(P-CB-6) Both UVB light and riboflavin contribute to platelet processing and storage lesions

Pathogen reduction technologies serve as an additional barrier for improving blood safety. However, they also contribute to platelet storage lesion. This study aimed to determine the individual contribution of UVB light and riboflavin to the platelet processing and storage lesion markers and analyze whether their combination use results in potentiation or attenuation.

Study

Design/Methods:

A four-arm experimental study was conducted using 10 plateletpheresis procedures (Trima Accel, Terumo BCT). Within the first four hours post-donation, the platelets from each procedure were divided into four 150 mL aliquots and assigned to the groups: saline (S), saline+UVB (SUV), riboflavin (R), and riboflavin+UVB (RUV) (Mirasol, Terumo BCT). Samples were aseptically taken before and immediately after each treatment and on days 3, 5, 7, and 9 of storage at 25°C under continuous agitation, for determination of platelet count and mean platelet volume (MPV) (BS30, Mindray), pH, aggregometry with ADP 20µM, epinephrine 300µM, collagen 10µg/mL, ristocetin 0.75mg/mL, TRAP-6 20µM, and hypotonic shock response (HSR) after four minutes (AggRAM, Helena), swirling and aggregates. Cultures for aerobic and anaerobic bacteria were performed 24 hours after each treatment. Results were expressed as mean±standard deviation (SD), and comparisons between treatments for each time were made using a generalized linear model with the Geisser-Greenhouse correction and Tukey's multiple comparisons test (p< 0.05). The statistical software GraphPad Prism v8.0 was used.

Results/Findings:

A decrease in pH was observed in the groups treated with R and RUV compared with saline. The aggregation response (area under curve, AUC) to ADP and epinephrine increased after treatment with SUV compared to S, after which it decreased in all groups and was lower on the third day in RUV compared to R. The responses to ristocetin, TRAP-6, and recovery from hypotonic shock were lower with UVB and R treatment than saline, and the effect was even higher with RUV. Swirling was reduced, and aggregates were increased in the RUV group compared to saline (Table 1). There were no differences in MPV or response to collagen. All cultures were negative after 10 days of incubation.

Conclusions:

Both UVB light and the addition of riboflavin contribute to platelet processing and storage lesions. In this model, aggregometry with ristocetin, TRAP-6, and recovery from osmotic shock were the most sensitive indicators of platelet injury. They showed a synergistic deleterious effect of the combination treatment with riboflavin and UVB. It is important to correlate these markers with post-transfusion survival and efficacy.