Inhibition of lysophosphatidic acid increase by prestorage whole blood leukoreduction in autologous CPDA‐1 whole blood

Abstract

Lysophosphatidylcholine (LPC) has been implicated in the onset of transfusion-related acute lung injury (TRALI). In plasma, LPC is converted to lysophosphatidic acid (LPA) by autotaxin (ATX). The effect of leukoreduction in the accumulation of these bioactive lipids and ATX in human autologous blood has not been fully investigated. The accumulation of choline-containing phospholipids (LPC, sphingomyelin [SM], and phosphatidylcholine [PC]), LPA, and ATX during the storage of autologous blood and the changes caused by leukoreduction were investigated. A total of 26 orthopedic patients were enrolled. Autologous blood was collected as whole blood and, after leukoreduction, preserved refrigerated until use. Prestorage leukoreduced (LR) and non-LR autologous blood samples were analyzed. The time-dependent changes and the effect of the filtration were compared. A time-dependent and significant increase in the levels of LPA was observed in both non-LR and LR samples. The concentration of LPA was significantly reduced in LR compared to non-LR samples. The concentration of LPC was higher in LR compared to non-LR samples. The levels of PC, SM, and ATX were not affected by either the storage period or the leukoreduction. Leukoreduction of autologous whole blood effectively reduced the accumulation of LPA. On the other hand, prestorage leukoreduction resulted in an increased concentration of LPC, without significantly affecting ATX. Further studies are necessary to confirm the role of LPA in the pathogenesis of adverse effects of blood transfusion, especially TRALI.