Non‐polar lipids accumulate during storage of transfusion products and do not contribute to the onset of transfusion‐related acute lung injury

Background and Objectives The accumulation of non‐polar lipids arachidonic acid, 5‐hydroxyeicosatetraenoic acid (HETE), 12‐HETE and 15‐HETE during storage of transfusion products may play a role in the onset of transfusion‐related acute lung injury (TRALI), a syndrome of respiratory distress after transfusion. Materials and Methods We investigated non‐polar lipid accumulation in red blood cells (RBCs) stored for 42 days, plasma stored for 7 days at either 4 or 20°C and platelet (PLT) transfusion products stored for 7 days. Furthermore, we investigated whether transfusion of RBCs with increased levels of non‐polar lipids induces TRALI in a ‘two‐hit’ human volunteer model. All products were produced following Dutch Blood Bank protocols and are according to European standards. Non‐polar lipids were measured with high‐performance liquid chromotography followed by mass spectrometry. Results All non‐polar lipids increased in RBCs after 21 days of storage compared to baseline. The non‐polar lipid concentration in plasma increased significantly, and the increase was even more pronounced in products stored at 20°C. In platelets, baseline levels of 5‐HETE and 15‐HETE were higher than in RBCs or plasma. However, the non‐polar lipids did not change significantly during storage of PLT products. Infusion of RBCs with increased levels of non‐polar lipids did not induce TRALI in LPS‐primed human volunteers. Conclusion We conclude that non‐polar lipids accumulate in RBC and plasma transfusion products and that accumulation is temperature dependent. Accumulation of non‐polar lipids does not appear to explain the onset of TRALI (Dutch Trial Register – NTR4455).