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)

This study of 49 patients with spontaneous venous and arterial thrombosis identified 27 with hypercoagulable states: 13 had only venous thrombosis (VT), six had episodes of VT followed by arterial thrombosis (AT) and eight had AT only. All 27 patients were less than 42 years of age; 22 had specific natural anticoagulant or fibrinolytic deficiencies: antithrombin III (nine patients), protein C (eight patients), protein S (three patients), heparin cofactor II (two patients), tissue plasminogen activator release (one patient) and mixed antithrombin III and protein S (one patient). The remaining five patients had recurrent thrombotic events associated with resistance to heparin anticoagulation, but no established laboratory diagnosis. Clotting complications included recurrent VT, pulmonary embolism, multiple failed arterial procedures and lower extremity amputation. The remaining 22 patients (mean age of 53 years, range of 46 to 63 years), 12 with VT and ten with AT, did not have laboratory evidence of hypercoagulability and none had recurrent vascular occlusions. All these patients were successfully treated by conventional therapy without any additional thrombotic events during the follow-up period. Young adults with spontaneous thrombotic events should be screened for possible hypercoagulable states. Additionally, these young patients need further evaluation and treatment of cardiovascular risk factors. Those with premature atherosclerosis have an especially poor prognosis despite surgical intervention and anticoagulant therapy.
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PMID:Hypercoagulable states as an evolving risk for spontaneous venous and arterial thrombosis. 792 7

Fibrin D-Dimer (D-Di), prothrombin activation fragment (F 1+2) and thrombin-antithrombin III complexes (TAT) were measured using ELISA procedures in the plasma of patients with an acute deep venous thrombosis (DVT), at presentation and on days 2, 6 and 10 after initiation of heparin treatment. Patients were randomly allocated into two treatment groups: 44 patients received adapted doses of continuous intravenous unfractionated heparin (UH) whereas 47 received 1 mg/kg every twelve hours of a low molecular weight heparin (enoxaparin) subcutaneously. A phlebography and a perfusion lung scan were performed before inclusion and on day 10. Failure of therapy (n = 9) was defined by venogram worsening or confirmed pulmonary embolism. Improvement (n = 44) or stationary state (n = 38) were defined by venogram evolution in the absence of new leg scan defects. At presentation, D-Di, F 1+2 and TAT were above cut-off values in 97, 66 and 89% of patients respectively. D-Di levels correlated with the extent of venous thrombosis whereas TAT and F 1+2 did not. Mean levels of D-Di decreased sharply during the first days of treatment but were still abnormal on day 10. A secondary increase of D-Di on days 6 or 10 by more than 3 micrograms/ml occurred in 4 of the 9 patients who developed a thromboembolic recurrence but in none of the 72 patients who had a more favorable outcome. F 1+2 and TAT time-courses were not related to clinical evolution. In the Enoxaparin group, there was no relationship between antifactor Xa activities and any biological markers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Markers of hemostatic system activation in acute deep venous thrombosis-evolution during the first days of heparin treatment. The DVTENOX Study Group. 816 10

Rudolf Virchow described not only his famous triad in the 1840s but also the relationship between thrombosis and pulmonary embolism. Deep vein thrombosis (DVT) was recognized as postoperative complication from the 1890s. The preventive measures were directed against the factor blood stasis until heparin was applied clinically in the 1930s. The Swiss surgeon K. Lenggenhager was probably the first who recommended low dose heparin prophylaxis in 1940 on a rational experimental basis. Perhaps because his results were published only in German this application form became not popular before the great studies of Kakkar in the 70s took place. The introduction of low molecular weight heparins in the 80s simplifies prophylaxis and therapy of DVT again. The descriptions of deficiency of natural coagulation inhibitors start with antithrombin III in 1961. The recent discovery of the molecular basis of activated protein C resistance made history today.
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PMID:[From the history of thrombosis prevention and treatment]. 865 46

Thirteen patients with hepatocellular carcinoma who underwent transcatheter arterial embolization (TAE) were studied to evaluate the incidence of pulmonary embolism and methods for diagnosing this complication. Pulmonary perfusion scans and changes in indexes of coagulation and of fibrinolysis, and in the partial pressure of oxygen in arterial blood were evaluated as possible signs of pulmonary embolism complicating TAE. In 3 out of 13 patients (23%), perfusion lung scans showed perfusion defects. These 3 patients were asymptomatic and their perfusion defects had disappeared by 4 weeks later. TAE was followed by significant decreases in platelet counts (p < 0.01) and in serotonin levels (p < 0.05); and by increases in A-aDO2 (p < 0.01), in levels of fibrinogen in plasma (p < 0.01), and in levels of thrombin-antithrombin III complex (TAT) (p < 0.05), with no significant increase in levels of D-dimer in plasma. Similar hematologic changes were observed in patients without perfusion defects after TAE. In 3 patients with perfusion defects, plasma levels of TAT before TAE were significantly higher than the levels in patients without perfusion defects (p < 0.01). Perfusion defects that occur after TAE may be caused by pulmonary thromboemboli, by pulmonary fat emboli, and by microatelectasis or discoid atelectasis, and the most common cause is probably pulmonary thromboemboli. We conclude that the risk of pulmonary embolism complicating TAE is higher in patients with hepatocellular carcinoma who have high levels of TAT in plasma.
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PMID:[Abnormalities in pulmonary perfusion scans after transcatheter arterial embolization of the liver]. 869 61

