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In‐vivo platelet activation correlates with red cell anionic phospholipid exposure in patients with β‐thalassaemia major
Author(s) -
Ruf Andreas,
Pick Marjorie,
Deutsch Varda,
Patscheke Heinrich,
Goldfarb Ada,
Rachmilewitz Eliezer A.,
Guillin Marie C.,
Eldor Amiram
Publication year - 1997
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 - 10.1046/j.1365-2141.1997.1502965.x
Subject(s) - phosphatidylserine , platelet , platelet activation , annexin , cd63 , flow cytometry , in vivo , red blood cell , red cell , thrombin , annexin a5 , p selectin , chemistry , medicine , microbiology and biotechnology , endocrinology , immunology , phospholipid , biology , biochemistry , membrane , gene , microrna , microvesicles
Several clinical and laboratory findings suggest the presence of a chronic hypercoagulable state in patients with β‐thalassaemia major (TM). We have previously shown that isolated TM red blood cells (RBC) strongly enhance prothrombin activation, suggesting an increased membrane exposure of procoagulant phospholipids (i.e. phosphatidylserine). In this study we quantitated the procoagulant activity of RBC in TM and thalassaemia intermedia (TI) patients. We also determined the fraction of activated platelets expressing p‐selectin (CD62p) or CD63 in these subjects. Both assays were performed by dual‐colour flow cytometry. A significantly ( P < 0.01) higher fraction of FITC‐annexin V‐labelled RBC was found in TM and TI patients, compared to the controls. A highly significant correlation ( P < 0.001) was found in TM patients between the number of RBC‐bound annexin V molecules and the fraction of CD62p (p‐selectin) or CD63‐positive platelets. This association between annexin V binding to TM RBC and the expression of platelet activation markers was also found in individual TM patients over time. Thus, the procoagulant surface of TM RBC may accelarate thrombin generation in vivo which, in turn, triggers platelet activation.