Search PubMed⌕ Search

Biomedical subjects

L Tengborn

Publications and source records attributed to L Tengborn.

At least 91 records · Page 5Linked to original sources
PubMed1988

Deep vein thrombosis of the axillary-subclavian veins: epidemiologic data, effects of different types of treatment and late sequelae.

Upper extremity deep venous thrombosis (DVT) is uncommon. In the city of Malmö, Sweden (240,000 inhabitants), 296 cases undergoing phlebography due to a suspicion of upper extremity DVT, during 1971-1986 were analysed. 165 arm phlebograms did not reveal any thrombi (56%). In 11 cases (4%) external compression of the vein was found. Thrombi in the axillary or subclavian vein were found in 120 cases (40%) and were classified as primary in 73 cases and secondary in 47 cases. Only seven cases of effort thrombosis were found. Four cases had neurovascular symptoms mimicking thoracic outlet syndrome and underwent elective first rib resection. None of the patients with primary DVT had a fatal pulmonary embolism (FPE). One patient had clinical signs suspicious of pulmonary embolism (PE), however, scintigraphy of the lungs was negative. Of the cases with secondary thrombi three cases had fatal, and one case had contributory PE at autopsy. Additionally, one patient had a non-fatal PE verified scintigraphically. Post-thrombotic sequelae from the arm were in no case so severe that the patient had to change occupation. Patients with primary DVT had moderate complaints in three and mild in fifteen cases. Those with secondary arm thrombi experienced only moderate symptoms in two cases and mild sequelae in fourteen. There was no correlation between the type of treatment and late post-thrombotic symptoms. From this study it can be concluded that phlebography must be undertaken before treatment can be started in patients with a suspected arm DVT. Primary DVT seems to be a "benign" disease, and in general treatment with anticoagulants is sufficient.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Characterizing hereditary and acquired defects of plasminogen.

Since plasminogen is the proenzyme of plasmin most acquired defects of plasminogen are associated with situations with an increased fibrinolytic activity. Congenital defects also have been described both such associated with thrombotic disease and such that are not. An increased fibrinolytic activity leading to an acquired plasminogen defect is seen 1) in situations complicated with a free proteolytic activity most often involving both the fibrinolytic and the coagulation systems, 2) as a result of locally increased fibrinolytic activity (angiomas), 3) during thrombolytic therapy using plasminogen activators (SK, UK, tPA). A congenital plasminogen defect characterized by 1) a low protein level as well as one with 2) a normal plasminogen protein level in plasma but a defect activation pattern has been reported. Plasminogen can be determined immunochemically, a method which does not differentiate between functionally active plasminogen/plasmin and complexes between these proteins and inhibitors. Plasminogen activity is measured in a chromogenic method using the chromogenic substrate S2251 (Kabi Diagnostica, Stockholm). In this latter method SK is used as a plasminogen activator and the total plasmin formed is measured amidolytically. Using both the immunochemical and the amidolytical methods it has been possible to identify congenital plasminogen defects characterized by a defective activation of plasminogen into plasmin, a defect that has been associated with thromboembolic disease. Another congenital plasminogen defect seems to be caused by a decreased synthesis of a normal plasminogen molecule. Such a defect may not be associated with thrombotic disease. In situations complicated with an increased fibrinolytic activity, decreased plasminogen levels (in both types of assay) are of diagnostic help. Values down to below 50% or even lower may be seen.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Coagulation Disorders↗
PubMed1988

Surgery in patients with congenital antithrombin III deficiency.

A retrospective study is presented of 23 patients with congenital antithrombin (AT) III deficiency who underwent 57 operations of various types. Thromboprophylaxis was given in 28 operations. Dextran was used in most cases, sometimes in combination with specific AT III concentrate. No patient given AT III concentrate alone or in combination with other methods had signs of thromboembolism. Deep venous thrombosis followed four of the operations with prophylaxis (3 patients). After the 29 operations without prophylaxis there were three cases of deep venous thrombosis, one with clinical signs of pulmonary embolism and another with superficial thrombophlebitis. Despite its inherent drawbacks, this retrospective study indicated that AT III concentrate can effectively prevent postoperative thromboembolism. But as the selection criteria for thromboprophylaxis are difficult to evaluate, a prospective study should be of great value.

