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)

Postoperative deep-vein thrombosis can lead to fatal pulmonary embolism on one side, and the development of a disabling postthrombotic syndrome, which can occur after some time. General thrombo-embolic prophylaxis can reduce the risk of postoperative thrombo-embolic complications. Predisposing factors include age, obesity, immobilization and recumbency. Cardiovascular diseases, malignant neoplasms, venous disorders, diseases associated with increased viscosity of blood, past deep-vein thrombosis and pulmonary embolisms, some infectious diseases with raised fibrinogen levels, and inherited or acquired clotting factor deficiency syndromes (antithrombin III, protein C, protein S) have an elevated risk of thrombosis. The surgery itself, when taking more than 20 minutes and performed under general anesthesia, is a major risk factor, as proven initiation of thrombosis is often on the operation table. Patients receiving regional or local anesthesia have a clearly reduced risk of thrombosis. After general surgery without thrombosis prophylaxis, a deep-vein thrombosis can be demonstrated by the fibrinogen uptake test in about 30% of all patients over the age of 40. After abdominal surgery an incidence of thrombosis of 14-33%, and after hip surgery an incidence of nearly 50%, have been established by means of the fibrinogen uptake test. However only 10% of these thromboses are expressed clinically. We therefore recommend Liquid Crystal Contact Thermography, which has a sensitivity of 94% and a specificity of over 80%, as a non-invasive, easily performed screening method in the diagnosis of deep-vein thrombosis. Apart from the physical methods, the use of heparin is also indicated in thrombo-embolic prophylaxis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The thrombo-embolic risk in surgery. 193 69

Fifty patients presenting with acute deep-vein thrombosis were randomized in a prospective, controlled study to determine the safety and efficacy of a treatment with low-molecular-weight (LMW) heparin compared with unfractionated heparin. LMW heparin (n = 24) was administered twice daily subcutaneously at a dose of 2 X 150 anti-Xa units/kg body weight, and unfractionated heparin (n = 26) was given intravenously by continuous infusion at a dose of 450 anti-Xa units/kg body weight daily for 10 days. Doses were adjusted to maintain peak anti-Xa levels between 0.5 and 1.0 anti-Xa units per milliliter. One patient in the unfractionated heparin group and 2 patients in the LMW heparin group suffered from bleeding complications. Two patients on LMW heparin and on unfractionated heparin had high evidence of pulmonary embolism based on defects on ventilation-perfusion scintigraphy. Control phlebography and duplex sonography demonstrated a significant improvement during both treatment regimens. Reperfusion of the deep-vein system was 70% with LMW heparin and 75% with unfractionated heparin. The anti-Xa levels were significantly higher in the LMW heparin group, and activated partial thromboplastin and thrombin clotting times were significantly higher in the group receiving unfractionated heparin. Thrombin-antithrombin III complexes and D-dimer concentration decreased during the treatment, but did not differ between the two regimens. At the end of the treatment period with LMW heparin, protein C and antithrombin III were significantly higher.
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PMID:Therapeutic application of subcutaneous low-molecular-weight heparin in acute venous thrombosis. 196 63

An 18 year old woman was hospitalized because of a vena cava inferior thrombosis, renal vein thrombosis, and pulmonary embolism due to an inherited protein C deficiency. She received 3 months of contraceptive treatment with estrogens. Protein deficiency was detected in 12 other members of her family; her father had a pulmonary embolism 12 years earlier and 2 other members of the family may have died of thromboembolism. (author's modified)
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PMID:[Protein C deficiency and the P pill]. 204 36

Every thromboembolic manifestation, especially in young subjects, calls for an aetiological study in which haemostasis is evaluated primarily with assays of physiological coagulation inhibitors: protein C, protein S and antithrombin III. Protein C deficiency is found in 6 to 7% of thromboembolic manifestations. We report the case of a 21-year old man who had phlebitis followed by pulmonary embolism without facilitating factors. Protein C level was 50% of normal value (0.50 IU/ml). The patient received heparin, subsequently replaced by oral anticoagulants after a long period of overlap between the two treatments. The outcome was favourable. Family investigation yielded a history of thromboembolic accidents in several members of the family, some of whom were protein C deficient (50% of normal value). Protein C synthesis is vitamin K-dependent. Protein C deficiency is transmitted as an autosomal dominant trait. Normal values range from 0.65 to 1.35 IU/ml. Clinically, 25% of the patients are said to be asymptomatic. The first thrombotic accidents occur in young subjects (mean age 29 +/- 14 years). Several points emerge from this case: full evaluation must be performed, especially in young subjects; family investigation consolidates the diagnosis and enables symptomatic protein C deficient patients to be treated and thrombotic manifestations to be prevented by effective anticoagulant therapy in high-risk situations; a prolonged period of heparin-oral anticoagulant overlap is needed to avoid cutaneous necrosis.
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PMID:[Recurrent thromboembolism disclosing protein C deficiency. Apropos of a case with familial investigation]. 207 65