Plasma levels of selected coagulation and fibrinolytic parameters (activated partial thromboplastin time, prothrombin time, fibrinogen, antithrombin III, protein C, thrombin-anti-thrombin III complexes (TAT), plasminogen activator inhibitor-1 (PAI-1), plasminogen, alpha 2-plasmin inhibitor) were evaluated in 90 patients with clinical suspicion of pulmonary embolism (PE). Plasma levels of fibrinogen, PAI-1 and TAT were significantly higher in patients than in controls (p < 0.01): evaluation of TAT displayed a sensitivity of 96.1% and specificity of 30.8%, and positive and negative predictive values of 64.5 and 85.7%, respectively. The number of nonperfused lung segments correlated directly with TAT levels (p < 0.01) and inversely with arterial pO2 values (p < 0.01). No significant difference was found in the other parameters between patients and controls. Our results suggest that the finding of normal TAT plasma levels can help to exclude PE in patients with clinically suspected PE.
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PMID:Thrombin-antithrombin III complexes as an additional diagnostic aid in pulmonary embolism. 869 74

In a multicenter, double-blind clinical trial in 1,968 inpatients 1 daily subcutaneous administration of LMW heparin plus 2 placebo injections or 3 x 5,000 IU unfractionated (UF) heparin was given for 10 (8-11) days. The primary end point was the incidence of proximal deep-vein thrombosis or pulmonary embolism. Patients were assessed during the study period for development of proximal deep-vein thrombosis by compression sonography at days 1 and 10 and for pulmonary embolism by scintigraphy in symptomatic patients. Aim of the study was to demonstrate the equivalence of both treatment regimens. A total of 1,968 patients were randomized to receive UF or LMW heparin. Of these, 378 patients were excluded during the study period, so that 780 patients on UF and 810 on LMW heparin were included in the efficacy analysis. Four primary end points were observed with UF and 6 with LMW heparin, demonstrating the equivalence of treatments (p = 0.012). Additionally, pulmonary embolism was suspected as the cause of death in 6 patients who died during the study (3 per treatment group). A higher frequency of death (n = 32) was observed in the LMW-heparin group (p = 0.02) particularly documented in a part of the centers. Safety analysis showed a higher frequency of local pruritus, local erythema and subcutaneous hematoma, a higher increase in plasma levels of triglycerides, total cholesterol, alanine aminotransferase and aspartate aminotransferase, and a decrease of antithrombin III in patients receiving UF heparin. A decrease in platelet count (values ranging between 40,000 and 80,000/microliter) was observed in 4 patients with UF and in none with LMW heparin. No severe thrombocytopenia was observed. Subcutaneous LMW heparin is as effective as UF heparin for prophylaxis of thromboembolism in bedridden, hospitalized medical patients.
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PMID:Subcutaneous low-molecular-weight heparin versus standard heparin and the prevention of thromboembolism in medical inpatients. The Heparin Study in Internal Medicine Group. 873 87

Hereditary protein S deficiency (HSPD) is a predisposing factor to recurrent venous thrombosis but is not currently associated with stroke. We report two cases of HSPD revealed by stroke in young adults. The first one was a 36-year-old patient whith a pure motor hemiplegia, who gradually recovered without sequelae. Total and free protein S was decreased (55 and 10%). One of his brothers died from pulmonary embolism at 20 years and a sister had low protein S level without clinical signs. The second case was a 26-year-old patient who had a right hemiplegia with aphasia due to an infarction in middle cerebral artery area. He partially recovered, but the course of the illness was complicated by deep venous thrombosis of the lower limbs and pulmonary embolism. Total and free serum protein S level was severely decreased (25 and 0%). The patient's mother and one of his sisters also had low protein S but never had clinical complications. In both case, dupplex scanning, transcranial doppler, echocardiography, serum antithrombin III and protein C were normal. Cigarette smoking was the only risk factor for arterial disease. These two cases suggest that HSPD must be investigated in young patients with stroke, even in cases of lacunar stroke.
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PMID:[Cerebrovascular complications and hereditary protein S deficiency: 2 cases]. 876 59

