title: Hemostatic function of buffy coat platelets in additive solution treated with pathogen reduction technology.
abstract: BACKGROUND
  Pathogen reduction technologies (PRTs) may influence the hemostatic potential of stored platelet (PLT) concentrates. To investigate this, buffy coat PLTs (BCPs) stored in PLT additive solution (SSP+) with or without Mirasol PRT treatment (CaridianBCT Biotechnologies) were compared by functional hemostatic assays.
  
  
  METHODS
  We performed in vitro comparison of PRT (PRT-BCP) and control pooled-and-split BCPs (CON-BCP) after 2, 3, 6, 7, and 8 days' storage. Hemostatic function was evaluated with thrombelastography (TEG) and impedance aggregometry (Multiplate), the latter also in a sample matrix (Day 2) with or without addition of red blood cells (RBCs), control plasma, and/or PRT-treated plasma.
  
  
  RESULTS
  PRT treatment of 8-day-stored BCPs influenced clot formation (TEG) minimally, with reductions in maximum clot strength (maximum amplitude, p = 0.014) but unchanged initial fibrin formation (R), clot growth rate (α), and fibrinolysis resistance. In the absence of RBCs and plasma, PRT impaired aggregation (Multiplate) in stored BCPs, with reduced aggregation against thrombin receptor activating peptide-6 (p < 0.001), collagen (p = 0.014), adenosine 5'-diphosphate (p = 0.007), and arachidonic acid (p = 0.070). Addition of RBCs and PRT-treated or untreated plasma to PRT-BCP and CON-BCP, respectively, enhanced aggregation in both groups.
  
  
  CONCLUSIONS
  Mirasol PRT treatment of BCPs had a minimal influence on clot formation, whereas aggregation in the absence of RBCs and plasma was significantly reduced. Addition of RBCs and plasma increased agonist-induced responses resulting in comparable aggregation between PRT-BCP and CON-BCP. The clinical relevance for PLT function in vivo of these findings will be investigated in a clinical trial.
authors: Section for Transfusion Medicine, Capital Region Blood Bank, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. sisse.ostrowski@gmail.com
authors: Sisse R
authors: SR
authors: Ostrowski
authors: Louise
authors: L
authors: Bochsen
authors: Nis A
authors: NA
authors: Windeløv
authors: José A
authors: JA
authors: Salado-Jimena
authors: Inge
authors: I
authors: Reynaerts
authors: Raymond P
authors: RP
authors: Goodrich
authors: Pär I
authors: PI
authors: Johansson
mesh_terms: D000244:Adenosine Diphosphate / Q000494:pharmacology; D016718:Arachidonic Acid / Q000494:pharmacology; D001792:Blood Platelets / Q000502:physiology*; D001793:Blood Preservation / Q000379:methods*; D058731:Blood Safety / Q000379:methods*; D017848:Blood-Borne Pathogens / Q000187:drug effects / Q000528:radiation effects; D002498:Centrifugation; D003094:Collagen / Q000494:pharmacology; D005337:Fibrin / Q000096:biosynthesis; D006487:Hemostasis; D006801:Humans; D010446:Peptide Fragments / Q000494:pharmacology; D019999:Pharmaceutical Solutions / Q000494:pharmacology*; D010974:Platelet Aggregation / Q000187:drug effects; D010979:Platelet Function Tests; D017713:Platelet Transfusion; D011897:Random Allocation; D012256:Riboflavin / Q000494:pharmacology; D013916:Thrombelastography; D010959:Tissue Plasminogen Activator / Q000494:pharmacology; D014466:Ultraviolet Rays
chemical_list: D010446:Peptide Fragments; D019999:Pharmaceutical Solutions; C082835:thrombin receptor peptide (42-47); D016718:Arachidonic Acid; D000244:Adenosine Diphosphate; D005337:Fibrin; D003094:Collagen; D010959:Tissue Plasminogen Activator; D012256:Riboflavin