Both PCTs significantly reduce thrombus formation rate but by different biochemical mechanisms.

Pathogen inactivation (PI) for platelet concentrates (PC) is a fairly recent development in transfusion medicine that is intended to decrease infectious disease transmission from the donor to the receiving patient. Effective inactivation of viruses, bacteria and eukaryotic parasites adds a layer of safety, protecting the blood supply against customary and emerging pathogens. Three PI methods have been described for platelets. These are based on photochemical damage of nucleic acids which prevents replication of most infectious pathogens and contaminating donor leukocytes. Because platelets do not replicate, the collateral damage to platelet function is considered low to non-existing. This is disputable however because photochemistry is not specific for nucleic acids and significantly affects platelet biomolecules as well. The impact of these biomolecular changes on platelet function and hemostasis is not well understood, but is increasingly being studied. The results of these studies can help explain current and future clinical observations with PI platelets, including the impact on transfusion yield and bleeding. This review summarizes the biomolecular effects of PI treatment on platelets. We conclude that despite a comparable principle of photochemical inactivation, all three methods affect platelets in different ways. This knowledge can help blood banks and transfusion specialists to guide their choice when considering the implementation or clinical use of PI treated platelets.

BACKGROUND Ultraviolet (UV) light illumination in the presence of exogenously added photosensitizers has been used to inactivate pathogens in platelet (PLT) concentrates for some time. The THERAFLEX UV‐C system, however, illuminates PLT concentrates with UV‐C light without additional photoactive compounds. In this study residual PLT function is measured in a comprehensive paired analysis of UV‐C–treated, gamma‐irradiated, and untreated control PLT concentrates. STUDY DESIGN AND METHODS: A pool‐and‐split design was used with buffy coat–derived PLT concentrates in 65% SSP+ additive solution. Thrombus formation kinetics in microfluidic flow chambers onto immobilized collagen was investigated with real‐time video microscopy. PLT aggregation, membrane markers, and cellular metabolism were determined concurrently. RESULTS Compared to gamma‐treated and untreated controls, UV‐C treatment significantly affected thrombus formation rates on Days 5 and 7, not Day 2. PLT degranulation (P‐selectin) and PLT apoptosis (annexin V binding) was slightly but significantly increased from Day 2 on. UV‐C treatment moreover induced integrin αIIbβ3 conformational changes reminiscent of activation. However, subsequent integrin activation by either PAR1‐activating hexapeptide (PAR1AP) or convulxin was unaffected. This was confirmed by PLT aggregation studies induced with collagen, PAR1AP, and ristocetin at two different agonist concentrations. Finally, UV‐C slightly increased lactic acid production rates, resulting in significantly decreased pH on Days 5 and 7, but never dropped below 7.2. CONCLUSION UV‐C pathogen inactivation treatment slightly but significantly increases PLT activation markers but does not profoundly influence activatability nor aggregation. The treatment does, however, attenuate thrombus formation kinetics in vitro in microfluidic flow chambers, especially after storage.

RF-PRT of single plasma units generates reactive oxygen species that adversely affect biomolecular integrity of relevant plasma constituents, a side-effect, which can be bypassed by applying hypoxic conditions during the pathogen inactivation process.

Edited by George CarmanPsoralen and ultraviolet A light (PUVA) are used to kill pathogens in blood products and as a treatment of aberrant cell proliferation in dermatitis, cutaneous T-cell lymphoma, and graftversus-host disease. DNA damage is well described, but the direct effects of PUVA on cell signal transduction are poorly understood. Because platelets are anucleate and contain archetypal signal transduction machinery, they are ideally suited to address this. Lipidomics on platelet membrane extracts showed that psoralen forms adducts with unsaturated carbon bonds of fatty acyls in all major phospholipid classes after PUVA.