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Role of platelet surface glycoprotein Ibα and P‐selectin in the clearance of transfused platelet concentrates
Author(s) -
Leytin Valery,
Allen David J.,
Gwozdz Adam,
Garvey Bernadette,
Freedman John
Publication year - 2004
Publication title -
transfusion
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.045
H-Index - 132
eISSN - 1537-2995
pISSN - 0041-1132
DOI - 10.1111/j.1537-2995.2004.04042.x
Subject(s) - platelet , in vivo , flow cytometry , in vitro , chemistry , platelet activation , p selectin , immunology , andrology , microbiology and biotechnology , medicine , biology , biochemistry
BACKGROUND: Role of P‐selectin (CD62) and glycoprotein (GP) Ibα in posttransfusion clearance of platelet concentrates (PCs) is unclear. STUDY DESIGN AND METHODS: Platelet (PLT) activation in vitro was determined by flow cytometry using anti‐CD62 and anti‐GPIbα. PC clearance in vivo was evaluated in an animal model using rabbits with an inhibited reticuloendothelial system, as measured by 0.5‐hour (R 0.5 ), 24‐hour (R 24 ), and total (R ∑ ) PLT recoveries, and survival time (ST). Correlations were analyzed between in vitro assays of PLT activation and in vivo clearance of conventional (Days 2‐5), outdated (Days 7‐8), and refrigerated PCs. RESULTS: Binding of anti‐CD62 to the PLT surface was significantly increased and of anti‐GPIbα decreased in outdated and refrigerated PCs compared to conventional PCs. Negative correlation was observed between in vitro anti‐CD62 binding and the fast (R 0.5 ) PLT clearance, but not with delayed (R 24 and ST) clearance. In contrast, anti‐GPIbα binding showed positive correlations with delayed but not with fast PLT clearance. Overall (R ∑ ) clearance correlated better with anti‐GPIbα than with anti‐CD62 binding. CD62 density on the PLT surface was decreased after PC transfusion, whereas GPIbα density remained unchanged. CONCLUSION: These data suggest that CD62 exposure on the PLT surface during PC storage triggers fast CD62‐mediated PC clearance, whereas in vitro GPIbα changes are involved in delayed GPIbα‐mediated PC clearance.