The effect of red blood cell transfusion on platelet function in critically ill patients

Autor: Rienk Nieuwland, Marleen Straat, Maike E. van Hezel, Michael W.T. Tanck, Nicole P. Juffermans, Boukje M. Beuger, Robin van Bruggen, Margit Boshuizen, Iris M. De Cuyper, Jaap Jan Zwaginga, Lisa van Manen, Dirk de Korte
Přispěvatelé: Graduate School, ACS - Heart failure & arrhythmias, AII - Inflammatory diseases, Laboratory for Experimental Clinical Chemistry, ACS - Microcirculation, Epidemiology and Data Science, APH - Methodology, Intensive Care Medicine, Landsteiner Laboratory
Rok vydání: 2019
Předmět:
Zdroj: Thrombosis research, 184, 115-121. Elsevier Limited
Thrombosis Research, 184, 115-121
ISSN: 0049-3848
Popis: Introduction Red blood cell (RBC) transfusion is associated with an increased risk of pro-thrombotic events, but the underlying mechanism is poorly understood. We hypothesized that RBC transfusion modulates platelet activity in critically ill patients with and without sepsis. Methods In a prospective cohort study, 37 critically ill patients receiving a single RBC unit to correct for anemia were sampled prior to and 1 h after transfusion. Platelet exposure of P-selectin, CD63 and binding of PAC-1 as well as formation of platelet-leukocyte complexes were measured by flow cytometry. The ability of plasma from critically ill patients to induce ex vivo platelet aggregation was assessed by flow cytometry after incubation with platelets from a healthy donor. Results RBC transfusion neither triggered the expression of platelet activation markers nor the formation of platelet-leukocyte complexes. Plasma from critically ill patients induced more spontaneous platelet aggregation prior to RBC transfusion compared to healthy controls, which was further augmented following RBC transfusion. Also collagen-induced platelet aggregation was already increased prior to RBC transfusion compared to healthy controls, and this response was unaffected by RBC transfusion. In contrast, ristocetin-induced platelet agglutination was decreased when compared to controls, suggesting impaired vWF-dependent platelet agglutination, even in the presence of high vWF levels. Following RBC transfusion, ristocetin-induced platelet agglutination further decreased. There were no differences between septic and non-septic recipients in all assays. Conclusion Ex vivo platelet aggregation is disturbed in the critically ill. Transfusion of a RBC unit may further increase the spontaneous platelet aggregatory response.
Databáze: OpenAIRE