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)

Three laboratory tests for the measurement of antithrombin III (AT III) were evaluated. The tests measured functional AT III in serum and plasma, and the third measured AT III antigen in plasma. Normal values for each method were obtained by testing samples from 20 normal subjects. Each test was then performed on specimens from 15 patients clinically suspected of having hypercoagulable states. Each determination was run in duplicate. The hypercoagulable states included disseminated intravascular coagulation, pulmonary embolism, and pregnancy. Two-thirds of these patients were found to have antithrombin III levels below the normal range by all three of the methods studied. Patients who had decreased AT III activity in the functional assays also had decreased AT III antigen.
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PMID:An evaluation of antithrombin III laboratory tests. 736 77

Congenital antithrombin III deficiency is a rare but well-documented abnormality. A young man presented with pulmonary embolism and was found to be suffering from this condition. His family history revealed numerous members with venous disease and its complications. Treatment of the acute episode and prophylaxis are discussed.
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PMID:Familial thrombosis associated with antithrombin III deficiency in a young adult male. A case report. 742 87

The authors report the observation of a new kindred with hereditary antithrombin III deficiency. In the last three generations, the family comprised 10 subjects, 7 of whom were affected: the grandmother had recurrent thrombophlebitis; her three sons died from pulmonary embolism at 22, 26 and 28 respectively and her daughter had repeated bouts of thrombophlebitis. In patients with hereditary antithrombin III deficiency, venous thrombosis occurs under similar conditions as, and is clinically similar to, thrombosis in patients without this defect. Usual tests of hemostasis are normal. The diagnosis is however suspected through an history of recurrent episodes and of similar cases in relatives. The diagnosis is confirmed by demonstration of low levels of antithrombin III in suspected patient and family. The disease is transmitted as autosomic dominant trait. Heparin is ineffective but oral anticoagulants may prevent occurence or recurrence of thrombosis in patients with this genetic defect.
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PMID:[Familial thromboembolic disease associated with antithrombin III deficiency (author's transl)]. 746 44

Activated protein C (APC)-protein C inhibitor (PCI) complex level was examined in 35 patients with acute pulmonary embolism (PE) and in 20 healthy volunteers. Thrombin-antithrombin III complex, plasmin alpha 2 plasmin inhibitor complex, and fibrin-D-dimer levels were significantly increased in the patients with PE compared to levels in healthy volunteers. Levels of plasminogen activator inhibitor-I, tissue type plasminogen activator, and von Willebrand factor antigens were also significantly increased in patients with PE. Plasma level of APC-PCI complex was increased in most patients with PE and APC-alpha 1 antitrypsin complex level was increased in 13 patients. These complexes were not detected in healthy volunteers. These findings suggested that plasma protein C was activated in patients with PE, and that PCI was the major inhibitor of APC generated in this condition. Thus, regulation of the protein C pathway might play an important role in the pathogenesis of PE.
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PMID:Increased activated protein C-protein C inhibitor complex levels in patients with pulmonary embolism. 751 16

Pulmonary embolism in reamed femoral nailing has been reported and discussed over recent years. Does an unreamed nailing technique with a solid nail prevent this rare but serious complication of intramedullary fixation? In an animal model in rabbits, we studied the pathophysiologic impact on pulmonary function and the impact on hemostasis of reamed and unreamed nailing of intact femora and tibiae, and of femoral fracture in relation to intramedullary pressure. No statistical difference of PaO2, PaCO2, and PCO2et was found in the femur whether a reamed or unreamed procedure was performed. Two of six animals with unreamed femoral nailing, one of six animal with reamed femoral nailing, and one of five animals with a femoral fracture fulfilled four of four or three of four criteria for embolization (increase of the difference of PaCO2 and PCO2et, decrease of PaO2, increase of blast cells in central-venous blood and bone marrow/fat in histologic section of the lungs and bone). Tibial nailing did not alter pulmonary function in either group. Intramedullary pressure was increased in all animals with perioperative impairment of pulmonary function (375 to 676 mbar). Analysis of the hemostatic results showed a significant difference of platelet activation in reamed versus unreamed nailing of the femur 1 hour after nailing (p < 0.01) and a significant decrease of fibrinogen and antithrombin III (p < 0.001/p < 0.01) in reamed femoral nailing. We conclude that unreamed nailing of the femur with a solid rod may also cause bone marrow embolization with alteration of pulmonary function as long as an important increase of the intramedullary pressure is generated during the nailing procedure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intramedullary nailing and pulmonary embolism: does unreamed nailing prevent embolization? An in vivo study in rabbits. 760 32

