Immune platelet transfusion refractoriness associated with anti‐ CD36 alloimmunisation in a Brazilian patient with platelet CD36 deficiency

Abstract Background and Objectives Immune platelet transfusion refractoriness (PTR) is usually mediated by anti‐HLA class I antibodies; immunisation against CD36 (platelet glycoprotein IV [GPIV]) is relatively rare. Platelet CD36 deficiency shows marked ethnic variability and is seldom reported in admixed Latin American populations. We describe the diagnostic and transfusional challenges of anti‐CD36 alloimmunisation in a Brazilian patient. Materials and Methods A 48‐year‐old Brazilian woman with a myeloid/lymphoid neoplasm with fibroblast growth factor receptor 1 (FGFR1) rearrangement developed severe PTR. Platelet antibodies were assessed by a Luminex‐based Pak‐Lx assay, CD36 expression by flow cytometry and CD36 genotyping by Sanger sequencing. Results Platelet counts remained <5 × 10 9 /L with absent corrected count increment and recurrent mucocutaneous bleeding. Platelet antibody testing showed isolated anti‐GPIV/CD36 reactivity (median fluorescence intensity [MFI] 4388); no additional HLA class I or human platelet antigen (HPA) antibodies were detected. No CD36 expression was detected on the patient's platelets by flow cytometry, and CD36 gene sequencing identified two heterozygous variants (c.975T>G and c.1079T>G) known to be associated with CD36 deficiency. Crossmatches remained incompatible with all available platelet units, including from an HLA‐identical brother, reflecting the scarcity of CD36‐negative platelet donors. The patient died of disease progression. Conclusion Anti‐CD36 alloimmunisation should be considered in severe PTR with negative HLA antibody screening, particularly in heavily transfused patients from admixed populations. To our knowledge, this is the first Brazilian case of anti‐CD36 alloimmunisation causing severe PTR; platelet CD36 deficiency has previously been reported in a Brazilian woman with anti‐CD36 antibodies in the context of pregnancy, underscoring the importance of considering this antibody specificity in persistent PTR despite negative HLA and HPA antibody screening.