The diagnosis of thromboembolic diseases is still difficult to establish before the occurrence of the pathological event, although it is now known that they are the result of a progressive alteration of the cardiovascular system. Introduction of new diagnostic tools for the evaluation of the thromboresistance capacity of the body or for the measurement of molecular markers allows the testing of the body defenses against thrombosis which is becoming a routine clinical diagnosis. Antithrombin III (AT III), protein C, protein S, and parameters of fibrinolysis have been recognized to be very important anticoagulant proteins and regulators of thrombin formation and thrombus extension. Furthermore, a normal factor V is necessary for the normal function of the protein C pathway. The presence of a factor V mutation leads to the activated protein C resistance syndrome. However, the major incidence of thrombotic events concerns the overall population. It has been epidemiologically related to the existence of risk factors producing blood activation, which progressively saturates the body's thromboresistance. This period is clinically silent for a long time. The new molecular markers recently introduced can show the existence of a preclinical state of blood activation at the plasma level (fibrinopeptide A, thrombin-antithrombin complexes, modified antithrombin III, fragments 1 + 2 of prothrombin, D-dimer) or at the platelet level (B-thromboglobulin, platelet factor 4, and thrombospondin), and promising developments concern the endothelial level (soluble thrombomodulin). The most universally used blood activation test is the D-dimer assay. This analyte has become very popular in past years for its high sensitivity, its long half-life, and its easy detection directly on citrated plasma. Its negative predictive value (in deep venous thrombosis or pulmonary embolism) as well as its use for monitoring of thrombotic risk in the post-operative period have been well documented clinically. New investigations are initiated to find analytes reflecting endothelial damage, an early platelet activation, or the involvement of blood cells (mainly monocytes and neutrophils) in abnormal processes. It also becomes possible to evaluate directly pathological causes inducing blood activation, such as the presence of antiphospholipid antibodies or other autoimmune antibodies.
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PMID:Thromboembolic diseases: biochemical mechanisms and new possibilities of biological diagnosis. 880 28

Intracranial surgery is often complicated by thromboembolic events including the life-threatening pulmonary embolism. After head trauma and in patients with brain tumors disseminated intravascular coagulation (DIC) can occur, characterized by the triggering of the coagulation cascade and the depletion of coagulation factors which ultimately leads to bleeding. The identification of patients at high risk as well as the early diagnosis of hemostatic problems uses routine laboratory parameters such as partial thromboplastin time and prothrombin time reflecting the intrinsic and the extrinsic pathway of the coagulation respectively. Thrombin antithrombin III complexes (TAT) and prothrombin fragment 1 + 2 (F1 + 2) are further indicators of an activation of the coagulation whereas fibrinogen degradation products (FDP) refer to the fibrinolytic system. The basic principles of coagulation and fibrinolysis are summarized as well as the changes of laboratory parameters accompanying DIC, hypercoagulability and hyperfibrinolysis.
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PMID:What the neurosurgeon needs to know about the coagulation system. 898 62

In the last 20 years within the clinical research on venous thromboembolism a major objective was to identify and develop increasingly effective and safe methods of prevention. This trend is justified by the high incidence of thromboembolism as well as by the relevant mortality for acute pulmonary embolism and postphlebitic sequels of difficult treatment. A significant contribution to the rational application of methods of prevention was given by the knowledge of risk factors. Together with acquired risks, as surgery, age, malignant tumors, in the last 30 years some conditions of thrombophilia were identified. They are caused by deficiencies in coagulation inhibitors (antithrombin III, protein C, protein S) or other alteration of the anticoagulation system as resistance to activated protein C or antiphospholipid antibodies. The primary prophylaxis of venous thromboembolism is aimed at the prevention of thrombosis by pharmacologic methods able to oppose the procoagulant alterations while avoiding hemorrhagic complications. The physical methods tend to reduce the stasis in the veins of the lower extremities. Subcutaneous calcium heparin at the dose of 5000 U twice or three times a day is the most common pharmacologic method used. It was shown to be safe and effective especially in postoperative prophylaxis of venous thromboembolism in general surgery. More recently, low molecular weight heparin fractions have been introduced. As compared to standard heparin they have the advantage of a single daily dose and a better efficacy in some groups of patients, as those undergoing hip replacement. Among the substances under clinical experimentation, dermatan sulfate seems promising. Most common physical prevention methods consist in the use of elastic graduated compression stockings and systems of intermittent pneumatic calf compression. The former can be used also in presence of a hemorrhagic risk as in neurosurgery. The latter have shown a good efficacy in increasing flow velocity and probably also in enhancing the fibrinolytic activity. The combination of physical and pharmacologic methods seems to be able of enhancing the efficacy of prophylaxis.
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PMID:Risk factors and prevention of venous thromboembolism. 906 62


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