A prospective, randomized, controlled clinical trial was performed comparing the antithrombotic efficacy of the low molecular weight heparin LMWH 21-23, (Braun) with an unfractionated heparin in elective general surgical patients over an observation period of 7 postoperative days. A total of 230 patients were admitted: 103 (group I) received low molecular weight heparin and 100 (group II) low-dose unfractionated heparin treatment given subcutaneously. In group I 41 patients (46%) were operated on for malignant disease and in group II 54 patients (54%). Due to the large amount of great abdominal procedures the intra- and perioperative application of hydroxyethyl starch was allowed for volume substitution. None of the patients died due to fatal pulmonary embolism. In group I four patients revealed positive 125I-labeled fibrinogen uptake (3.9%); two patients belonged to the hydroxyethyl starch subgroup. In group II five patients displayed a positive fibrinogen uptake (5%); two belonged to the hydroxyethyl starch subgroup. The results of the hemostaseological investigations (e.g., prothrombin time, activated partial thromboplastin time, thrombin clotting time, fibrinogen, antithrombin III, protein C, plasminogen, alpha 2-antiplasmin, tissue-type plasminogen activator, plasminogen activator inhibitor) revealed no statistically significant differences between groups I and II or their subgroups, although a tendency to prolonged clotting times was observed. The antifactor Xa activity values, however, displayed a statistically significant difference between the two groups (P < 0.05). The antifactor Xa activity measured up to 0.16 U/ml for the low molecular weight heparin (group I) and 0.05 U/ml for the unfractionated heparin (group II) in the postoperative period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prospective randomized clinical study in general surgery comparing a new low molecular weight heparin with unfractionated heparin in the prevention of thrombosis. 789 22

A young man with a history of deep vein thrombosis and pulmonary embolism 11 years ago presented again with acute pulmonary embolism and was treated initially with intravenous heparin at our institution. Five days later he had another massive bout of pulmonary embolism causing hypotension. Pulmonary angiography confirmed the presence of thrombi in both pulmonary arteries, with complete obstruction of the left pulmonary artery. He was treated successfully by emergency pulmonary embolectomy. Blood investigations later confirmed the diagnosis of protein S deficiency and he was started on warfarin therapy for life. Massive pulmonary embolism should be treated aggressively. Thrombolytic therapy accelerates clot lysis, reduces pulmonary pressures, restores pulmonary capillary volume and reverses right heart failure faster than heparin alone. There is also a trend towards decreased mortality with thrombolysis. In the presence of shock, the patient should be resuscitated and if facilities for emergency embolectomy are available, surgery is a viable alternative to thrombolysis, especially if the clot burden is massive. In young patients with recurrent venous thromboembolism in the absence of obvious predisposing factors, it is important to exclude inherited plasma protein deficiencies of protein S, protein C, antithrombin III, plasminogen and fibrinogen.
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PMID:Massive acute pulmonary embolism in protein S deficiency--a case report. 794 58

