A case of platelet transfusion refractoriness in a CD36‐negative patient with acute myeloid leukemia: Diagnostic and therapeutic management

To the Editor, CD36 deficiency is responsible for CD36 iso-immunizations following pregnancy causing fetal and neonatal alloimmune thrombocytopenia (FNAIT) and sometimes early fetal loss or platelet transfusion, inducing platelet transfusion refractoriness and, in some cases, post-transfusion purpura; We report the case of a 25-year-old man originating from Mali (Africa) treated for acute myeloid leukemia secondary to treatment for Hodgkin's lymphoma. The patient received induction course with idarubicin (9 mg/m from day [D] 1 to day 5) and cytarabine (200 mg/m from D1 to D7), inducing aplasia. Because two platelet transfusions with a dose >0.5 10/kg of patient weight were ineffective, HLA and HPA alloantibodies were screened. The anti-HLA antibody screening (One Lambda, Inc., Canoga Park, CA) by the Luminex technique and the anti-HPA antibodies by MAIPA (Monoclonal Antibody-specific Immobilization of Platelet Antigens, ApDia, Turnhout, Belgium) were negative. Surprisingly, anti-CD36 iso-antibodies (iso-Abs) using a beadbased multiplex assay PakLx (Immucor, Waukesha, WI) were detected with an MFI (mean fluorescence intensity) of 5236. A reference laboratory (HPA/HLA Laboratory, EFS Bretagne, Rennes, France) confirmed the detection of CD36 iso-Abs using MAIPA with clone FA6.152 anti-CD36 Moab. Homemade sequencing highlighted a mutation in exon 12 of the CD36 gene, NM_000072.3:c.975T > G, inducing a stop codon at position 325 of the mature protein, already recorded as rs567787470 in the international database. To limit inefficiency platelet transfusion, three strategies were developed during his treatment. The different strategies and platelet concentrates transfused following the chronological order of the treatment sequences are described in Table 1.