Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis
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Blood Coagul. Fibrinolysis · Aug 1994
A lupus anticoagulant neutralization procedure using the patient's own platelets.
An auto platelet neutralization procedure (APNP) which assists identification of lupus anticoagulants (LA) is described. Patient platelet-rich plasma is frozen then thawed (PRPF) and an activated partial thromboplastin time (aPTT) is performed on both platelet-poor plasma and PRPF. The degree of correction between the two plasmas is calculated and the percentage APNP is obtained. ⋯ In three patients with normal aPTT, LA was suspected and APNP ranged from 21 to 28%. An intermediate APNP range of 20-25% may be suggestive of LA in patients with normal aPTT. The APNP did not appear to be effected by platelet count in the samples tested unless the platelet count in PRP was less than 175 x 10(9)/1.(ABSTRACT TRUNCATED AT 250 WORDS)
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Blood Coagul. Fibrinolysis · Aug 1994
Studies on the mechanisms of action of aprotinin and tranexamic acid as plasmin inhibitors and antifibrinolytic agents.
Both aprotinin and tranexamic acid are effective inhibitors of fibrinolysis in vitro and in vivo and both agents can act as plasmin inhibitors in purified systems, although there is some debate on their exact mechanism of action in vivo. The studies reported here using an in vitro clot lysis system designed to provide precise inhibition constants show that aprotinin remains a very potent inhibitor of plasmin even in the presence of fibrin with Ki = 2 nM. Plasmin-aprotinin interactions in solution are not affected by a number of kringle binding ligands, aminohexanoic acid, tranexamic acid or CNBr-fibrinogen fragments with Ki = 0.4 nM. ⋯ Inhibition of fibrinolysis by tranexamic acid is not readily analysed by a simple inhibition model which may be due to multiple overlapping ligand-kringle interactions or tranexamic-fibrin interactions. Experiments using combinations of aprotinin and tranexamic acid in the clot lysis system confirm the complementary nature of inhibitory mechanisms and suggest a slight synergism. These results support the idea that aprotinin inhibition of plasmin is a primary mode of action in vivo, and suggest that combination therapy of aprotinin with tranexamic acid might be more effective than either inhibitor alone.