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 < or = 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 < or = 0.002), among which M yielded higher values than I (p < or = 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 > or = 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.
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 < or = 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 < or = 0.002), among which M yielded higher values than I (p < or = 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 > or = 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.