Official Journal of the British Blood Transfusion Society Transfusion Medicine | LETTER TO THE EDITOR Risk of Rh (D) alloimmunisation after Rh (D) positive platelet transfusions in patients undergoing haematopoietic stem cell transplantation Dear Sir, Transfusion of Rh (D) positive blood products to Rh (D) neg- ative patients is not a rare practice in blood banks and depends largely on Rh (D) negative blood products availability. Platelets (PLTs) do not carry Rh antigens but PLT concentrates can be contaminated by red blood cells, mainly if they are obtained from whole-blood by bufy coat system (Bartley et al, 2009). Alloim- munisation rates against D and other Rh antigens caused by PLT transfusions is variable and ranges from 0 to 18.7% according to published studies (Shaz & Hillyer, 2011). To our knowledge there is no specifc data of Rh (D) alloimmunisation in patients under- going haematopoietic stem cell transplantation (HSCT) receiv- ing Rh (D) positive PLT transfusions. Tese patients are severely immunocompromised, so is expected there would be a trend to lower rate of alloimmunisation. We retrospectively reviewed the clinical and transfusion records of patients who underwent HSCT in our hospital for a 14 year-period (2000–2013). Platelet concentrates were pre- pared from whole-blood donations (WBD) according to the bufy coat method by the Regional Transfusion Centre. Only a small percentage of platelets (7%) were from a single donor apheresis. Te antibody screen test (IAT) to detect anti-D was performed in the automated system ORTHO Autovue Innova using the gel test (Ortho Clinical Diagnostics, High Wycombe, UK). Sera of patients with positive tests were tested for speci- fcity using panels of RBC with known antigens (Ortho Clinical and Diagnostics, Diamed and Makropanel). Inclusion criteria were as follows: to have a negative IAT before transplantation and to have performed another IAT at least 14days afer hos- pital discharge, to receive HSCT from Rh (D) negative donors. Tus, 47 patients were available for analysis: 27 men and 20 female, median age 50.6 years (range: 22·8–69·0), 29 patients underwent autologous HSCT and 18 received and allogeneic HSCT. Te 47 patients analysed received a median of 3 Rh (D) positive PLT transfusions (range: 1–49). Two patients both diagnosed of multiple myeloma who underwent autologous HSCT developed anti-D (4·2%). One Correspondence: Pilar Solves, Transfusion Service, Hematology Unit, Blood Bank, Hospital Universitari I Politècnic La Fe, Avda de Fernando Abril Martorell, 106, Valencia 46026, Spain. Tel.: 00 34 96 341 12 99; fax: 00 34 96 124 62 01; e-mail: solves_pil@gva.es patient developed anti-D + anti-E 11 days afer one Rh (D) positive WBD PTL transfusion. Tis patient was a woman and a secondary immunologic response can not be excluded. Another patient developed anti-D 10 months afer transfusion of nine Rh (D) positive platelet concentrates (six WBD and three apheresis PLTs). Cid et al. (2002) have communicated absence of alloimmu- nisation in a small series of 22 Rh (D) negative haematologic patients transfused with Rh (D) positive PLTs. However, in a larger study including 1014 immunocompetent and immuno- suppressed Rh (D) negative patients, these authors have found 3·8% patients developing anti-D afer Rh (D) positive PLT trans- fusions (Cid et al., 2011). Our analysis show similar results also in immunosuppressed patients undergoing HSCT. On the other hand, in a recent study O’Brien et al. (2014) have reported the lack of immunisation in 130 Rh (D) negative patients trans- fused with Rh (D) positive apheresis platelets. Te type of trans- fused PLTs seems to be key to explain the diferences among studies: whole-blood-derived platelets have a greater quantity of red blood cells and therefore higher risk of alloimmunisation (O’Brien et al., 2014) as compared with apheresis platelets (Shaz & Hillyer, 2011). In conclusion, our results show that transfusion of WBD Rh (D) positive PLTs produce anti-D alloimmunisation even in patients that are severe immunocompromised, as those receiving an HSCT. ACKNOWLEDGMENTS P. S. and N C. designed the study and wrote the paper, I. Gomez and R. Hernani collected and analysed the data, and G. F. S. and M. A. S. analysed the data and critically reviewed the paper. P. Solves, N. Carpio, I. Gómez, R. Hernani, G. F. Sanz & M. A. Sanz Transfusion Service, Hematology Unit, Hospital Universitari I Politècnic La Fe, Valencia, Spain First published online 4 March 2015 © 2015 British Blood Transfusion Society doi: 10.1111/tme.12179