Original article

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Platelet concentrates in platelet additive solutions generate less complement activation products during storage than platelets stored in plasma

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Key words: platelet transfusion, platelet storage, complement activation products, nucleosomes, HMGB1
Publication Date: 2022-03-07

Abstract

Background - Platelet transfusions can be associated with adverse reactions, such as febrile non-haemolytic transfusion reaction (FNHTR). It has been suggested that damage-associated molecular patterns (DAMP) and complement play a role in FNHTR. This study investigated the nature of DAMPs and complement activation products contained in platelet concentrates during storage, with a specific focus on different platelet storage solutions.
Materials and methods - Buffy coats (BC) from healthy donors were pooled (15 BC per pool) and divided into three groups of the same volume. After addition of different storage solutions (plasma, platelet additive solutions [PAS]-C or PAS-E; n=6 for each group), BC pools were processed to platelet concentrates (PC). Leukoreduced PCs were stored on a shaking bed at 20-24°C and sampled on days 1, 2, 6 and 8 after collection for selected quality parameters: platelet activation, DAMPs (High Mobility Group Box 1 [HMGB1],
nucleosomes), and complement activation products.
Results - During storage, equal levels of free nucleosomes and increasing concentrations of HMGB1 were present in all groups. Complement activation was observed in all PC. However, by day 8, the use of PAS had reduced C3b/c levels by approximately 90% and C4b/c levels by approximately 65%.
Discussion - Nucleosomes and HMGB1 were present in PCs prepared in plasma and PAS. Complement was activated during storage of platelets in plasma and in PAS. The use of PAS is associated with a lower amount of complement activation products due to the dilution of plasma by PAS . Therefore, PC in PAS have less complement activation products than platelets stored in plasma. These proinflammatory mediators in PC might induce FNHTR.

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Authors

Yasmin E.S. de Wit - Department Immunopathology Sanquin Blood Supply, Amsterdam, the Netherlands

Richard Vlaar - Department Blood Cell Research Sanquin Blood Supply, Amsterdam, the Netherlands

Eric Gouwerok - Department Blood Cell Research Sanquin Blood Supply, Amsterdam, the Netherlands

Hind Hamzeh-Cognasse - SAINBIOSE, INSERM, U1059, University of Lyon, Université Jean-Monnet-Saint-Etienne, France

Gerard van Mierlo - Department Immunopathology Sanquin Blood Supply, Amsterdam, the Netherlands

Ingrid Bulder - Department Immunopathology Sanquin Blood Supply, Amsterdam, the Netherlands

Johan W.M. Lagerberg - Department Blood Cell Research Sanquin Blood Supply, Amsterdam, the Netherlands; Department Product and Process Development, Sanquin Blood Supply, Amsterdam, the Netherlands

Dirk de Korte - Department Blood Cell Research Sanquin Blood Supply, Amsterdam, the Netherlands; Department Product and Process Development, Sanquin Blood Supply, Amsterdam, the Netherlands

Fabrice Cognasse - SAINBIOSE, INSERM, U1059, University of Lyon, Université Jean-Monnet-Saint-Etienne, France; Etablissement Français du Sang Auvergne-Rhône-Alpes, Saint-Étienne, France;

Anja ten Brinke - Department Immunopathology Sanquin Blood Supply, Amsterdam, the Netherlands

Sacha S. Zeerleder - Department Immunopathology Sanquin Blood Supply, Amsterdam, the Netherlands; 6Department Hematology and Central Hematology Laboratory, Inselspital, Bern University Hospital, University of Bern and Department for BioMedical Research, University of Bern, Bern, Switzerland

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