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

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Immunohematology

American National Red Cross

Subject: Medical Laboratory Technology

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ISSN: 0894-203X
eISSN: 1930-3955

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VOLUME 35 , ISSUE 4 (December 2019) > List of articles

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

S.S. Khatri / B.R Curtis / C. Yamada *

Keywords : platelet transfusion refractoriness, anti-CD36, desensitization, bone marrow transplant

Citation Information : Immunohematology. Volume 35, Issue 4, Pages 139-144, DOI: https://doi.org/10.21307/immunohematology-2020-028

License : (Transfer of Copyright)

Published Online: 16-February-2021

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ABSTRACT

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 crossmatch-compatible 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.

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