• Sisse R Ostrowski, Louise Bochsen, José A Salado-Jimena, Henrik Ullum, Inge Reynaerts, Raymond P Goodrich, and Pär I Johansson.
• Section for Transfusion Medicine, Capital Region Blood Bank, Department of Clinical Immunology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. sisse.ostrowski@gmail.com
• Transfusion. 2010 Oct 1;50(10):2210-9.

BackgroundPathogen 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 MethodsIn 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.ResultsPRT 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.ConclusionPRT 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.© 2010 American Association of Blood Banks.

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