Letter: Platelet and coagulation studies in patients treated with bromocriptine.
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Biomedical subjects
Publications and source records attributed to M Samama.
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Certain new data about the nature of Willebrand factors are discussed, its activity being considered as part of the activity of the antihemolytic factor VIII. An one-stage method for its determination is described based on the absence of thrombocytic aggregation in the presence of ristocetin in the patients with Willebrand disease as well as the illustration of one case.
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A simple, rapid and sensitive spectrophotometric method for the evaluation of plasminogen level is presented. After activation of plasminogen by streptokinase, plasmin is determined using its amidasic action on a tripeptidic substrate bound with paranitroanlin.
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Fibrinogen has been purified from normal and dysfibrinogenemia Metz plasmas, and from normal and from the patient's platelets. There are differences in the pattern of disc polyacrylamide gel electrophoresis between normal plasma and normal platelet fibrinogens, but the migration of the A alpha chain is similar. The abnormality of the electrophoretic mobility of the A alpha chain of plasma fibrinogen from Metz dysfibrinogenemia is not found in platelet fibrinogen of this patient. This result clearly establishes that platelet fibrinogen is a different protein from plasma fibrinogen.
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Platelets from patients with myotonic dystrophy showed a normal pattern of aggregation in response to adenosine diphosphate (A.D.P.) and collagen but were unusually sensitive to adrenaline, aggregation being detectable with adrenaline concentrations as low as 0.041 mumol per litre. In other diseases in which such sensitivity has been reported this has been accompanied by a similarly altered response to A.D.P. The increased platelet aggregation could be due to increased uptake of Ca++ by platelets or to a decrease in phosphorylation of the platelet membrane.
Studies were performed to analyse the inhibitory effect of a myeloma globulin (IgG) on fibrin formation. This inhibitory activity was very intense and caused a severe bleeding disorder which proved fatal. The isolated myeloma globulin inhibited all three stages of fibrin formation: the proteolytic action of thrombin on fibrinogen, the aggregation of fibrin monomers and the stabilization of fibrin by cross-linkages in the gamma and alpha chains. Purified factor XIII, even in excess, previously activated by the addition of thrombin and calcium, did not correct this defect in cross linking. Our results suggest that this myeloma globulin induced a blockage of some receptors near the cross linking sites.
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Six cases of post-embolic chronic cor pulmonale are presented. All six were treated with thrombolytic agents (4 with streptokinase, 2 with urokinase), and in only one case was improvement maintained at the end of one year. Two patients underwent a disobliterative procedure of the pulmonary artery, together with ligation of the inferior vena cava. One of these operations was unsuccessful, and the other had a successful outcome, as confirmed by objective assessment with angiography, scintigraphy and haemodynamic studies. The literature is reviewed at this stage. It was found that the fibrinolytic agents had some chance of working only if the condition was less than a few months old. One major drawback to surgical disobliteration that cannot be foreseen before operation is the presence of thromboses at the arteriolar level in subjects whose main arteries are already blocked proximally. Nervertheless it is possible to obtain good results by surgery, and the operation is worth attempting in young subjects, given the poor prognosis of the untreated condition.
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