Adult↗
PubMed1987

Properties and catabolism of heat treated antithrombin III concentrate.

Heat treatment is employed to diminish the transmission of hepatitis when blood products are administered. It is possible that such a procedure could reduce the biological activity of the proteins and induce changes in structure and aggregation state. We have therefore made in vitro and pharmacokinetic studies of heat treated antithrombin III (AT III) concentrate using both radiolabelled and non-labelled preparations. The purification, heat treatment and the radiolabelling procedures did not induce any changes in the AT III molecules with exception of a decrease in heparin affinity in about 10% of the molecules. The in vivo studies using 125I AT III showed that the fractional catabolic rate was increased and the half-life was shortened by about 20-25% compared to our previous studies on non-heat treated AT III concentrate. Our present findings indicating a mean half-life of 3.0 days are quite comparable to studies by others on non-heat treated AT III, however.

Antithrombin III↗
PubMed1987

Cell saver versus hemofilter for concentration of oxygenator blood after cardiopulmonary bypass.

Concentration of superfluous blood in the oxygenator after the termination of a cardiopulmonary bypass was studied in 46 aortocoronary bypass patients. 15 patients were treated with a centrifugation system, the Haemonetics Cell Saver, 16 patients were treated with the Gambro Hollow Fibre Hemofilter and the remaining 15 patients received as much as possible from the untreated oxygenator contents and served as controls in a coagulation study. Both methods functioned well, the time consumption for operation of the two systems was similar. The products differed greatly as centrifugation revealed highly concentrated red cells in saline solution while hemofiltration produced protein-rich concentrated whole blood. A coagulation study of the patients who had received the concentrated products showed no signs of activation of the coagulation factors nor of the fibrinolytic system.

Adult↗
PubMed1987

Mediastinal drainage blood. Potentialities for autotransfusion after cardiac surgery.

The rate of postoperative bleeding was studied in 32 patients with aortocoronary bypass surgery and in 18 with aortic valve replacement. In 12 of the 50 patients, more than 500 ml of shed mediastinal blood could be saved within 8 postoperative hours. Aerobic and anaerobic cultures of such blood were obtained from the suction reservoir in 20 cases 2, 4 and 6 hours postoperatively. The results were negative, apart from Staphylococcus albus in one 6-hour sample. The blood, which was in some degree hemolyzed, contained acceptable amounts of red cells and albumin. Alterations of the coagulation and fibrinolytic systems indicated massive proteolysis with degradation of the proteins to an extent that precluded coagulation. This proteolysis had taken place in the mediastinum, resulting in total defibrinogenation of the blood. The authors conclude that in about one-fourth of cases in cardiac surgery, postoperatively shed blood is worth saving for red cell and volume substitution.

Aortic Valve↗
PubMed1987

Postoperative autotransfusion of concentrated drainage blood in cardiac surgery. Experience with a new autotransfusion system.

A new autotransfusion system was evaluated postoperatively in six patients undergoing aortocoronary bypass surgery. A hollow fiber hemofilter was integrated in the system, making it possible to concentrate the shed blood. The device functioned well, 825 ml diluted mediastinal drainage blood with a hematocrit of 23 was concentrated to a volume of 475 ml with a hematocrit of 36 and retransfused. Proteins were preserved, thus albumin concentration increased from 23 to 37 g/l in the autotransfusate. No negative side effects were registered after autotransfusion. A thorough coagulation study after retransfusion did not reveal any sign of activation of the coagulation cascade, nor were there any signs of an increased fibrinolysis.

Aged↗
PubMed1986

Return to normal of 99mTc-plasmin test after deep venous thrombosis and its relationship to vessel wall fibrinolysis.

