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Autologous cryopreserved platelets to overcome immune platelet refractoriness

P latelet refractoriness (PR) describes a clinical state in which the anticipated increase in platelet (PLT) count from a PLT transfusion is not achieved. The precise definition of PR varies, but it is widely accepted as an inappropriately low PLT increment usually determined by the 1-hour corrected count increment, after repeated PLT transfusion of fresh, ABO-compatible PLT concentrates. There are both nonimmune and immune causes for PR and often the etiology of PR is multifactorial. Alloimmunization to Class I HLA expressed on PLTs is the most important cause of immune PR after repeated PLT transfusions and was present in a variable frequency between 7 and 55% before the routine use of leukoreduction, depending on study, patient population, and number and type of transfusions. Because alloimmunization to HLA antigens accounts for the majority of immune causes of PR, PLTs can be selected on the basis of HLA matching. However, for broadly alloimmunized persistently refractory patients, finding an appropriate number of HLA-matched or HLAcompatible PLTs may be extremely difficult, and several treatments have been used with limited success to overcome immune PR including intravenous immune globulin; plasma exchange or protein A adsorption; rituximab, bortezomib, or other immunosuppressive agents; and massive prophylactic PLT transfusion to adsorb antibody. Adjunctive therapies include the use of antifibrinolytic agents, a slow near-continuous infusion of otherwise incompatible PLT products, and increasing the hematocrit to 30% or higher. Additional options include the use of recombinant Factor VIIa, thrombopoietic agents, and autologous cryopreserved PLTs (CPPs). In this issue of TRANSFUSION, Gerber and colleagues report their experience in Switzerland using autologous CPPs to support patients with thrombocytopenia with immune PR who had few or no available HLA-matched PLT donors. In contrast to the original cryopreservation method, Gerber and colleagues used 10% dimethyl sulfoxide (DMSO) and omitted the centrifugation step before freezing, as well as the washing and centrifugation steps after thawing. Therefore, the technical complexity was reduced and the transfusion process was shortened. The Swiss authors performed a retrospective study and they reported the results of their PLT cryopreservation program from 2002 to 2012. In 11 years, the authors collected autologous PLTs in 14 patients and transfused 40 autologous CPPs to nine patients. Three points of this study deserve to be pointed out. First, in addition to clinical data, the authors presented in vitro data from CPPs that were not transfused, giving readers a general overview of the process of cryopreservation of PLTs. Second, from the in vitro data, the authors concluded that cryopreservation of PLTs led to activation of a proportion of PLTs, but still a relevant fraction of PLTs preserved full functionality. A similar conclusion was also supported by data obtained in our laboratory. Using perfusion studies, we showed that CPPs retained adhesive and aggregating properties and supported a moderate increase in the rate of thrombin generation and clot formation while presenting no evidence of stimulating a hypercoagulable state. Finally, from the presented in vivo data, the present study adds more knowledge regarding the transfusion of autologous CPPs in the setting of thrombocytopenia in patients with hematologic diseases. Gerber and coworkers reported that the median 1-hour count increment was significantly higher with autologous CPPs when compared to ABO-matched, HLA-unselected PLTs (0 3 10 and 6 3 10/L; p < 0.001). In an excellent review performed by Slichter and coworkers, the authors collected data from 13 studies with the transfusion of 1215 autologous CPPs to 356 patients. Three studies reported fresh transfusion data along with autologous CPP data suggesting that responses to cryopreserved autologous PLTs and allogeneic PLTs are not different from 5to 7-day 228C-stored PLTs. Taken together, the data from the Slichter review and data from the current study, it can be concluded that CPPs can provide effective clinical hemostasis without serious adverse events. Although the reported history of CPPs is full of in vitro data showing a PLT phenotype of moderate activation, clinical data suggest that CPPs in DMSO may prevent hemorrhagic events in thrombocytopenic patients with similar efficacy to that of standard PLTs, and no cases of thromboembolic complications have been reported. In summary, the report by Gerber and colleagues in this issue of TRANSFUSION provides another compelling study with supporting in vivo and in vitro data showing that the use of autologous CPPs to doi:10.1111/trf.13758