BACKGROUND: Pathogen reduction technologies (PRTs) may induce storage lesion in platelet (PLT) concentrates. To investigate this, buffy coat PLTs (BCPs) in PLT additive solution (AS; SSP+) with or without Mirasol PRT (CaridianBCT Biotechnologies) were assessed by quality control tests and four-color flow cytometry. STUDY DESIGN AND METHODS: In vitro comparison of PRT and control pooled-and-split BCPs after 2, 3, 6, 7, and 8 days of storage was made. PLT concentration, count per unit, swirl, metabolism, activation (CD62P, PAC1, CD42b/GPIb, CD63, CD40L/CD154, CD40, annexin V), and microparticle, sCD40L, and sCD62P release were evaluated. RESULTS: PRT induced a minor initial PLT loss (Day 2 [mean±SD], 302×10(9) ±44×10(9) PLTs/unit vs. 325× 10(9) ±46×10(9) PLTs/unit; p<0.001) but the decline was comparable to control BCP. Swirling was comparable and declined with similar rates in PRT-treated and control BCPs during storage. PRT enhanced PLT metabolism and activation, evidenced by lower pH(22) ; increased glucose consumption and lactate production rates (p<0.01); early increases in CD62P-, PAC1-, CD63-, CD40L-, CD40-, and annexin V-positive PLTs; reduced GPIb expression; and enhanced release of PLT-derived MPs and sCD40L (all p<0.05). CD62P and PAC1 expression changed with different kinetics during storage and varying GPIb expression was displayed within the CD62P/PAC1-positive PLT subsets. CONCLUSION: PRT treatment of BCP in AS induced a minor initial PLT loss and enhanced metabolism and PLT activation. The clinical relevance for PLT function in vivo of these findings will be investigated in a clinical trial.
BACKGROUND: Pathogen reduction technologies (PRTs) may induce storage lesion in platelet (PLT) concentrates. To investigate this, buffy coat PLTs (BCPs) in PLT additive solution (AS; SSP+) with or without Mirasol PRT (CaridianBCT Biotechnologies) were assessed by quality control tests and four-color flow cytometry. STUDY DESIGN AND METHODS: In vitro comparison of PRT and control pooled-and-split BCPs after 2, 3, 6, 7, and 8 days of storage was made. PLT concentration, count per unit, swirl, metabolism, activation (CD62P, PAC1, CD42b/GPIb, CD63, CD40L/CD154, CD40, annexin V), and microparticle, sCD40L, and sCD62P release were evaluated. RESULTS: PRT induced a minor initial PLT loss (Day 2 [mean±SD], 302×10(9) ±44×10(9) PLTs/unit vs. 325× 10(9) ±46×10(9) PLTs/unit; p<0.001) but the decline was comparable to control BCP. Swirling was comparable and declined with similar rates in PRT-treated and control BCPs during storage. PRT enhanced PLT metabolism and activation, evidenced by lower pH(22) ; increased glucose consumption and lactate production rates (p<0.01); early increases in CD62P-, PAC1-, CD63-, CD40L-, CD40-, and annexin V-positive PLTs; reduced GPIb expression; and enhanced release of PLT-derived MPs and sCD40L (all p<0.05). CD62P and PAC1 expression changed with different kinetics during storage and varying GPIb expression was displayed within the CD62P/PAC1-positive PLT subsets. CONCLUSION: PRT treatment of BCP in AS induced a minor initial PLT loss and enhanced metabolism and PLT activation. The clinical relevance for PLT function in vivo of these findings will be investigated in a clinical trial.