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)

The relation of intravascular fibrin to the leucocytic sticking reaction in ear chambers of rabbits injured by heat was investigated in two ways. First, attempts were made to destroy the thin layer of fibrin believed to coat the surfaces of cells involved in the sticking reaction. Second, white cell sticking was studied after fibrinogen had been removed from the blood stream. The results of these experiments were as follows:- 1. Activation of fibrinolysin in vivo by streptokinase did not impair sticking of white blood cells. 2. Administration of streptokinase parenterally did not lower fibrinogen blood levels appreciably even when the amount used was large. 3. Thromboplastin infusions alone reduced circulating fibrinogen to low levels but leucocytic sticking was not prevented. Furthermore, frequent death of animals due to pulmonary embolism made such experiments prohibitive. 4. Addition of streptokinase to thromboplastin infusions protected against embolic deaths but did not influence sticking even though the fibrinogen levels achieved were quite low. 5. Finally, when thrombin was added to infusions of thromboplastin and streptokinase, no circulating fibrinogen could be detected. Under such circumstances leucocytic sticking following heat injury occurred without reduction. These findings were interpreted as evidence against a primary role of the blood clotting mechanism in causing the sticking of white blood cells to injured endothelium. Alternative explanations were discussed.
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PMID:Studies on the pathogenesis of acute inflammation. II. The relationship of fibrinogen and fibrin to the leucocytic sticking reaction in ear chambers of rabbits injured by heat. 1379 25

Venous thromboembolism is a common and potentially fatal disease. If properly used, anticoagulation therapy is effective in preventing recurrence of venous thromboembolism and in improving survival. Symptomatic patients with an objective diagnosis of acute deep vein thrombosis (DVT) or pulmonary embolism (PE) should receive immediate systemic heparin anticoagulation at dosages sufficient to rapidly prolong the activated partial thromboplastin time into the laboratory-specific therapeutic range; this range corresponds to a plasma heparin concentration of 0.2 to 0.4 IU/ml (as measured by protamine sulfate titration), or 0.3 to 0.7 anti-Xa IU/ml. An oral vitamin K antagonist (e.g. warfarin) should be started within 24 hours after starting heparin; the starting dose should be the estimated patient-specific daily dose with no loading dose. Heparin and warfarin anticoagulation should be overlapped for at least 4 to 5 days and until the international normalized ratio (INR) is within the therapeutic range (2.0 to 3.0) on 2 measurements made at least 24 hours apart. The duration of warfarin anticoagulation should be individualized based on the respective risks of venous thromboembolism recurrence and anticoagulant-related bleeding. In general, warfarin should be continued for at least 3 months, and longer for patients with recurrent or idiopathic venous thromboembolism, malignant neoplasm, neurologic disease with extremity paresis, obesity, or laboratory evidence of a lupus anticoagulant/anticardiolipin antibody, homozygous carrier or combined heterozygous carrier for the factor V R506Q (Leiden) and prothrombin G20210A mutations, and possibly deficiency of either antithrombin, protein C, or protein S. Low molecular weight heparin (LMWH) is effective and well tolerated as acute therapy for patients with DVT or stable PE, and does not require laboratory monitoring or dose adjustment. Outpatient LMWH therapy is also well tolerated and cost effective for most patients with DVT, and possibly for selected patients with PE.
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PMID:Current management of acute symptomatic deep vein thrombosis. 1472 51

Platelets from protease-activated receptor 4 (PAR4)-deficient mice are unresponsive to thrombin, and Par4-/- mice have prolonged bleeding times and are protected against thrombosis. However, in addition to its role in platelets, PAR4 contributes to thrombin signaling in cells in the blood vessel wall that might participate in hemostasis and thrombosis, such as endothelial cells. To determine whether the hemostatic and thrombotic phenotypes of Par4-/- mice were due to loss of PAR4 function in hematopoietic vs. other cell types, tail bleed times and thromboplastin-induced pulmonary embolism were examined in lethally irradiated mice reconstituted with Par4+/+ or Par4-/- bone marrow. In Par4+/+ and Par4-/- mice reconstituted with Par4+/+ marrow, the median tail bleed times were 2.0 and 1.7 min, respectively, vs. > 10 min for both Par4+/+ and Par4-/- mice reconstituted with Par4-/- marrow. In the pulmonary embolism model, Par4+/+ and Par4-/- mice reconstituted with Par4+/+ marrow survived a median of 3.7 and 2.8 min, respectively, after administration of thromboplastin, vs. > 20 min for both Par4+/+ and Par4-/- mice reconstituted with Par4-/- marrow. Further, the phenotype of mice reconstituted with Par4-/- marrow was almost as dramatic as that seen in Nf-e2-/- mice, which lack platelets. These data strongly suggest that increased tail bleed times and protection against thrombosis in Par4-/- mice are accounted for by lack of PAR4 function in platelets, emphasize the importance of thrombin signaling in platelets among the multiple pathways and cell types that govern hemostasis and thrombosis.
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PMID:Impaired hemostasis and protection against thrombosis in protease-activated receptor 4-deficient mice is due to lack of thrombin signaling in platelets. 1530 51

