A case of platelet transfusion refractoriness due to anti-CD36 with a successful treatment outcome

CONCLUSIONS: Antibodies (Abs) against antigens on platelets (PLTs), including glycoprotein IV (CD36), can cause PLT refractoriness. Transfusing PLTs to patients with anti-CD36 is challenging because of the rarity of CD36-negative (CD36-) donors and the possibility of additional HLA Abs. We report a case of PLT refractoriness due to anti-CD36 and HLA Abs. A 21-year-old man (group O, D+) with assumed drug-induced aplastic anemia received multiple PLT transfusions and developed severe PLT refractoriness. He was found to have anti-CD36 as well as HLA class I Abs, with a CD36- phenotype on both PLTs and monocytes. He was diagnosed with type 1 CD36 deficiency and received intravenous immunoglobulin (IVIG) and rituximab to decrease future Ab production. The PLT corrected count increment (CCI) improved significantly with subsequent transfusions of flow crossmatchcompatible as well as uncrossmatched PLTs. He eventually received a bone marrow transplant and has been doing well since. The mean CCI before and after IVIG/rituximab treatment was 0.2 and 6.2, respectively. Soon after IVIG started, the patient's CCI after receiving CD36-, group AB, D+, and HLA untested PLTs was 0.8, but his CCI after receiving flow crossmatch-compatible PLTs was 12.6. Two months after IVIG was started, the mean CCIs for uncrossmatched apheresis PLTs and crossmatch-compatible PLTs were comparable (6.1 versus 6.0, respectively). Desensitization treatment with IVIG and rituximab lowered anti-CD36 and HLA Ab levels, and the CCI of PLT transfusion improved significantly. This case demonstrates that immune suppression is effective for successful PLT transfusion of patients with anti-CD36.