Fourteen patients with deep venous thrombosis (DVT) and a positive 99mTc-plasmin test were followed up to determine how soon a negative test was obtained. Localization and extension of the thrombi were determined by phlebography. Plasminogen activator activity in vein walls and local fibrinolytic activity after venous occlusion were measured in order to find out what the prerequisites for impaired thrombolysis are. The time required to obtain a negative 99mTc-plasmin test showed considerable variation, ranging from less than 1 week to more than 6 months. The 99mTc-plasmin test had returned to normal in 64% of the patients after 6 months. No relationship was found between vessel wall fibrinolysis and time to normalization. Instead, we found an association between the time to normalization of the 99mTc-plasmin test and the size of the thrombus, according to phlebography, as well as between the time to normalization of the 99mTc-plasmin test and the extension of leg points with a positive 99mTc-plasmin test at admission. The finding of abnormal 99mTc-plasmin test results more than 6 months after acute DVT is of practical importance and warrants caution when evaluating patients with symptoms and signs suggestive of acute recurrent DVT.

Adult↗
PubMed1985

Management of haemophilia A with antibodies--the effect of combined treatment with factor VIII, hydrocortisone and cyclophosphamide.

Immune tolerance has by several methods been induced in haemophiliacs with antibodies. A conversion of "high responders" into "low responders" was previously reported after repeated moderate factor IX doses over periods of 7-10 days in combination with cyclophosphamide and steroids in two patients with haemophilia B and inhibitors. This paper reports similar results in a haemophilia A patient by giving factor VIII, cyclophosphamide, and steroids during relatively short periods of time (7-8 days). The anamnestic response markedly decreased already following the first treatment and never exceeded a level of 1 u/ml (approximately 3 BU/ml) even when boosted with ordinary factor VIII doses for only 3 days. It is concluded that the markedly decreased secondary antibody response is most probably the result of factor VIII given at short intervals (twice a day) for periods of up to about one week when given in combination with cyclophosphamide and steroids. The same effect may be achieved by other methods. The treatment schedule suggested in the present paper is, however, simple and avoids long periods of high antibody levels. Furthermore, the total factor VIII dose used is lower than suggested in most other treatment schedules, which makes the treatment substantially less expensive.

Antibody Formation↗
PubMed1985

Two different mechanisms in patients with venous thrombosis and defective fibrinolysis: low concentration of plasminogen activator or increased concentration of plasminogen activator inhibitor.

Fibrinolytic components after venous occlusion and concentrations of tissue plasminogen activator inhibitor were studied in 100 consecutive patients with confirmed recurrent deep vein thrombosis or pulmonary embolism. After 20 minutes of venous occlusion the fibrinolytic response was decreased in 33 patients, as measured both amidolytically with S-2251 and on fibrin plates. Two different mechanisms responsible for the poor fibrinolytic response could be distinguished. Twenty two of the patients in whom the response was poor released normal amounts of tissue plasminogen activator antigen, as assayed by immunoradiometric assay, but had appreciably increased concentrations of tissue plasminogen activator inhibitor. The 11 other patients in whom the response was poor had both low tissue plasminogen activator activities and low tissue plasminogen activator antigen concentrations but normal concentrations of tissue plasminogen activator inhibitor. The results show not only that defective synthesis or release of tissue plasminogen activator may be important in the pathogenesis of venous thrombosis but also that a large group of patients with thrombosis have an increased concentration of the inhibitor to tissue plasminogen activator.

Adolescent↗
PubMed1985

A Swedish family with abnormal antithrombin III.

An abnormal variant of antithrombin III is reported in a young male with deep vein thrombosis. The heparin cofactor, progressive thrombin inhibition, and factor Xa inactivation are decreased. The abnormality seems to be a mutation which is transmitted in an autosomaldominant way. The half-life and fractional catabolic rate of 125I antithrombin III concentrate is the same in this patient as in patients with the classic type of antithrombin III deficiency and in a control.

Adult↗
PubMed1983

Pre- and postoperative levels of antithrombin III with special reference to thromboembolism after total hip replacement.

