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)

Six patients suffering from solitary cryofibrinogenaemia are described. In one patient idiopathic cryofibrinogenaemia was present, while the others showed secondary cryofibrinogenaemia associated with borrelia infection, chronic venous insufficiency with pulmonary embolism, primary biliary cirrhosis, diabetes mellitus or von-Willebrand syndrome. Subcutaneous injections of the thrombin-like snake poison batroxobin/ancrod were administered over a period of several weeks. Five patients experienced almost complete remission of their symptoms, especially of pain following cold exposure. In one patient partial relief was achieved. Overall we found a 75% reduction of symptoms. When blood fibrinogen levels are carefully monitored this therapy is an efficient and safe form of treatment for cryofibrinogenaemia.
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PMID:[Cryofibrinogenemia--successful therapy by decreasing fibrinogen]. 186 Jul 98

Nineteen patients with symptoms of chronic venous insufficiency (CVI) were treated with 13-week cycles of intermittent pneumatic compression (IPC) during 2 h sessions twice weekly, with most treatments at home. At study completion, quantitative subjective scores for total symptomatology were improved in 16/19 patients (84%). Enhancement of fibrinolytic potential in vivo was detected in 86% of observations on specimens from CVI patients over 2 h of IPC, with accelerated euglobulin clot lysis times (ELT) noted within 15 min of initiating compression. The enhanced fibrinolytic potential was attributed to increased urokinase plasminogen activator (u-PA), probably released from perturbed endothelial cells by IPC. Significant decreases in total t-PA antigen (mass concentration) but not t-PA activity, were produced by IPC in CVI patients only (P = 0.0001), with greater effects noted in the non-anticoagulated versus the anticoagulated cohort. Plasminogen activator inhibitor type 1 (PAI-1) levels rose rapidly after IPC only in the controls and non-anticoagulated CVI patients. PAI-1 decreased in those receiving anticoagulation. No platelet perturbation was detected during IPC by measuring levels of beta-thromboglobulin or the thromboxane A2 metabolite, 11-dehydrothromboxane B2; however, significant (P < 0.003) decreases in plasma prostacyclin (PGI2) levels (measured as the stable 6-ketoprostaglandin F-1-alpha-metabolite) were observed after 15 min of IPC in non-anticoagulated CVI patients only. There was no evidence of increased thrombin generation by IPC, determined by urinary excretion of fibrinopeptide A and prothrombin fragment 1. Concurrent anticoagulation appears to mediate more favorable biochemical alterations in CVI, although subjective improvement did not correlate with anticoagulation. The mechanism(s) by which these physiologic changes compliment the mechanical effects of IPC remain to be elucidated and will require adequately controlled and powered studies.
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PMID:Intermittent pneumatic compression in chronic venous insufficiency favorably affects fibrinolytic potential and platelet activation. 883 95

Venous valves are more frequent in distal veins and venulae, providing a protecting action against blood skin reflux. Structurally simple, collagen and endothelium, they allow a cavity to be formed by distension, when occlusion occurs. Venous angioscopy can distinguish bicuspid floating valves, reinforced, reinforcing valves with free edges and seat valves as well as the presence of apertures of small collateral vessels in the sinus, of which they play a role in the filling up. Valves are inefficient in supine and in standing among 20% of the adult population. Sinuses allow vortices to be created, low recirculating zones, where blood flow move slowly in niches, at a low shear rate, independently from the main stream. A deep vortex is located in sinus, usually empty, but likely to receive red cell aggregates and leukocytes in the condition of stasis and hyperviscosity. Such a vortex is hypoxic, cause of endothelial activation. In such areas fibrin-leucocytic nidus are created, histologically recognized, of which sub-endothelium has become thick and thrombogenic. Two stages characterized its progression: stage I: a few alteration in the valves, little thrombin generation, taken over by the coagulation inhibitors: AT III, APC and TFPI. Stage II: damaged valves, local consumption of the inhibitors and extended generation of thrombin over the platelets, through factor IXa. Hereditary inhibitor deficits increase the risk (frequent factor Leyden V). When the coagulation cascade is considered, VIIa-tissue factor complex appears to be the thrombotic pathway, leading first to wall linked thrombin, uneasily reached by AT III and facteur IXa non inhibited by TFPI, therefore explaining the platelet extension. Monocytes, which can bear tissue factor, may be "lodged" inside the niches. Besides this important role in deep venous thrombosis, incompetent venous valves are responsible for the skin venous hypertension, a subsequent ground for ulcers. Their role in chronic venous insufficiency is uncertain. In the near future, venous angioscopy will bring about new findings about the pathophysiology of venous valves.
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PMID:[Venous valves in the legs: hemodynamic and biological problems and relationship to physiopathology]. 948 Mar 31

