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In vitro cell quality of buffy coat platelets in additive solution treated with pathogen reduction technology.
Ostrowski, Sisse R. 1; Bochsen, Louise 1; Salado-Jimena, Jose A. 1; Ullum, Henrik 1; Reynaerts, Inge 1; Goodrich, Raymond P. 1; Johansson, Par I. 1
[Miscellaneous Article] Transfusion. 50(10):2210-2219, October 2010.

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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 x 109 /- 44 x 109 PLTs/unit vs. 325 x 109 /- 46 x 109 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 pH22; 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.