We studied 84 consecutive patients referred with the suspicion of pulmonary embolism (PE) to investigate the influence of clinical and hematological profiles on the diagnosis and severity of this disease and recovery. Diagnosis of PE was confirmed in 48 out of 84 patients by perfusion scintigraphy and/or pulmonary arteriography. Severity of PE and entity of recovery were investigated by measuring standard PaO2 on blood gas analysis and the number of unperfused lung segments ULS on perfusion scintigraphy. Most common clinical predisposing conditions were more frequent, though not significantly so, in embolic patients and a very low prevalence of PE was appreciable in patients without clear predisposing conditions. Among coagulation factors, only thrombin-antithrombin (TAT) complexes were twice as high in embolic as in nonembolic patients (14.0 +/- 13.6 vs. 7.0 +/- 4.2 ng/ml; p < 0.02), while there was no statistically significant difference between embolic and nonembolic patients for activated partial thromboplastin time, prothrombin time, antithrombin III, protein C, fibrinogen, plasminogen, alpha 2-plasmin inhibitor, and plasminogen activator inhibitor-1. Sensitivity and specificity of TAT complexes in diagnosis of PE were 95.8% and 30.5%, respectively. Therefore, normal values of TAT complexes may help exclude the diagnosis of PE, while abnormal values allow to reinforce the clinical suspicion of PE. No relation was found between coagulation parameters and the severity of PE. The follow-up of 48 patients with confirmed PE was favorable on the average; however, neither the presence of predisposing conditions nor abnormal coagulation parameters allow to predict the degree of functional and scintigraphic improvement during follow-up.
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PMID:Clinical, anamnestic and coagulation data in patients with suspected or confirmed pulmonary embolism. 800 95

There have been few reports of neonatal ischemic necrosis of the testis without torsion of the spermatic cord, which may be caused either by compression in utero or by transient torsion of the spermatic cord resolving spontaneously before surgery. The patient reported herein developed an inflammatory swelling of the right scrotum and an ecchymotic plaque over the left thigh at four days of age. Ischemic necrosis of the right testis without torsion was found upon surgery. When the patient was ten days of age, he developed an inflammatory swelling in the left scrotum; ischemic necrosis of the left testis without torsion was again found upon surgery. Thrombosis of the spermatic vessels was suspected. Postoperatively, ecchymotic and necrotic skin lesions developed, followed by pulmonary embolism and cerebral thrombosis. Outcome was fatal. Hematologic tests in the neonate and his parents established the diagnosis of inherited antithrombin III deficiency. Ischemic necrosis of the testes was thus probably due to hypercoagulability. No similar cases have been reported to date.
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PMID:[Neonatal testicular ischemic necrosis without torsion, associated with antithrombin III deficit]. 812 35

Thrombectomy with arteriovenous fistula was performed between 1977 and 1988 in 103 patients (41 females, 62 males, mean age 46.7 years, 114 involved extremities) with embolizing deep-vein thrombosis (DVT). The sole aim of the surgical procedure was prevention of recurrent embolization. On the basis of the proximal extent of the thrombosis the source of embolization was identified as the iliac veins or inferior vena cava in 63% of the patients; 48% presented with a post-phlebitic vein and/or an older thrombosis, and 46% had already had recurrent pulmonary emboli. Unsuccessful aggressive procedures had been carried out previously in 11%. The rate of intraoperative pulmonary embolism (PE) was 3% (one fatal case). The perioperative mortality was 6.8%, but only one death was related to the surgical treatment itself. During follow-up (8-140 months postoperatively, mean 55 +/- 34 months) late recurrent PE was confirmed in two patients (antithrombin III deficiency, contralateral DVT) and was reported as the suspected cause of death in a third (3.6%). Venous thrombectomy with arteriovenous fistula is a reliable and effective procedure for management of embolizing DVT and is indicated especially in young patients. The rates of early- and late-recurrent PE are low, introduction of artificial material into the vein can be avoided, and long-term preservation of valve function is occasionally possible.
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PMID:Thrombectomy with arteriovenous fistula for embolizing deep venous thrombosis: an alternative therapy for prevention of recurrent pulmonary embolism. 813 16


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