In the treatment of venous insufficiency unsuitable for surgical correction in replanted digits, a small ungual window was surgically created to infiltrate subcutaneous heparin in the congested digit. The initial heparin dose was 1000 units. This dose made possible a continuous bleeding during 24 to 48 hours, solely through the ungual window. Further doses were applied based on the degree of congestion of the replanted digit, but usually it was necessary to infiltrate up to 500 units of heparin every 24 to 48 hours until vascular stability was achieved. Three patients were treated with this technique. One opted for quitting the treatment. A replanted thumb suffered venous congestion on the seventh postoperative day and was treated with local subcutaneous heparin for 3 days. A replanted fingertip suffered venous thrombosis 24 hours after surgery and was treated likewise for 18 days. In these two patients, success was attained. Blood transfusions were carried out in the latter two, and none had any systemic changes in partial thromboplastin or thrombin time. This treatment is based on the mechanism of action of heparin at high doses but applied only to the congested segment. Besides their anticoagulant effect through antithrombin, high doses of heparin slow platelet aggregation, may induce angiogenesis, and have a longer-than-normal half-life. With the above technique, heparin has been applied to the congested segment at an approximate dose of 33,000 to 40,000 units/kg, and continuous bleeding solely through the ungual window for 24 to 48 hours has been achieved, which has allowed us to save two replanted segments with no complications at all. This method may offer another alternative for the medical treatment of venous insufficiency in replanted segments.
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PMID:Local subcutaneous heparin as treatment for venous insufficiency in replanted digits. 1083 37

Patients with chronic venous insufficiency arguably have been relegated to a standard of care that is lower than that for those with the more appealing entity of peripheral arterial disease. Fortunately, the collaboration of an expanding group of clinicians (including cardiologists and vascular medicine specialists) with vascular surgeons is stimulating a renewed interest in the management of patients afflicted with venous disease. With the increased level of awareness of venous disease, technologic advances undoubtedly will augment the armamentarium available for the treatment of patients with chronic venous insufficiency. The focus on the prevention of venous thromboembolic complications has been advanced greatly, as witnessed by the growth of new pharmacologic agents, such as heparinoids, antiplatelet agents, direct thrombin inhibitors, thrombolytics, and pentasaccharides. In addition, the more aggressive strategy of intervening in acute deep venous obstruction by using thrombolytic agents and adjunctive mechanical thrombectomy devices potentially may obviate the future sequelae of chronic venous insufficiency. The tremendous growth of endovascular techniques in recent years has revolutionized the management of problems due to acute and chronic arterial obstructive disease. The application of these techniques in the future may have a similar impact in improving the clinical outcomes of patients with chronic venous disease and potentially, if proven safe and efficacious in clinical trials, may lower the threshold for intervention to an earlier disease stage. Similarly, with the advent of endovascular and endoscopic techniques, surgical procedures will also continue to evolve, with these procedures complementing one another, as opposed to serving as surrogates, which traditionally has been the case.
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PMID:Chronic Venous Insufficiency. 1268 8