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Platelet function assessed by shear‐induced deposition of split triple‐dose apheresis concentrates treated with pathogen reduction technologies
Author(s) -
Picker Susanne M.,
Schneider Volker,
Gathof Birgit S.
Publication year - 2009
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.1537-2995.2009.02092.x
Subject(s) - apheresis , platelet , pathogen , reduction (mathematics) , medicine , function (biology) , chemistry , immunology , biology , microbiology and biotechnology , mathematics , geometry
BACKGROUND: Pathogen inactivation/reduction technology (PRT) may alter quality of stored platelet (PLT) concentrates (PCs). Therefore, PLT adhesion and aggregation should be studied before transfusion of PRT‐treated PLTs. STUDY DESIGN AND METHODS: A three‐arm in vitro study on triple‐dose apheresis PCs (n = 9) was conducted. Split single units were designated to PRT treatment with either a riboflavin (M)‐ or a psoralen (I)‐based technique and compared to untreated controls (C). Samples were taken on Days 0, 1, 5, 7, and 8 to assess PLT function via a cone and plate(let) analyzer, flow cytometric P‐selectin expression, and turbidometric aggregation response to thrombin receptor–activating peptide 6 (TRAP‐6). RESULTS: P‐selectin expression increased and TRAP‐6–inducible expression decreased steadily in all units until reaching a plateau on Day 5 of storage. PRT‐treated units demonstrated significant (p ≤ 0.008) differences to C units due to a more pronounced upregulation in P‐selectin expression after PRT treatment. The same was true for TRAP‐6 after Day 5 of storage. C units were significantly superior over PRT‐treated units (p ≤ 0.002), among which M yielded higher values than I (p ≤ 0.008). Although M demonstrated increased shear‐induced PLT deposition that remained stable during storage (p = 0.082), surface coverage significantly declined in C (p = 0.047) and especially in I (p = 0.003), but differences between M, C, and I did not reach significance. All units exhibited a slight increase in aggregate size that remained comparable throughout storage (p ≥ 0.141). CONCLUSIONS: Irrespective of storage‐related changes in PLT activation and turbidometric aggregation response, riboflavin‐based PRT seemed to benefit shear‐induced PLT adhesion. The impact of this finding for PLT function and thrombogenesis in vivo must await clinical evaluation.