Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The use of fibrinolytic agents to control the fibrinolytic enzyme system and lyse pathologic fibrin deposits or thrombus has now assumed a position with anticoagulants and vascular surgery in the physician's therapeutic armamentarium. The principal exogenous activators that are used clinically are streptokinase, urokinase, and tissue plasminogen activator. Acute arterial occlusions are more likely than chronic occlusions to respond to thrombolytic therapy, especially if treatment is instituted within a few hours of onset of symptoms and if the disease is due to embolic material rather than in situ thrombosis. Since the duration of drug infusion necessary to lyse arterial thrombus cannot be predicted, patients in whom tissue viability cannot be determined or in whom ischemia cannot be tolerated during the drug infusion interval are not candidates for intraarterial fibrinolytic drug infusion. In treating patients with venous occlusion, thrombolytic therapy is more effective against proximal clots than in calf thrombosis. No protective effect from pulmonary embolism has been noted in trials comparing heparin with streptokinase. Fifty percent of patients with an initial episode of deep venous thrombosis treated within 72 hours of onset will have complete resolution of thrombus with preservation of valve function.
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PMID:Application of thrombolytic therapy in vascular occlusive disease. A surgical view. 311 28

In eighty-three patients with confirmed deep vein thrombosis, the fibrinolytic system was studied before and after a 10-minute venous occlusion. Blood was collected at least 3 months after the last acute episode, and PAI-1 antigen and activity, as well as tissue-type plasminogen activator (t-PA) antigen, urokinase-type plasminogen activator (u-PA) antigen, and fibrinolytic activity were measured in these samples. During venous stasis, plasminogen activator inhibitor (PAI) activity decreased in almost all patients (81 of 83), from a median value of 8.2 to 2.9 U/mL (P less than .001, Wilcoxon signed-rank test). Because PAI-1 antigen augmented from a median value of 16 to 19.2 ng/mL (P less than .001), the decline in PAI activity was attributed to an increase in t-PA antigen from a median value of 10 to 21.7 ng/mL (P less than .001). Neutralization of PAI activity thus reflects the patient's capacity to overcome basal inhibitory potential through t-PA release. Based on residual PAI activity after 10-minute stasis, patients were classified as good or bad responders (PAI activity below detection limit, ie, less than or equal to 1.0 and greater than 1.0 U/ml, respectively). Good responders had a significantly higher fibrinolytic response after stasis than bad responders (median euglobulin clot lysis time 60 v 180 minutes; dilute whole blood clot lysis time 60 v 120 minutes; fibrinolytic activity on fibrin plates 7.7 v 0 U/mL). Furthermore, good responders, as compared with bad responders, had higher t-PA release (median 16.5 v 11.5 ng/mL), lower basal PAI activity (median 4.8 v 11.2 U/mL), and lower basal PAI-1 (median 11 v 21 ng/mL) and u-PA antigen (median 7.9 v 9.0 ng/mL, P less than .02). Hypofibrinolysis, as defined by the inability of released t-PA to overcome PAI-1 basal inhibitory potential, was observed in 45 of 83 patients (54%) and resulted either from an insufficient release of t-PA or from an increased basal PAI activity.
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PMID:Residual plasminogen activator inhibitor activity after venous stasis as a criterion for hypofibrinolysis: a study in 83 patients with confirmed deep vein thrombosis. 313 60

This study examines the comparative efficacy, safety, and cost associated with treatment of deep vein thrombosis with streptokinase or urokinase. Sixty patients were analyzed retrospectively, 30 treated with streptokinase and 30 treated with urokinase. Statistically significant greater fibrinogenolysis was noted when streptokinase was used to treat patients with deep venous thrombosis (p = 0.01). The mean decrease in fibrinogen from preinfusion value was 83% in the streptokinase treated group and 61% in the urokinase treated group. Five of 30 (17%) of the streptokinase treated patients experienced major complications. No major complications were seen in the urokinase treated group (p = 0.019). Cost analysis demonstrates that therapy with urokinase was $11.40 per patient more than streptokinase. If complications are not included in the cost analysis, then urokinase becomes only $650 per patient more expensive than streptokinase therapy. These data support that deep vein thrombosis treatment with urokinase is effective, safer and more cost efficient when compared to streptokinase.
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PMID:Comparison of cost effectiveness of streptokinase and urokinase in the treatment of deep vein thrombosis. 314 16

