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Platelet prothrombin converting activity in hereditary disorders of platelet function
Author(s) -
Bevers E. M.,
Comfurius P.,
Nieuwenhuis H. K.,
LEVYTOLEDANO S.,
Enouf J.,
Belluci S.,
Caen J. P.,
Zwaal R. F. A.
Publication year - 1986
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1986.tb05557.x
Subject(s) - prothrombinase , thrombasthenia , platelet , phosphatidylserine , coagulation , bernard–soulier syndrome , chemistry , thromboplastin , medicine , endocrinology , clot retraction , immunology , thrombin , biochemistry , platelet aggregation , phospholipid , membrane
Summary. Prothrombinase activities of platelets have been measured in diluted platelet‐rich plasma using a chromogenic substrate assay and purified coagulation factors. No abnormalities in prothrombinase activities were found for platelets from patients with storage pool disease (dense‐body deficiency), grey platelet syndrome, and Glanzmann's thrombasthenia. It is concluded that neither release of dense bodies and a‐granules nor aggregation of platelets are essential prerequisites for exposure of a procoagulant surface. Platelets from patients with Bernard‐Soulier syndrome, however, have approximately 10‐fold higher prothrombinase activities in the non‐stimulated form than normal non‐stimulated platelets. The increased procoagulant activity cannot be completely ascribed to an increase in platelet size. It is suggested that the increased prothrombinase activity reflects an increased exposure of phosphatidylserine at the outer surface of non‐stimulated Bernard‐Soulier platelets, earlier described byPerretetaI(1983).