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)

Plasma beta-thromboglobulin (beta TG) levels were measured in 103 healthy controls and 112 patients suffering from either peripheral vascular disease (PVD), or cerebrovascular disease (CVD) or deep vein thrombosis (DVT). Plasma beta TG was significantly elevated in 46 PVD patients and 24 recent DVT patients compared to controls, but did not differ significantly in 18 chronic DVT and 24 old CVD patients. In addition, heparin neutralizing activity (HNA) and platelet aggregation induced by adenosine diphosphate, 1-epinephrine and thrombin were compared in 33 out of the 46 PVD patients to 33 controls. The mean HNA was significantly shorter in the PVD patients than in controls. The rate and extent of platelet aggregation were increased in PVD patients compared to controls, but the difference was not statistically significant. Platelet production time (PPT) was measured in 20 controls, 35 PVD patients, nine chronic DVT and 12 chronic CVD patients; significantly shorter PPT was only observed in 14 patients with advanced PVD compared to controls, suggesting increased platelet consumption in these patients. All four assays (plasma beta TG, HNA, platelet aggregation and PPT) were performed in 25 patients; no correlation between the four tests was found in these patients suggesting that the tests were measuring various aspects of platelet function. These results suggest that in vivo platelet consumption as well as platelet aggregation and 'release reaction' are presumably enhanced in PVD and recent DVT patients and that plasma beta TG and PPT assays may be better and more specific indicators of in vivo platelet activation than in vitro platelet aggregation test.
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PMID:beta-Thromboglobulin, platelet production time and pletelet function in vascular disease. 9 36

Twenty-seven patients with peripheral vascular disease had studies of thrombin generation, antithrombin III -alues, factor VIII values, platelet adhesitivity, and activated partial thromboplastin time. Of the studies performed, the thrombin generation index, antithrombin III values, and, to a lesser extent, activated partial thromboplastin time were reliable in confirming clinically suspected hypercoagulability. When patients were placed into groups with and without operative complications, it was noted that the group with operative complications had higher average values of thrombin generation index and lower average values of antithrombin III and activated partial thromboplastin time than did the group without operative complications. It is thought that these tests may be useful in selecting those patients with a high risk of thrombotic complications from vascular surgery and who may benefit from anticoagulant management while undergoing necessary vascular reconstructive procedures.
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PMID:Hypercoagulability in patients with peripheral vascular disease. 115 13

Platelets hyperaggregability and hypersecretion fibronectin (Fn) are known to occur in peripheral vascular disease (PVD) and diabetes mellitus (DM) with microangiopathy. To determine whether an increase in platelet membrane bound Fn constitutes to hyperaggregability of platelets, washed platelets from normal subjects and from patients with peripheral vascular disease and patients with diabetes mellitus were examined for the presence of fibronectin (Fn) by means of fluorescein linked antibody to Fn. Platelets from peripheral vascular disease and diabetes mellitus patients tended to aggregate during preparation and apparently exhibited greater fluorescence in platelet "smears" than was observed in smears from controls. In contrast, when washed platelet "smears" were prepared from platelet preparations containing iloprost, an analogue of prostacyclin, platelet aggregates did not form and the 'excess' of fluorescence disappeared from all the three groups. When platelets were stained for Fn fluorescence in suspensions, no fluorescence was observed on the surface of platelets from peripheral vascular disease and diabetes mellitus patients or controls. On stimulation with thrombin washed platelet suspension showed fluorescence for Fn. Platelet activation leads to Fn appearing on platelet surface but this effect cannot be quantified by optical fluorescence microscopy.
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PMID:A study of platelet fibronectin immunofluorescence in peripheral vascular disease and diabetes mellitus. 248 53

Platelets play an important role in the development of atherosclerosis. The arachidonic acid, whose oxygenated metabolites are potent regulators of the platelet-vessel wall interactions, is released from membrane phospholipids by the phospholipase (s) system (s). These membrane-linked phenomena are strongly modulated by the membrane physical properties. The present study was carried out to investigate the relationship between membrane fluidity and arachidonic acid metabolism in platelets from atherosclerotic patients. Twenty-one patients with peripheral vascular disease and twelve controls were studied. Platelets from patients showed an increase in membrane fluidity and enhanced thrombin-stimulated thromboxane synthesis. No alterations were found, however, in total phospholipid fatty acid composition. A significant decrease in the cholesterol/phospholipid ratio could account for the alterations in the membrane physical properties described in the platelets from patients.
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PMID:Membrane fluidity and thromboxane synthesis in platelets from patients with severe atherosclerosis. 309 71

