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)

An IGG lambda was purified and its binding properties analyzed from the serum of a woman who had suffered a pulmonary embolism after taking an oral contraceptive (50 mcg ethinyl estradiol and 500 mcg norethisterone) for over 2 years. The purification steps were 1) precipitation with 25% ammonium sulfate; 2) gel filtration on DEAE Sepha dex A25-Sephadex G-25 at pH 10.5 with 6 M urea; 3) repeat gel filtration, but at pH 8.6 without urea; 4) chromatography on Sepharose 4B CNBr coupled with ethinyl estradiol. The activities of the fractions were analyzed by double diffusion immunoelectrophoresis. Scatchard plots by both dialysis and by ultracentrifugation generated an association constant of 2.7 X 10 7 M -1 for ethinyl estradiol, .4 X 10 7 M -1 for 17beta-estradiol, and a valence of 2. Normal human sera had such low affinities for ethinyl estradiol that the Ka could not be calculated. Immunoelectrophoresis showed only a single protein, of about 150,000 molecular weight in polyacrylamide gel. Equilibrium dialysis against other steroids demonstrated that the IgC was specific for ethinyl estradiol, but binding was inhibited to a lesser extent by the following, in order of potency: 17beta-estradiol, progesterone, estr adiol, testosterone, and estrone. The Ka was midway between that of albuinn and the highly specific steroid binding protein. The relationships between oral contraception, this apparent monoclonal gammapathy, and the pulmonary embolism are discussed.
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PMID:[Monoclonal human immunoglobulin (IgG lambda) with antiethinylestradiol activity, oral contraceptives, and arterial pulmonary thrombosis]. 80 20

Arteriosclerotic plaques were found in the aorta and arteries of rabbits given homocysteine thiolactone, methionine or homocysteic acid, both parenterally and in a synthetic diet. Animals given large doses of parenteral methionine or homocysteine thiolactone died of pulmonary embolism and pulmonary infarct. Pyridoxine prevented thrombosis and pulmonary embolism but did not prevent arteriosclerotic plaques. These findings and previous work, showing a new matabolic pathway for sulfate ester synthesis from methionine, the somatotrophic activity of homocysteic acid, and control of cellular growth and intercellular matrix synthesis by homocysteine derivatives, suggest a theory to explain aspects of the pathogenesis of arteriosclerosis.
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PMID:Homocysteine theory of arteriosclerosis. 119 72

Electromechanical dissociation (EMD) may be primary, due to disease of the heart muscle itself, or secondary to alterations in loading conditions of the heart. Factors such as internal hemorrhage, acute cardiac tamponade, tension pneumothorax, acute pulmonary embolism, and inflow or outflow obstructions of the heart may be responsible for changes in loading. Myocardial ischemia, myocardial depressant overdose, and other conditions may also contribute to secondary EMD. If detected early, these secondary forms of EMD may respond to treatment. Drugs for resuscitation of a patient with EMD include epinephrine, atropine sulfate, and, in selected instances, calcium.
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PMID:Electromechanical dissociation. Treatable causes of a dire cardiac emergency. 194 21

A congenitally abnormal fibrinogen (Vlissingen) was isolated from the blood of a young woman suffering from massive pulmonary embolism. Fibrinogen Vlissingen showed an abnormal clotting time with both thrombin and Reptilase. The release of the fibrino-peptides A and B by thrombin was normal, but fibrin polymerization was impaired both in the presence and absence of Ca2+ ions. On sodium dodecyl sulfate-polyacrylamide gel electrophoresis performed according to Laemmli the gamma-chain of fibrinogen Vlissingen showed two bands, one normal and one having an apparently lower molecular mass of about 1,500 daltons. The previously described protective effect of Ca2+ ions on plasmin degradation of the carboxyl terminus of the gamma-chain of normal fibrinogen was only partially detectable in fibrinogen Vlissingen. In addition the binding of Ca2+ ions was decreased. Fibrinogen Vlissingen bound 2.4 Ca2+ ions per fibrinogen molecule at pH 7.4, whereas normal fibrinogen bound 3.1 Ca2+ ions. At pH 5.8 fibrinogen Vlissingen bound 1.1 Ca2+ ions, whereas normal fibrinogen bound 2.0 Ca2+ ions per molecule fibrinogen in the D-domains, again indicating a structural change in the carboxyl terminus of fibrinogen. The structural defect was determined by sequence analysis of DNA amplified by use of the polymerase chain reaction. Exons VIII, IX, and X of the gamma-chain gene were amplified and the DNA sequence of the amplified fragments was determined. A 6-base deletion was found in 50% of the fragments corresponding to exon VIII, indicating that the patient was heterozygous for the mutation. This deletion codes for amino acids Asn-319 and Asp-320 in the normal fibrinogen gamma-chain. The data indicate that Asn-319 and Asp-320 are crucial for maintaining the integrity of the carboxyl-terminal polymerization sites, the protective effect of Ca2+ ions on plasmin degradation of the carboxyl terminus of the gamma-chain, and the calcium binding domain at the carboxyl terminus of fibrinogen.
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PMID:A congenitally abnormal fibrinogen (Vlissingen) with a 6-base deletion in the gamma-chain gene, causing defective calcium binding and impaired fibrin polymerization. 207 11

