1,720,991 research outputs found
Bidimensional immunoelectrophoresis abnormal migration of serum antithrombin III in coumarin-treated patients.
No full textDeterminants of plasma levels of plasminogen activator inhibitor-1 : A study of normotensive twins
No full textAbnormal migration of serum antithrombin III in patients on coumarin therapy by cross-immunoelectrophoresis.
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Heterozygous protein C deficiency associated with multiple congenital hemangiomas--a case report.
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Additional evidence against the presence of inhibitors in vit. K deficiency and in coumarin-treated patients.
No full textI.F. 3,41
Urokinase-type plasminogen activator release after DDAVP in von Willebrand disease: different behaviour of plasminogen activators according to the synthesis of von Willebrand factor.
No full textNine healthy volunteers and 23 patients with various types of von Willebrand disease were studied before and after DDAVP infusion. We investigated the behaviour of factor VIII/von Willebrand factor measurements, and of tissue plasminogen activator and urokinase-type plasminogen activator. In mild von Willebrand disease the increase of both plasminogen activators was similar to that seen in normal controls. A different fibrinolytic behaviour was found in the type I platelet low and in the type III von Willebrand disease patients. An impaired and absent fibrinolytic response to DDAVP was seen in the former and in the latter von Willebrand disease, respectively. A close relation between either u-PA and t-PA or von Willebrand factor was observed. The possibility of a linkage among these three proteins was discussed
Unusual thrombotic-like retinopathy (Coats' disease) associated with congenital plasminogen deficiency type I.
No full textAbstract. A new kindred with heterozygous plasminogen deficiency type I is described. The proband, a 17-year-old male, showed a peculiar thrombotic-like retinal picture compatible with Coats' disease. Extensive coagulation studies revealed decreased levels of both plasminogen activity and antigen to about 50% of normal values. Five out of 13 family members from the paternal side showed the same fibrinolytic defect. In two cases, a history of recurrent phlebites of the lower limbs was present. One unaffected patient also had a superficial phlebites at a young age; her plasminogen levels were shown to be within normal limits, but a long-standing oestroprogestinic intake could have influenced and normalized the results. No other family member showed retinal abnormality.
This is the first case of hypoplasminogenaemia associated with Coats' disease. A possible role of the fibrinolytic defect in the pathogenesis of this unusual retinopathy is suggested. Finally, the occurrence of thrombotic manifestations in other affected family members supports the opinion that plasminogen deficiency should be considered as a potential risk factor for thrombosis
Improvement of fibrinolytic capacity after steroid therapy withdrawal, in kidney transplantation
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