A common misconception among microsurgeons is that free tissue failure is an "all-or-none" phenomenon. In other words, there is an instantaneous cessation of blood flow to a flap primarily due to thrombosis at the arterial or venous anastomotic site (primary thrombosis) with complete flap loss as a result. Contrary to this belief, we have found that free tissue transfers occasionally "die" a slow, progressive, and partial death. This most likely is due to gradual "shutting down" of the microcirculation by the showering of microemboli downstream from the arterial anastomosis (secondary thrombosis). We discuss our clinical experience during the past 6 years with 10 patients in whom free flap failure was not an all-or-none phenomenon and describe the expectant management of these failing free flaps. Microvascular reconstruction of the lower extremities was performed for recalcitrant sickle cell ulceration, chronic venous stasis ulceration in a patient with anti-thrombin III deficiency, dry gangrene of the plantar surface of the foot and toes secondary to posterior tibial artery injection in an intravenous drug abuser, Gustillo type IIIc injury requiring reconstitution of the femoropopliteal artery after an automobile bumper injury, Gustillo type IIIb injury resulting from gunshot wounds, an open ankle joint in a patient with severe peripheral vascular disease, and osteomyelitis. Other cases included cheek soft tissue reconstruction after wide resection of a recurrent dermatofibrosarcoma protuberans of the parotid gland, chest wall coverage after claviculectomy for osteoradionecrosis, and thumb replantation complicated by refractory vasospasm. Latissimus dorsi (four patients), rectus abdominis (three patients), scapular (one patient), and radial forearm fasciocutaneous (one patient) flaps were used. Flap compromise was detected between 4 hours and 6 weeks after surgery. Salvage attempts included Fogarty thrombectomy (four patients), anastomotic revision (two patients), streptokinase instillation (one patient), and leech application (one patient). Failing free flaps were managed expectantly with the use of daily dressing changes. This allowed for the survival of sufficient soft tissue to effect coverage of exposed bone, tendon, or joint. Hyperbaric oxygen was not administered. Tangenital excision of the eschar was performed between 6 and 51 days after free tissue transfer. Skin grafting was delayed for 15 to 80 days. In all cases, a successful outcome was achieved ultimately by either a single skin-grafting procedure (seven patients) or groin flap coverage (one patient). Follow-up ranged from 2 to 35 months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Free tissue failure is not an all-or-none phenomenon. 763 89

Platelet aggregates, stabilized by fibrin, rapidly form hemostatic plugs when blood vessels are severed or arterial thrombi at sites of vessel injury, such as ruptured atherosclerotic plaques, or regions where blood flow is disturbed, such as at stenoses. These thrombi cause the thromboembolic complications of atherosclerosis: heart attacks, strokes, and peripheral vascular disease. Platelet adhesion to subendothelial components such as collagen activates signalling pathways that lead to thromboxane A2 formation and secretion of platelet granule contents, including ADP. Both these substances cause platelet aggregation, a process in which the integrin, glycoprotein IIb/IIIa, becomes a receptor for fibrinogen, which forms bridges between adjacent platelets. On the surface of stimulated platelets, coagulation is accelerated and thrombin is generated; it is a potent inducer of platelet aggregation and secretion and also causes fibrin to form around the aggregates, stabilizing them. There are receptors on the platelet surface for thrombin, thromboxane A2, collagen, ADP, platelet-activating factor, fibrinogen, von Willebrand factor, and other ligands. Agents that inhibit platelet aggregation and the signalling pathways that are activated by the various aggregating agents are under intensive investigation in many laboratories.
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PMID:Role of platelets in thrombosis and hemostasis. 806 74

von Willebrand factor and soluble thrombomodulin are established plasma markers of endothelial cell dysfunction, whilst beta thromboglobulin is an established plasma marker of platelet activity. Soluble P-selectin may be the product of either or both types of cell and levels of all four molecules have been previously found to be increased in atherosclerosis. To determine the relationship of soluble P-selectin to the endothelial cell and platelet products, we measured the four indices in a case control study of 55 patients with peripheral vascular disease and 55 age and sex matched controls. von Willebrand factor (p < 0.0001), beta thromboglobulin (p = 0.0006), soluble P-selectin (p = 0.0021) and soluble thrombomodulin (p = 0.021) were all raised in the patients. Soluble P-selectin correlated with beta thromboglobulin (r = 0.34, p = 0.019) but failed to correlate with either endothelial cell marker. Co-culture of endothelial cells in vitro with bovine thrombin resulted in increased levels of von Willebrand factor in the supernatants but levels of soluble thrombomodulin and soluble P-selectin were not enhanced. Exposure of endothelial cell monolayers to elastase resulted in different patterns of release of von Willebrand factor, soluble thrombomodulin and soluble P-selectin. We suggest that soluble P-selectin is unlikely to arise from the endothelium and may be a new marker of platelet activation in atherosclerosis.
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PMID:Soluble P-selectin in atherosclerosis: a comparison with endothelial cell and platelet markers. 924 35