Leakage of viscous bone cement into venous blood possibly resulting in pulmonary embolism may occur during percutaneous vertebroplasty. Our aim was to study if bone cement surface or cement liquid component could induce platelet aggregation or plasma coagulation in vitro. Two types of commonly used methyl-methacrylate bone cement, Palacos (Heraeus Kulzer, Germany) and Vertebroplastic (DePuy, Acro Med, England), were smeared on thin glass slides that were inserted over the bottom of cuvettes immediately or after 24 h, and platelet aggregation was recorded over 10 min. Bone cement liquid component, containing methyl-methacrylate monomer and N,N-dimethyl-p-toluidine, was tested in 2% and 4% final concentration. Partial thromboplastin time (PTT) was determined by the hook method in the presence of bone cement-smeared glass slides or 6% bone cement liquid. Both types of bone cement, either fresh or aged, did not promote platelet aggregation, whereas collagen-coated glass slides induced substantial platelet aggregation (65 +/- 37%). On the other hand, bone cement liquids reduced platelet aggregation induced by collagen solution to an average of less than 15% (p < 0.01). Bone cement, fresh or aged, had no effect on PTT, but bone cement liquids significantly prolonged PTT: median and 1st-3rd interquartile range 149 (96-171) s for Vertebroplastic and 132 (99-194) s for Palacos, p = 0.03 for both comparisons with normal pool plasma without additives that had PTT of 69 (62-71) s. We conclude that the surface of fresh or aged bone cement is not thrombogenic in vitro. The bone cement liquid inhibits platelet aggregation and plasma clotting in relatively high concentrations that cannot be expected in vivo.
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PMID:Methyl-methacrylate bone cement surface does not promote platelet aggregation or plasma coagulation in vitro. 1534 14

The clinical significance of lower extremity deep vein thrombus (DVT) propagation in the setting of anticoagulation therapy remains unclear. The purpose of this study is to compare results of thrombus outcome found with repeat duplex ultrasonography to the incidence of pulmonary embolism and mortality. During a recent 18-month period, 457 patients were diagnosed with lower extremity DVT with duplex ultrasonography and their data were retrospectively analyzed. Repeat examinations were available for review in 118 patients (51 men, 67 women). Results of repeat duplex exams were divided into 4 groups: resolved, improved, unchanged, or extended proximally. All patients received heparin and warfarin therapy. Ventilation-perfusion (V/ Q) scans were obtained only for signs and symptoms of pulmonary embolism (n=30). Mortality, the prevalence of high-probability V/ Q scans, frequency of intracaval filter insertion, gender, mean age, mean prothrombin time (PT), mean partial thromboplastin time (PTT), mean number of repeat ultrasounds per patient, and mean time over which the repeat ultrasounds took place were compared among the 4 groups. Patients who had proximal extension of DVT (19%) on repeat duplex ultrasound had an increased prevalence of pulmonary embolism (p<0.05). Also, patients whose DVT resolved were younger (p<0.05). There was no difference among the 4 groups in mortality, placement of Greenfield filters, mean PT, mean PTT, mean number of ultrasound exams per patient, or mean follow-up time over which the exams took place. Proximal extension of DVT documented by repeat duplex ultrasound is a significant risk factor for pulmonary embolism. Repeat duplex ultrasound can identify a group of patients who may benefit from insertion of an intracaval filter device.
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PMID:Does repeat duplex ultrasound for lower extremity deep vein thrombosis influence patient management? 1559 33

A 28-year-old man presented with mental retardation, peculiar facial features, radioulnar synostosis, hypogonadism, aplasia of the right kidney, a moderate degree of proteinuria, and peripheral cyanosis. The activated partial thromboplastin time was shortened, and the level of plasma factor VIII was high. A chromosomal analysis revealed a 49, XXXXY karyotype. From the 10th hospital day, he suffered from sudden dyspnea following swelling of the left leg. He was diagnosed as having deep vein thrombosis and pulmonary embolism, and was successfully treated with anticoagulant therapy. This is the first case of the 49, XXXXY syndrome complicated with unilateral renal aplasia, proteinuria, and venous thromboembolism.
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PMID:49, XXXXY syndrome with unilateral renal aplasia, proteinuria, and venous thromboembolism. 1564 56

