Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma concentrations of antithrombin III (AT III), plasminogen (Plg), and protein C (PC) were assayed in 28 patients with venous thrombosis of lower extremities without distinct underlying disorders. Three abnormalities were found in 5 cases (17.8%) in relation to coagulation and fibrinolytic system (3 with congenital AT III deficiency, one each with dysplasminogenemia and congenital PC deficiency). In the patients with either one of these abnormalities, characteristic features of thrombosis are summarized as follows; 1. early onset of clinical symptoms. 2. high frequency of superficial vein thrombosis. 3. high recurrence rate. 4. high frequency of pulmonary embolism.
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PMID:[Congenital abnormalities related to coagulation and the fibrinolytic system in patients with vein thrombosis of the lower extremities]. 375 31

Considerable interest in plasminogen activators as human thrombolytic drugs has stimulated rapid biotechnologic progresses. These enzymes have been classified in two immunochemically distinct groups: "urokinase-like" activators or u-PA which do not interact with fibrin and "tissue activator-like" activators or t-PA which interact with fibrin. Plasminogen activators are widely distributed in normal and malignant tissues and they are implicated in various physiological and pathological processes. They maintain the functional integrity of the vascular system and their presence may be of importance in tissue remodeling and cell migration. Urokinase and streptokinase are used in human thrombolytic therapy. However, the properties displayed by t-PA suggest that this enzyme may be a superior fibrinolytic agent. The primary structures of urokinase and t-PA are known; both enzymes have been synthesized by DNA technology. In order to produce t-PA in large quantities by gene cloning, intensive studies are conducted by pharmaceutical industries. Clinical trials using t-PA for dissolving thrombi in coronary heart disease, strokes and pulmonary embolism are in progress. This review presents the molecular and structural properties of plasminogen activators, as well as related physiological, pathological and therapeutic aspects.
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PMID:[Plasminogen activators: general aspects and recent developments]. 391 65

A case of double right and left intraventricular thrombosis diagnosed by 2D echocardiography is reported in a 20 year old man with nephrotic syndrome with eosinophilia and hypercoagulability, admitted as an emergency for a staphylococcal septicaemia in shock and anuria. Anticoagulation with heparin did not prevent two episodes of pulmonary embolism. Complete dissolution of the thrombi was obtained by peripheral administration of fibrinolytic therapy (urokinase and plasminogen). The authors discuss the differential diagnosis of echocardiographic appearances of biventricular masses and possible causes of these thrombi are suggested.
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PMID:[Biventricular thrombosis in nephrotic syndrome with hypercoagulability and hypereosinophilia]. 392 Sep 99

Two patients, aged 64 and 47 years, had a massive pulmonary embolism one day after cholecystectomy. Ultra-short fibrinolysis was undertaken with 1.5 million units of streptokinase. Both patients rapidly improved, with a fall in heart rate, pulmonary artery or central-venous pressure, and a rise in arterial pO2. There were no significant bleedings. Ultra-short fibrinolysis (maximally over one hour) can thus successfully lyse emboli--consisting of fresh plasminogen-rich coagulation thrombi in the early postoperative period--without re-opening wound- and capillary beds during this short period.
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PMID:[Fibrinolytic therapy of massive pulmonary embolism on the 1st postoperative day following cholecystectomy]. 394 64

The effects of peroperative electrical calf muscle stimulation with groups of impulses giving a short lasting tetanus of the calf muscles on postoperative deep venous thrombosis (DVT) and pulmonary embolism (PE) were compared with that of dextran 40 given per and postoperatively. The incidence of DVT and PE during the first 4-6 postoperative days was recorded. The diagnosis of DVT was based on the 125I-fibrinogen uptake test and phlebography and of PE on pre- and postoperative perfusion pulmonary scintigram and chest X-ray examination. Both methods reduced the incidence of PE. Calf muscle stimulation reduced the DVT incidence in patients with malignant disease while the reduction in DVT incidence for the whole group only was significant in the stimulation as well as the dextran 40 group. Mean values for preoperatively determined levels of antithrombin III, beta-thromboglobulin, fibrinopeptide A, plasminogen and ability to release fibrinolytic activity during venous stasis did not differ between those patients who developed or those who did not develop postoperative DVT or PE. However, antithrombin III levels below 80 per cent appeared to predispose to postoperative thromboembolism. The two prophylactic methods have similar effects on the incidence of postoperative thromboembolism. The stimulation method has certain advantages due to its safety and simplicity.
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PMID:Prediction and prophylaxis of postoperative thromboembolism--a comparison between peroperative calf muscle stimulation with groups of impulses and dextran 40. 618 44

