In a case of Ehlers-Danlos syndrome, a platelet defect is described. It is characterized by a defect of ADP and platelet factor 3 release, absence of secondary curve in ADP, adrenalin and distilled water-induced aggregation and a defective collagen aggregation. It is pointed out that this defect, which occurs in primary thrombopathy, also exists in connective tissue diseases such as Ehlers-Danlos syndrome, osteogenesis imperfecta, etc
SummaryPurified bovine platelet cofactor I substituted for adsorbed plasma in the thromboplastin generation test when Ac-globulin was also supplied. Only 70 gamma/ml were needed. Purified bovine autoprothrombin II substituted for serum in the test. Only 9 gamma were equivalent to serum. Platelet cofactor I thus takes the place of the antihemophilic factor and autoprothrombin II substitutes for PTC and Stuart-Prower factor. We regard the autoprothrombin II preparation used as a single component derived from prothrombin.
Thrombi were electrically induced in dogs. The alterations of the vessel wall were studied in samples obtained on the 8th day from control and treated animals. Changes in coagulation parameters were monitored daily. Animals were treated with 600 mg defibrotide (Crinos) daily for a week, starting 24 h after the induction of thrombi. In the control dogs there was thickening of intima with endothelial hyperplasia and smooth muscle proliferation. The treated animals did not show any morphological or ultrastructural alterations (SEM). This observation encourages us to examine the role of fibrinolytic and endothelial supportive therapy for prevention of development of vascular changes.
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