hg after BMV. These data indicate that platelet function, coagulation status, and fibrinolytic activity are increased regionally in the left atrium and in the systemic circulation in patients with MS and sinus rhythm in the absence of LA thrombus. Successful BMV induces a significant reduction of prethrombotic status in patients with low LA pressure after the procedure. Patients with high LA pressure after BMV maintain a high prethrombotic state and may be considered at an increased risk of thromboembolism after the procedure.
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PMID:Immediate effect of balloon valvuloplasty on hemostatic changes in mitral stenosis. 1107 9

There is evidence that the coagulation system is activated in patients with peripheral arterial occlusive disease (PAOD). The beneficial effects of the vasoactive drug prostaglandin E1 (PGE1) may rely in part on the modulation of the coagulation system. The study was designed to evaluate the effects of PGE1 on hemostatic and fibrinolytic variables in patients with intermittent claudication. Therefore molecular markers of thrombin (prothrombin fragment 1+2, PTF 1+2; thrombin-antithrombin III complexes, TAT) and fibrin formation (fibrinopeptide A, FPA) and markers of the fibrinolytic activity (fibrin degradation products, D-dimers) were determined before and immediately after the first PGE1 dose (60 microg in 100 ml NaCl over 2 h i.v.) as well as after 4 weeks of daily infusion therapy in 12 PAOD patients and in eight control patients before and after a single placebo infusion. Plasma levels of PTF1+2, TAT, FPA and D-dimers tended to decrease after the initial dose of PGE1. Infusion therapy with PGE1 for 4 weeks led to a decrease of all hemostatic and fibrinolytic parameters with most pronounced changes for PFT1+2, D-dimers and plasminogen activator inhibitor-1 decreasing by 11% (P<0.05), 20% (P<0.05), and 7% (P<0.05), respectively. These variables remained unchanged in controls with placebo infusion. In summary, infusion therapy with PGE1 in patients with PAOD reduces thrombin formation and results in a decrease of fibrin degradation. PGE1 may thus reduce fibrin deposition involved in the pathogenesis of atherosclerosis.
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PMID:Hemostasis and fibrinolysis in patients with intermittent claudication: effects of prostaglandin E1. 1109 Feb 53

Synthetic colloids have been reported to cause haemorrhagic complications. The effects of perioperative volume replacement with 4% gelatin (n = 20), 6% low-molecular weight (LMW) hydroxyethyl starch (HES) (Mw: 70,000 dalton; HES 70/0.5; n = 20) and 6% medium-molecular weight (MMW) HES (Mw: 200,000 dalton; HES 200/0.5; n = 20) on haemostasis were assessed in patients undergoing major abdominal surgery. Volume was administered to keep central venous pressure (CVP) between 10 and 14 mm Hg. Conventional global coagulation tests, molecular markers of coagulation, and platelet function (using a platelet function analyser (PFA-100) with ADP as inductor) were monitored prior to surgery (T0), at the end of surgery (T1), 4 h after the end of surgery (T2), and on the morning of the first postoperative day (T3). Significantly more gelatin (2900 (SD 320) ml) than HES 200 (2150 (312) ml) was given during the study period. Bleeding and the use of allogeneic blood-blood products were similar in all groups. Markers of thrombin generation (F1 + 2), of thrombin neutralization (TAT III complex), and of fibrin formation and its degradation (D-dimer) increased significantly during and after surgery without showing significant group differences. Factor VIII and von Willebrand factor (vWF) also increased in all groups beyond the normal range, showing the significantly highest increase in the gelatin-treated group (VIII: from 173 (36) to 266 (33) U dl-1; vWF: from 164(33) to 238 (31) U dl-1). Platelet function remained within the normal range and without group differences throughout the study period. We can conclude that all three solutions can be used safely in patients undergoing major abdominal surgery with regard to the haemostatic process.
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PMID:Influence of different colloids on molecular markers of haemostasis and platelet function in patients undergoing major abdominal surgery. 2168 26

Elevated plasma concentrations of endogenous thrombin generation markers and thrombotic events have been reported in children with leukemia. The aim of this study was to evaluate the effects of cancer and its treatment on thrombin generation (TAT levels) in children with acute lymphoblastic leukemia (ALL). The authors evaluated 32 children (23 M, 9 F) aged between 1 and 15 years (mean 6) affected by ALL (immunophenotypic subgroups: 16 common, 7 T, and 9 pre-B type). In all patients TAT levels at onset and after 5-6 doses of L-asparaginase were evaluated. TAT levels were higher in patients both at onset (13.04 +/- 10.90 ng/L) and after the 5-6 doses of L-asp (19.41 +/- 11.05 ng/L) with respect to controls (4 +/- 1 ng/L) (p < .001 and p < .001). TAT levels after 5-6 doses of L-asp were higher than those at onset (p < .001). Factorial ANOVA showed that at onset there was a significant effect of leukemia immunophenotypic subgroups upon TAT levels (p < .05) and no effect of inherited thrombotic risk factors. These results indicate that in children with ALL an important role is played by acquired thrombotic risk factors, among which the indirect cancer procoagulant activity has its importance.
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PMID:Thrombin generation in children with acute lymphoblastic leukemia: effect of leukemia immunophenotypic subgroups. 1112 98


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