A quantitative model of venous thrombosis in the beagle dog is described. The model was adapted to permit ageing of isolated experimental clots in vivo. A model of acute pulmonary embolism in this species is also described. In the venous thrombosis model, infusion of streptokinase (SK) or SK-activated human plasmin gave significant lysis but bolus doses of SK. plasmin complex were ineffective. Active site anisoylated derivatives of SK. plasminogen complex, SK-activated plasmin and activator-free plasmin were all active when given as bolus doses in both models. At lytic doses, the acyl-enzymes caused fewer side-effects attributable to plasminaemia than the corresponding unmodified enzymes.
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PMID:Acyl-enzymes as thrombolytic agents in dog models of venous thrombosis and pulmonary embolism. 623 76

By activating plasminogen into plasmin, which in turn dissolves fibrin, fibrinolytic agents can dissolve pathologic thrombi. Streptokinase, a fibrinolytic agent derived from group C beta-hemolytic streptococci, is antigenic and can elicit allergic reactions. Urikinase, a fibrinolytic agent obtained by purification from human urine or from human fetal kidney cell culture, is not antigenic, and for this reason can be used repeatedly, if needed, whereas streptokinase cannot be used for retreatment within six months of a course of therapy. Either agent can be introduced into the circulation systemically (intravenously) or locally (via catheter). The indications for systemic therapy include deep-vein thrombosis, pulmonary embolism, and arterial thrombosis and embolism. The indications for local therapy include acute myocardial infarction, arterial thrombosis and embolism, and the clearing of occluded arteriovenous cannulae and access shunts. Contraindications include an actively bleeding lesion, a vascular intracranial disorder, or uncontrolled hypertension; relative contraindications include pregnancy; a recent wound, fracture, surgery, or deep closed biopsy; or a general contraindication to anticoagulation, such as coagulopathy, uremia, or severe liver disease. During thrombolytic therapy, invasive procedures, intramuscular injections, and the use of other anticoagulant or antiplatelet agents should be avoided. Measurement of fibrinogen levels, the titer of fibrin/fibrinogen degradation product, or thrombin time can be used to monitor therapy.
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PMID:Fibrinolysis and its current usage. 634 82

The fibrin-mediated enhancement of the activation of plasminogen by tissue-type plasminogen activator observed with normal fibrin, is strongly decreased with fibrin Dusard, although the binding of tissue-type plasminogen activator to this fibrin is normal. This impaired fibrin-mediated plasminogen activation is most likely related to the history of recurrent thrombosis and pulmonary embolism observed in this family.
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PMID:Dysfibrinogenemia (fibrinogen Dusard) associated with impaired fibrin-enhanced plasminogen activation. 653

Major pulmonary embolism occurring insidiously over several weeks (subacute massive pulmonary embolism) has a high mortality and may not respond well to standard anticoagulant or thrombolytic treatment. A priming dose of plasminogen was used to enhance thrombolysis produced by a streptokinase infusion in five consecutive patients with subacute massive pulmonary embolism. In each patient a dramatic clinical improvement occurred with a substantial increase in pulmonary blood flow. All five patients survived to leave hospital. Malignant disease was the underlying cause of embolism in three patients, two of whom died of their malignant disease in the six months after treatment of their pulmonary embolism. The third patient with malignant disease had a choriocarcinoma; at least some of the pulmonary obstruction may have been tumour tissue but this obstruction was dramatically cleared by the treatment. The use of a combination of plasminogen with streptokinase should be considered in severely ill patients with subacute massive pulmonary embolism, particularly if other treatment, including streptokinase alone, has failed.
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PMID:Subacute massive pulmonary embolism treated with plasminogen and streptokinase. 666 49

Recent deep vein thrombosis of the iliofemoral segment often leads to pulmonary embolism and to impaired valve function. Although more common, occlusions in the calf veins are less dangerous, and often a self-limiting disorder as almost half of these thrombi lyse spontaneously. Approximately 70% of fresh deep venous thrombi dissolve under intensive and prolonged thrombolytic treatment with streptokinase and long-term follow-up studies indicate that normal valve function is preserved in those patients in whom thrombus clearance was obtained. Thrombosis with streptokinase or urokinase appears to be the current treatment of choice for most cases of massive and severe, life-threatening pulmonary embolism; those patients surviving more than an hour or so after massive infarction comprise a prognostically better group, in whom the chances of surviving embolectomy is today smaller than the probability of survival without surgery but with thrombolytic treatment. Obviously there are problems in the evaluation but also in the thrombolytic treatment with streptokinase and urokinase of deep venous thrombosis and pulmonary embolism. These problems do not concern the principle of thrombolysis, but are largely due to the fact that the drugs so far used also induce a systemic fibrinogenolysis resulting in a bleeding risk. There is already good evidence that tissue activator of plasminogen is highly specific for fibrin and can induce thrombolysis in experimental animals without inducing systemic fibrinogenolysis.
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PMID:[Actual state of thrombolytic treatment of recent vein thrombosis and pulmonary embolism (author's transl)]. 719 77


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