We have studied the effects of urokinase (UK) on concentration changes of alpha 2 antiplasmin (alpha 2 AP) and on fibrino(geno)lysis. Medium dose (480,000 u) or large dose (960,000 u) of UK was given to each of seven normal volunteers by intravenous drip infusion within six hours, and then blood and urine analyses were carried out. Total alpha 2 AP, which includes free alpha 2 AP and alpha 2 AP-plasmin complex, decreased to about 50% of the original value with large dose of UK. alpha 2 AP-plasmin complex appeared in the plasma one hr after UK infusion and increased up to 50% of total alpha 2 AP at the end of UK infusion. B beta peptides, which are liberated from fibrin(ogen) at the very early stage of fibrino(geno)lysis, increased significantly with UK infusion, and was 65 times as much as the normal range at the end of UK infusion. Urinary B beta peptides increased as well as plasma B beta peptides. On the other hand, fibrin(ogen) degradation products (FDP) measured with enzyme immunoassay (EIA) increased only slightly, and moreover, urinary FDP was not detectable at any time. Plasma fibrinogen levels did not decrease and changed within the normal range in both groups. We then gave 960,000 u of UK to four patients with deep vein thrombosis and blood analyses were carried out as with normal volunteers. The most significant observation different from that of normal volunteers was shown in FDP levels. Serum FDP levels of four patients increased significantly in comparison with normal volunteers. Urinary FDP increased as significantly as plasma FDP. In conclusion, the infusion of 960,000 u of UK caused only very early stage of fibrinogenolysis without advanced fibrinogenolysis in normal volunteers, but in thrombotic patients, advanced fibrinolysis was observed.
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PMID:Fibrinogenolysis and fibrinolysis in normal volunteers and patients with thrombosis after infusion of urokinase. 316 Dec 12

Pulmonary embolism following postoperative deep venous thrombosis is a very serious complication with a high mortality rate. Though this disorder has been thought to be rare in Japanese, its occurrence seems to be increasing recently because of changes in eating habits, increase of average age and the frequent practice of venous catheterization. Two cases of the pulmonary embolism following deep venous thrombosis after surgery are reported, and possible causes of the deep venous thrombosis are discussed. Case 1: A 48 year-old obese female was operated on for a posterior fossa dural arteriovenous malformation. On the 4th postoperative day, she developed a pain and swelling in the left leg and low back pain. On the 18th postoperative day, she fell into a state of shock following the sudden onset of a severe back pain and respiratory distress. After diagnosis of the pulmonary embolism, she was immediately treated with urokinase, warfarin and aspirin. Her obesity was considered to be one of the risk factors of the postoperative deep venous thrombosis. Case 2: A 62 year-old female with a ruptured cerebral aneurysm could not get out of bed because of postoperative mental disturbance. A central venous pressure catheter was inserted into the right femoral vein for two weeks postoperatively. One month after surgery, she complained of swelling and a dull pain in the right leg without cardiorespiratory symptoms. Lung perfusion scintigraphy showed asymptomatic pulmonary embolism. She was treated immediately. Both long bed rest and femoral venous catheterization were considered as risk factors possibly leading to deep venous thrombosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Postoperative pulmonary embolism in neurosurgical practice: report of two cases]. 321 Dec 80

Since the introduction of thrombolytic treatment based on the activation of plasminogen (PLG) by streptokinase (SK) and urokinase (UK) the search for new and improved methods has been continuing. The pivotal issue is how to achieve clot-specific fibrinolysis without producing systemic fibrinogenolysis. One out of various approaches to enhance lysis rates has been the use of PLG either alone or in combination with UK or SK in the light of the fact that fibrinolytic treatment, particularly using SK, is associated with a consumption of PLG, and that thrombi contain relatively small amounts of native PLG, however, are capable of incorporating added PLG in vitro. PLG-concentrates from various manufactures have been administered intravenously for treatment of deep venous thrombosis, mainly in combination with SK, and of pulmonary embolism in combination with UK. Local intracoronary and intraarterial administration in combination with UK has been reported in patients with myocardial infarction, and peripheral arterial occlusions, respectively. Lysis rates obtained in these studies were in most cases superior to results obtained with SK or UK alone, without increasing the incidence of bleeding complications. In addition, excellent results in larger group of patients with cerebral thrombosis were obtained with PLG alone. The encouraging results of these studies may be explained by the fact that all of the preparations used contained partially activated forms of PLG (commonly designated lys-PLG) to a greater or lesser extent. Lys-PLG has a higher affinity for fibrin than the native glu-PLG and is activated by UK or SK by a manyfold faster. These properties allow for a rapid formation of plasmin which--bound to fibrin--is also protected from the attack of neutralizing antiplasmin. The design and results of previous studies with lys-PLG concentrates will be reviewed and approaches to further improve fibrinolytic regimens with lys-PLG-concentrates discussed.
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PMID:Review of studies with plasminogen concentrates and proposals for further therapeutic strategies with plasminogen concentrates. 328 Apr 22