Although macroangiopathies such as peripheral vascular disease (PVD), cerebral vascular disease (CVD), and coronary heart disease (CHD) can often be observed in patients with diabetes mellitus, they are not specific for diabetes mellitus. Moreover, it is unclear whether their progressive mechanism is different. In the present study, we compared the risk factors among the diabetic macrovascular complications. Univariate analyses showed that in all patients, age at examination, duration of diabetes, thrombin-antithrombin III complex (TAT) level, fibrinogen level, lipoprotein (a) (Lp(a)) level, total cholesterol (T-Chol) level, and existence of microagiopathy were risk factors for PVD. Age, duration of diabetes, insulin level, TAT level, fibrinogen level, HDL cholesterol (HDL-Chol) level, hypertension, and nephropathy were risk factors for CVD. Only fibrinogen level was a risk factor for CHD. Moreover, Lp(a) level was a risk factor for PVD and CVD in male patients, but not in females. On the other hand, insulin level was a risk factor for CVD in female patients, but not in males. Multivariate analyses showed that TAT level, T-Chol level, and neuropathy were independent variables for PVD and that age, TAT level, and HDL-Chol level were independent variables for CVD. On the other hand, only fibrinogen level was the independent variable for CHD in males. Our results suggest that the progressive mechanism of PVD and CVD might be different from that of CHD and might differ according to gender in Japanese diabetic patients.
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PMID:Comparison of risk factors of macrovascular complications. Peripheral vascular disease, cerebral vascular disease, and coronary heart disease in Japanese type 2 diabetes mellitus patients. 1112 Apr 54

The aim of the study was to determine whether folic acid treatment in subjects with homocysteinemia would change their coagulation and oxidative status. Thirty-three patients with peripheral vascular disease and 26 elderly subjects with no symptoms of atherosclerosis, all of whom had total homocysteine >20 microM, were treated with folic acid (5 or 10 mg) for 3 months. In the 33 patients with peripheral vascular disease, homocysteine levels decreased from a median of 26.7 microM at baseline to 20.0 microM (p < 0.0001), whereas in the 26 asymptomatic elderly subjects, homocysteine level decreased from 24.4 microM to 18.6 microM (p < 0.0001). Plasma fibrinogen decreased whereas plasminogen and anti-thrombin increased; the differences between pre- and posttreatment values were significant in both patients and healthy subjects. Oxidative status markers showed a shift toward lower oxidative stress. This effect was observed in both study groups. An association of the therapeutic effect with the genetic polymorphism of 5,10-methylenetetrahydrofolate reductase was not detected. Folic acid supplementation to hyperhomocysteinemic subjects resulted in a decrease in total blood homocysteine concentrations; moreover, there was a tendency to reverse the coagulation status and oxidative stress.
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PMID:Treatment of hyperhomocysteinemia with folic acid: effects on homocysteine levels, coagulation status, and oxidative stress markers. 1202 79

The femoral approach is the most commonly used route for diagnostic cardiac catheterization and coronary interventions today. Manual compression and pressure bandages usually lead to immobilisation of the patient for several hours and may result in significant discomfort. Since the introduction of the first femoral closure device in 1991, many devices have proven their efficacy in significantly reducing time to hemostasis while simultaneously improving patient comfort. Twenty four closure device systems with different concepts are on the market, e. g. pure collagen, collagen + thrombin, collagen + anchor, vascular suture, hemostatic patches and pads, staples and more. The four predominantly used are Angio-Seal (46 %), Perclose (32 %), VasoSeal (14 %) and Duett (3 %). The effectiveness of all four systems has been proven in a prospective, randomized, controlled multicenter trial each. Efficacy and safety were analyzed using data from ten comparative studies in 8832 predominantly or exclusively interventional patients, however none of the closure systems proved to be superior. Fortunately, recent years have shown a trend toward a reduction in local complications by vascular closure devices compared to manual compression. Closure devices are thus becoming increasingly cost effective. Vascular closure systems should be preferred when the prolonged supine position is not tolerated, a protein IIb/IIIa-inhibitor was used during the procedure, or early discharge of patient is anticipated. In the presence of peripheral vascular disease, small diameter of the femoral vessels or stenotic lesions in the femoral artery, closure devices should be used with caution. Closure systems for immediate femoral puncture site hemostasis are now an important tool of invasive cardiology today.
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PMID:[Immediate hemostasis of the femoral artery after heart catheterization: the present situation of closure systems]. 1529 87


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