In this retrospective study, the hemorrhagic and thrombotic events are reported at presentation and during induction in 34 consecutive acute promyelocytic leukemia (APL) patients treated in a single referral center. The most consistent hemostatic abnormality was decreased fibrinogen level (<150 mg/dL) found in 21 patients (61%), partial thromboplastin time (PTT) was normal almost in all patients. A mildly prolonged prothrombin time (PT) was observed in 14 patients (44%). Median platelet count was 30.10(9)/L (range 3-191.10(9)/L). Life-threatening bleeding manifestations occurred in 10 patients (29%). By multivariate analysis, severe bleeding complications did not correlate with hemostatic parameters but did correlate with white cell count at presentation. Four patients (12%) had severe thrombotic events, two cerebral sagital sinus thrombosis, one pulmonary embolism, and one subclavian vein thrombosis. Two other patients had pseudotumor cerebri. Three out of six patients with thrombotic events were found to have thrombophilia. These results may suggest an association between thrombophilia and thrombosis in APL patients. Two patients suffered from combined severe bleeding and thrombosis. Hemostatic parameters are not helpful in predicting neither hemorrhage nor thrombosis.
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PMID:Predictive factors of bleeding and thrombosis during induction therapy in acute promyelocytic leukemia-a single center experience in 34 patients. 1590 24

Tissue factor (TF) mRNA levels in leukocyte and TF antigen in plasma were examined in patients with deep vein thrombosis (DVT). Although TF mRNA levels in leukocytes were higher in patients with DVT than in healthy volunteers, they were lower in patients with DVT than in those with solid cancer and those with disseminated intravascular coagulation (DIC). On the other hand, the plasma levels of TF antigens were markedly high in patients with DVT/pulmonary embolism (PE). Analysis of the role of underlying disease of DVT showed no significant difference in TF mRNA levels and TF antigens among patients with solid cancer, post-surgical, other diseases and those free of underlying diseases. In patients with VTE, plasma levels of D-dimer, soluble fibrin, GE-XDP and plasminogen activator inhibitor-1 did not correlate with TF mRNA or TF antigen. In analysis of 18 patients with PE with and without DVT, TF mRNA levels in leukocytes correlated with the plasma levels of D-dimer. These findings suggest that TF in leukocytes is more likely to be involved in the development of thrombosis in PE than DVT.
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PMID:Elevated levels of leukocyte tissue factor mRNA in patients with venous thromboembolism. 1603 15

The presence of antiphospholipid antibodies is associated with arterial and venous thrombosis. A young female with initial presentation of dyspnea and cough that lasted for days is reported. A computed tomographic scan of her chest and echocardiography showed features of thrombus formation over the right atrium, complicated with pulmonary thromboembolism. Antiphospholipid syndrome was diagnosed according to elevated activated partial thromboplastin time, high serum titers of anticardiolipin antibody, and the presence of intracardiac thrombus with pulmonary embolism. This thrombus was subsequently removed successfully with surgical intervention, and the patient's recovery was uneventful.
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PMID:Antiphospholipid syndrome presenting as intracardiac thrombus with pulmonary embolism. 1619 33

Heparin-induced thrombocytopenia (HIT) is an uncommon but potentially serious complication of hemodialysis, and subsequent reexposure to heparin after the disappearance of antiheparin-PF4 complex antibodies (HIT antibody) has been controversial. We report a 60-year-old woman who was sensitized to unfractionated heparin (heparin) as anticoagulant during hemodialysis (HD) and heparin flush on a nonsession day. The patient suddenly developed acute systemic reactions with acute pulmonary embolism a few minutes after manipulation with heparin flush on day 9, a nonsession day. Although there was no evidence of pulmonary embolism on a pulmonary scintigram on the next day, the fifth HD session was discontinued owing to recurrence of acute systemic reactions and massive clots in the dialyzer 30 min into the session. After confirmation of the presence of HIT antibody and maturation of vascular access fistula, a sixth HD session was carried out with argatroban, a synthetic direct thrombin inhibitor, with a bolus of 10 mg and continuous infusion of 0.5 mg/kg/hr as an alternative to heparin. Optimal dose adjustment of argatroban through activated partial thromboplastin time (APTT) monitoring led to a bolus of 5 mg and continuous infusion of 0.15 mg/kg/hr. The patient's HD treatment at the same doses 3 times a week followed an uneventful course over 6 months. HIT antibody was seronegative about 40 days after the cessation of heparin treatment. Reexposure to heparin was attempted with the monitoring of HIT antibody and platelet counts before and after the sessions on day 210. The titers of HIT antibody compared with before the level of reexposure showed a transient insignificantly small peak, and dialysis with heparin has been maintained to date with no recurrence of HIT. The measurement of HIT antibody titer could be useful in assessing not only the effect of argatroban to replace heparin but also in predicting the recurrence of HIT due to reexposure.
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PMID:Heparin-induced thrombocytopenia in a uremic patient requiring hemodialysis: an alternative treatment and reexposure to heparin. 1745 28


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