A prospective study of antithrombin III, determined by electroimmunochemical assay or an amidolytical method, was carried out with special reference to thromboembolism after total hip replacement. Two hundred and seven patients were randomly allocated to thromboembolic prophylaxis with dextran 70 or low dose heparin combined with dihydroergotamine. Deep vein thrombosis determined by phlebography of the operated leg or pulmonary embolism diagnosed with perfusion/ventilation scintigraphy developed in 51% of the total material and did not differ significantly between the two groups of prophylaxis or between patients with a preoperative At III below normal and those with a normal value. The correlation between the two assay methods for At III was 0.61. An initial, postoperative decrease in At III was noted with a parallel fall in hematocrit and fibrinogen, later followed by an increase of the plasma proteins. It is concluded that the immediate postoperative decrease of At III is mostly due to hemodilution.

Antithrombin III↗
PubMed1982

Demonstration of 99mTc-labelled plasmin on the surface of ex vivo thrombi.

In an vitro system using the Chandler model for the preparation of in vitro thrombi trace amounts of porcine or human 99mTc-labelled plasmin was found to adsorb to the surface of a preformed thrombus. A radioactive lining of the thrombus could be demonstrated using autoradiography after addition of 99mTc-labelled plasmin in concentrations of 0.04 - 0.07 or 0.4 - 0.7 CTA u/thrombus made from 2 ml whole blood (0.035 - 0.35 microM). The same pattern was found for porcine as for human plasmin. The presence of tranexamic acid in concentrations of 3 to 12 mM did not affect the binding of plasmin indicating that the plasmin binding to fibrin was independent of the lysine binding sites. Furthermore alpha 2-antiplasmin was demonstrated on/in the thrombus also when no plasmin was present indicating a binding of alpha 2-antiplasmin to the thrombus. The plasmin bound to the thrombus was proteolytically inactive. In order to obtain thrombolysis most of the alpha 2-antiplasmin in the surrounding medium had to be neutralized.

Animals↗
PubMed1982

Pregnancy in women with congenital antithrombin III deficiency: experience of treatment with heparin and antithrombin.

The incidence of thromboembolic complications (TE) during pregnancy in women with congenital antithrombin III (AT) deficiency has retrospectively been estimated to be about 70%. 8 women with congenital AT deficiency were studied during 9 pregnancies. Subcutaneous or intravenous heparin in doses to prolong the activated partial thromboplastin time (APTT) was given during pregnancy as prophylaxis or therapeutic treatment. During delivery and abortion the AT level was brought to normal by infusion of AT concentrate and the heparin was reduced or withdrawn. Four pregnancies were uncomplicated with regard to TE and resulted in 4 healthy children. Five pregnancies were terminated by induced or spontaneous abortion. 1 woman had TE during heparin prophylaxis and 2 women had TE before the prophylaxis was started. 1 of the latter suffered from a new TE during continued heparing treatment. Insufficient prolongation of APTT was registered at the time of TE in both women with TE during heparin treatment.

Adult↗
PubMed1982

Prospective study of a phenformin-like substance (moroxydine chloride) in patients with deficient vessel wall fibrinolysis.

It is known that ethylestrenol and/or phenformin can normalize deficient fibrinolysis in the vessel walls and prevent recurrent thromboembolism (Hedner et al., 1976; Nilsson et al., 1975, 1981). Because of the side-effects of phenformin, we studied the effect of a phenformin-like substance: moroxydine chloride (Kabi 1886), which unlike phenformin, does not cause lactic acidosis. A prospective randomized clinical trial was carried out on 49 patients with a decreased release capacity of fibrinolytic activity (venous occlusion test for 20 min as described by Robertson et al. (1972) on at least two occasions. They received either moroxydine chloride in a dose of 0.04 g/kg a day or no specific treatment. Most of the patients had earlier at least one episode of deep venous thrombosis. At review 6 months after entering the trial, it was found that out of 26 patients receiving moroxydine chloride, the release capacity was normal in 16 (62%), compared with 5 (22%) of the 23 controls. Dicoumarol alone did not seem to have any effect on the fibrinolysis. The only side-effects were occasional diarrhea in two, which was controlled by reduction of the dose, and itching requiring withdrawal of the drug in one. Moroxydine chloride, thus, seems to normalize a defective release capacity of vessel wall in a fair percentage of cases.

Adolescent↗