[Two-dimensional immunoelectrophoresis for the determination of factor-VIII-associated protein. Variation in the von Willebrand-Jürgens syndrome].
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Biomedical subjects
Publications and source records attributed to V Tilsner.
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Dacron prostheses for replacement of the thoracic aorta were sealed with bioadhesive following the Viennese method. Native human fibrinogen was brought to coagulation by adding thrombin. Factor XIII was also added in order to accelerate polymerisation and to reinforce fibrin formation in the presence of thrombin and CaCl2, thus producing a stable thrombus. In order to avoid local fibrinolysis a fast but short-acting as well as a slow but longer-acting antifibrinolytic agent was added. This method was applied in twenty patients. The prostheses remained completely impermeable to blood after resuming circulation in spite of full heparinization. No post-operative haemorrhages from the prostheses were observed.
The degree of intraoperative myocardial injury was determined in two groups undergoing different methods of myocardial protection by observing the LDH and its isoenzymes up to the 11th postoperative day. Both groups consisted of patients who underwent mitral- and aortic-valve replacement. In the first group myocardial protection consisted of Kirsch cardioplegia (2) combined with conventional coronary perfusion in cases of aortic-valve replacement. In the second group the same initial cardioplegic procedure was followed by the noncorpuscular, hypothermic and aerobic coronary perfusion by Bleese and Döring (1). No difference was noted among the mitral valve patients. During the 11 days postoperative period, the aortic valve patients in the first group demonstrated a significantly higher LDH activity than the mitral-valve cases whereas LDH activity of aortic-valve patients in the second group resembled that of the mitral valve cases. Since the length of extracorporal circulation and ischemia did not vary significantly, the LDH behavior in the aortic-valve cases of the first group may be explained by the inferiority of the myocardial protection method used. In comparison with the other methods conventional coronary perfusion resulted in more myocardial injury.
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In postoperative and posttraumatic states, thromboembolic prophylaxis results in tenfold lower occurrence of pulmonary embolism and venous thrombisis--on which the postthrombotic syndrome is based--without a determinable increase of bleeding risk. Heparin is the treatment of choice. The dosage should be calculated on the basis of body weight. A minimal laboratory program of control measurements can diminish side effects.
Hemorrhage due to thrombocytopathies can in most cases be stopped by application of the homologous coagulation-active phospholipide complex Fibraccel, as shown in a study in which 78 patients suffering from various thrombocytopathies were checked. This effect is especially important in patients with immunothrombocytopathies which do not permit any thrombocyte substitution. Recalcification time and thromboelastogram should be normalised during Fibraccel treatment. In existing extravascular coagulation Fibraccel treatment is contraindicated, especially in cases of inadequate protection by heparin.
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Compared with streptokinase, thrombolytic treatment with urokinase has the advantages of being better tolerated and of practically unlimited applicability. Its disadvantage is the high cost. A good lytic action can be obtained with a dosage of 150,000 Ploug Units/12 hours for a duration of lysis of 8-14 days combined with heparin, the therapy being monitored by determination of the products of fibrinolysis. This dosage is not possible if the time factor plays a decisive role in the success of the treatment, e.g. in myocardial infarction. Urokinase is indicated when streptokinase cannot be used, or if continuation of the streptokinase therapy is necessary because of extensive thromboses.
A case report is presented of a 20 year old patient with an acute promyelocytic leukemia. The presenting symptom was a macrohematuria caused by a consumption coagulopathy. Consumption coagulopathy has only been observed in acute promyelocytic leukemia in contrast to other coagulopathies in acute leukemia. The clotting disorder was successfully treated by administration of urokinase.
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