Protein C deficiency has been reported to be associated with a high risk for thromboembolism. We report three patients with protein C deficiency: one suffered from left renal vein thrombosis, another from recurrent venous thrombosis of the legs complicated by pulmonary embolism and the third from an extensive thrombosis of the splanchnic veins with partial Budd-Chiari syndrome. We discuss the unusual sites of venous thrombosis in protein C deficient patients, the factors which may act as thrombotic trigger and the strategy of long-term prevention.
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PMID:Protein C deficiency associated with venous thromboembolism. 216 13

Plasma protein C exerts anticoagulatory effects by inactivating factors V and VIII. Hereditary protein C deficiency is transmitted as an autosomal dominant disorder. Homozygous individuals usually develop purpura fulminans as newborns; heterozygous protein C-deficient individuals are at increased risk for venous thrombosis and pulmonary embolism. However, arterial thrombosis has been only rarely observed. We describe a young patient with heterozygous protein C deficiency who experienced a severe stroke due to thrombotic occlusion of the left middle cerebral artery.
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PMID:Ischemic stroke due to protein C deficiency. 219 15

Protein C and antithrombin III represent main inhibitors of the plasmatic coagulation system. Due to the lack of practicable assays the clinical importance of protein C was only established during the last six years. In familial protein C deficiency 77% of patients present with recurrent venous thromboses, half of them below the age of 30. In addition to recurrent superficial thrombophlebitis more serious manifestations like deep vein thrombosis and pulmonary embolism have been described. Mesenteric vein thrombosis has been reported in only 5 cases all of which could be controlled by conservative treatment. In our patient protein C deficiency was discovered 10 years after the angiographic diagnosis of portal and mesenteric vein thrombosis. Thereafter, the patient complained of recurrent abdominal discomfort. Intestinal ischaemia due to mesenteric vein thrombosis required segmental resection twice. Postoperatively the patient was heparinized. After excluding a secondary protein C deficiency due to a lack in vitamin K, hepatic disease, or disseminated intravascular coagulation, long-term anticoagulation by dicumarol was implemented as therapy of first choice.
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PMID:[Protein C deficiency with recurrent infarct of the small intestine]. 231 54

We describe two families with heterozygous plasminogen deficiency. In the first the patient was a 27 year-old female who suffered an acute episode of ischemic cerebrovascular disease affecting the left temporal lobe documented by arteriographic, gammagraphic and CAT studies. She had no family history of thrombotic conditions. In the other family the propositus was a 31 year-old man with spontaneous deep venous thrombosis in the left leg. His father was also symptomatic, with a history of recurrent thrombotic complications after predisposing factors, that included multiple venous thrombosis and a pulmonary embolism. Laboratory data showed normal hemostasis test results. Antigenic and functional levels of protein C, protein S and antithrombin III were within normal limits. The only abnormality found was decreased plasminogen activity in plasma; antigenic and functional levels were reduced to about half-normal levels. In both cases crossed immunoelectrophoresis revealed a normal migration pattern of plasminogen. Thus, we conclude that our patients were carriers of congenital hypoplasminogenemia or familial type I plasminogen deficiency, due to decreased synthesis. We also reported on fibrinolytic response to infusion of DDAVP, a synthetic analogue of the antidiuretic hormone. Fibrinolytic activity was normal in basal conditions as well as in response to DDAVP infusion.
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PMID:[Plasminogen deficiencies in 2 Spanish families. Response to the administration of DDAVP]. 236 94

A heterozygote protein C deficit was found in 4 members of the same family. The propositus is a 40 year old male with a clear thrombotic tendency. This included repeated thrombophlebitis of the right leg, and one episode of pulmonary embolism. Arterial thrombosis was not noted. The anticoagulant therapy undertaken by the patient appears to be of some benefit in the sense that no recurrence of thrombotic manifestations occurred. One brother and two nephews of the propositus, even though asymptomatic showed reduced levels of Protein C both as activity and antigen. The parallel reduction of Protein C activity and antigen points towards a "true" deficit of Protein C. The normal, although reduced, pattern in the crossed immunoelectrophoresis supplies further confirmation to this interpretation.
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PMID:The report of an Italian family with heterozygous protein C deficiency. 246 57

Since most patients with thrombophilia in Israel are referred for diagnosis to our center, it was possible to estimate the relative frequency of the hereditary disorders leading to thrombophilia. 107 unrelated patients were evaluated over 4 years. Diagnoses were established in 23 patients (21.5%) while in 84 (78.5%) no abnormality was detected. Antithrombin III deficiency was found in 8 patients (7.5%), dominant protein C deficiency in 6 (5.6%), recessive homozygous protein C deficiency in 1, protein S deficiency in 3 (2.8%) and dysfibrinogenemia in 1. Four additional patients (3.7%) had a lupus anticoagulant. The frequency of deep vein thrombosis and pulmonary embolism was similar in patients with and without a definite diagnosis. Thrombosis of visceral or cerebral vessels and a positive family history were more frequent among patients in whom a definite diagnosis was made. In both groups there was a substantial lag between the time of presentation of the first thrombotic episode and the time of evaluation. Since the number of referred patients with thrombophilia has gradually increased over the period of the study, it is at present impossible to establish the prevalence of the various hereditary disorders leading to thrombophilia in the population.
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PMID:The relative frequency of hereditary thrombotic disorders among 107 patients with thrombophilia in Israel. 252 86


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