Hemostatic function of buffy coat platelets in additive solution treated with pathogen reduction technology.
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.
Ostrowski
Sisse R
SR
Section for Transfusion Medicine, Capital Region Blood Bank, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. sisse.ostrowski@gmail.com
Bochsen
Louise
L
Windeløv
Nis A
NA
Salado-Jimena
José A
JA
Reynaerts
Inge
I
Goodrich
Raymond P
RP
Johansson
Pär I
PI
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
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