The venous function has been assessed after deep vein thrombosis (DVT) by Doppler, strain gauge plethysmography (55 patients) and exercise plethysmography (10 patients) for a mean period of 63 weeks. Venous volume and venous outflow remain significantly lower throughout the study, whatever the site of thrombosis and the initial therapy (Heparin, local or general Urokinase). There are no significant correlations between clinical and functional parameters except for patients with proximal obstruction and popliteal valvular incompetence. Exercise plethysmography evaluates the importance of the calf pump in the postphlebitic syndrome. Static plethysmographic measurements prove to be unreliable for the long term prognosis whereas associated dynamic tests should be a better way to assess the haemodynamic changes after DVT and to control the efficiency of the prevention of the post-phlebitic syndrome.
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PMID:Haemodynamics of the postphlebitic syndrome. 332 54

A newly developed thrombus imaging agent, 67Ga-DFO-DAS-fibrinogen (67Ga-fibrinogen), was used for 22 studies in 20 cases of suspected deep venous thrombosis. Increased accumulation of 67Ga-fibrinogen in venous thrombi was depicted at 48 h after injection in 10 of the 15 cases (10 of 17 studies) who showed abnormal findings in radionuclide venography. A hot spot in the lung emboli was visualized in two cases. Seven of the eight cases having anticoagulant therapy showed increased 67Ga-fibrinogen uptake, while follow-up 67Ga-fibrinogen scintigraphy after the administration of heparin and urokinase did not reveal an abnormal hot spot in one case. 67Ga-fibrinogen can be made available simply by adding 67Ga solution to a vial containing fibrinogen-DAS-DFO conjugate. In conclusion, 67Ga-fibrinogen is considered to be a promising agent for detecting active venous thrombi and to assess the effect of anticoagulant therapy.
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PMID:Positive imaging of venous thrombi and thromboemboli with Ga-67 DFO-DAS-fibrinogen. 339 Dec 13

In 1933 Streptokinase (SK) was isolated from bacterial strains of haemolytic Streptococci. Since then it has become the widest spread drug for fibrinolysis. SK, a protein, consists of 415 aminoacids and has a molecular weight of 47,000u. Together with the plasminogen (PLG) of the blood it forms activator complexes, which then convert other PLG molecules of the blood to plasmin. Plasmin attacks and dissolves fibrin deposits. As a substance produced by bacteria SK stimulates antibody formation in the body, the titer will increase during therapy, and SK lysis should be terminated after 6 days of treatment. Usually SK is administered intravascularly to treat a wide range of diseases, associated with pathological activation of hemostasis, like deep vein thrombosis, pulmonary embolism, myocardial infarction etc.. Contraindications can be traced back to the effects of SK on coagulation and the immune system. Bleeding is the most common side effect, but also a few anaphylactic reactions, caused by massive antigen-antibody precipitation have been observed. The rate of lethality of the treatment was established at 0.7% of the cases. To reduce the incidence of side effects modifications of the drug have been proposed, such as activator complex, light B chain SK, and acylated activator therapy. Compared with Urokinase, SK shows a higher rate of side effects, especially in the field of the immune system. Therapy with Urokinase can be controlled more easily. Nevertheless because of considerable price differences and logistics, SK is preferred in Europe and the USA. If strict guidelines in therapeutic use are followed, the rate of side effects of the drug can be curtailed and will be comparable to those of Urokinase.
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PMID:Review and current status of thrombolytic therapy with streptokinase. 354 44

Arterial embolism or thrombosis are very rare complications of the fibrinolytic therapy of deep venous thrombosis. The characteristics symptoms of these illness are the acute arterial failure of the concerned extremity during venous thrombolysis. The diagnosis take place by angiography, by ultrasonics, and in particular cases by the skin thermographic method. If the arterial occlusion is not operable, the thrombolysis by urokinase is discussed. This seems to be the last possible method to support the extremity.
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PMID:[Acute arterial occlusive syndrome in streptokinase treatment of deep venous thrombosis--successful therapy with urokinase]. 363 Feb 81


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