Hydroxycholoroquine sulfate has been administered for prophylaxis against pulmonary embolism following total hip arthroplasty. A significant reduction was observed in the rate of fatal emboli, with relatively few and minor side effects, on daily doses of 1200 mg.
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PMID:Hydroxychloroquine sulfate prophylaxis for pulmonary embolism for patients with low-friction arthroplasty. 242 99

Use of urokinase to treat heparin-associated thrombocytopenia and thrombosis in one patient is described, and various treatments proposed for this syndrome are discussed. A 56-year-old man received an intravenous bolus dose of heparin sodium at his local hospital and was transferred to another institution for treatment of suspected pulmonary embolism; he had received heparin two weeks earlier during coronary angiography. The patient's platelet count was reported to be normal before heparin administration. When embolism was confirmed, heparin was discontinued and streptokinase was given for 24 hours. Heparin infusion was then restarted at 1000 units/hr and continued for four days. Platelet count on admission to the second hospital was 47,000/cu mm; 12 hours later it was 19,000/cu mm, and it remained low despite platelet transfusions. Five days after admission, deep-vein thrombosis developed in the left leg. Heparin was discontinued and urokinase and warfarin were started. Urokinase was infused at 320,000 IU/hr for 12 hours and continued at dosages of 160,000-320,000 IU/hr for a total of 40 hours. The initial warfarin sodium dose was 15 mg, followed by a dosage of 10 mg/day. Symptoms of deep-vein thrombosis improved within 12 hours and platelet count increased after heparin was discontinued. If it is recognized early enough, heparin-associated thrombocytopenia can be reversed by discontinuation of heparin. Transfusions of platelets are of little benefit. Dipyridamole, cyclo-oxygenase inhibitors such as aspirin, and protamine sulfate may be useful. Long term anticoagulation with warfarin is recommended to prevent recurrent thrombosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thrombolytic therapy in heparin-associated thrombocytopenia with thrombosis. 348 69

A new method is described for identifying low concentrations of circulating derivatives of fibrinogen and fibrin, even when present in heterogeneous mixtures. This technique is applicable to plasma and serum and uses electrophoresis in 2% agarose in the presence of sodium dodecyl sulfate (SDS) followed by immunological identification of separated derivatives, using radiolabeled antifibrinogen antiserum and autoradiography. Unique electrophoretic patterns distinguish plasmic derivatives of crosslinked fibrin from those of fibrinogen and also identify crosslinked fibrin polymers produced by the combined action of thrombin and factor XIII on fibrinogen. The assay is sensitive to a concentration of 0.1 micrograms/mL of fibrinogen in serum or plasma. Fibrin polymers, plasmic degradation products of fibrinogen, and plasmic degradation products of crosslinked fibrin were detected in the plasma or serum of a patient with disseminated intravascular coagulation. Plasmic derivatives of both fibrinogen and crosslinked fibrin appeared in serum in the course of fibrinolytic therapy for pulmonary embolism, whereas during acute myocardial infarction a marked increase in the proportion of fibrin polymers in plasma was found in comparison with normal controls. Thus, the procedure can distinguish between the simultaneous processes of fibrin polymer formation, fibrinogenolysis, and fibrinolysis, and is sufficiently sensitive to detect relevant quantities of derivatives in pathologic conditions.
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PMID:Specific identification of fibrin polymers, fibrinogen degradation products, and crosslinked fibrin degradation products in plasma and serum with a new sensitive technique. 397 Oct 42

Pulmonary embolism is described as an infrequent complication of axillary and subclavian vein thrombosis. We have reported our recent clinical experience with 14 patients admitted to the Harbor-UCLA Medical Center who had a clinical diagnosis of axillary and subclavian vein thrombosis documented by phlebography of the thrombosed arm. The causes of thrombosis were effort (three patients), trauma (three patients), drug abuse (four patients), underlying neoplastic disease (three patients), and congenital venous malformation (one patient). Pulmonary emboli were diagnosed by arteriogram, ventilation perfusion scans, and arterial blood gas abnormalities in five patients with respiratory symptoms for an incidence of 35.7 percent. Immediate anticoagulation with heparin, then switching to warfarin sulfate after 5 days, was the standard therapy in all patients. Follow-up examinations between 3 and 24 months demonstrated mild postphlebitic syndrome consisting of pain and minimal swelling in two patients. We conclude that pulmonary emboli may be a more frequent complication of axillary and subclavian vein thrombosis than has generally been recognized.
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PMID:Pulmonary embolism secondary to venous thrombosis of the arm. 669 95

The case of a 63-year-old woman is presented to whom a barium sulfate enema was administered accidentally into the vagina. During inflation of the stop manchette a deep bilateral laceration of the vaginal mucosa occurred which was neglected initially. Thus, venous vessels were ruptured and the subsequent insufflation of the barium sulfate suspension resulted in a direct injection to the afferent veins and a peracute, massive pulmonary embolism. Within 1 min irreversible heart failure followed. The case differs in some aspects from two similar cases referred to in the literature, where death occurred 15 h and 3 days, respectively, after enema.
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PMID:[Lethal barium sulfate embolism after accidental vaginal application (author's transl)]. 746 78

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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