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Severe Platelet Transfusion Refractoriness in Association with Antibodies Against CD36. Lab Med 2020 Sep 01;51(5):540-544

Date

01/12/2020

Pubmed ID

31925433

DOI

10.1093/labmed/lmz091

Scopus ID

2-s2.0-85090173258 (requires institutional sign-in at Scopus site)   6 Citations

Abstract

Platelet-transfusion refractoriness (PTR) is common in patients with hematological malignancies. The etiology of immune PTR is typically human leukocyte antigen (HLA) antibodies (Abs) from pregnancy or previous transfusion. Herein, we report PTR in the setting of induction chemotherapy for acute myelogenous leukemia (AML) from Abs against CD36/glycoprotein (GP)IV. A 66-year-old African American woman presented with anemia and thrombocytopenia. She was found to have transfusion-dependent AML, and a 7 + 3 regimen (7 days of standard-dose cytarabine and 3 days of an anthracycline antibiotic or an anthracenedione, most often daunorubicin) was initiated. The patient developed profound thrombocytopenia, with platelet nadir of 0 by day 13. The results of HLA antibody screening were negative. However, the results of a screening test for platelet-specific antibodies screen showed Abs against cluster of differentiation (CD)36. The platelets of the patient lacked expression of CD36, and DNA analysis showed mutations in the CD36 gene. HLA Ab-mediated PTR is common in patients with hematological malignancies. However, once HLA Abs are excluded, other less-frequent Abs should be considered, particularly in patient populations of Asian, African, or Middle Eastern descent.

Author List

Schmidt AE, Sahai T, Refaai MA, Sullivan M, Curtis BR

Author

Brian Curtis PhD Director in the Platelet & Neutrophil Immunology Laboratory department at BloodCenter of Wisconsin




MESH terms used to index this publication - Major topics in bold

Aged
Antimetabolites, Antineoplastic
Blood Platelet Disorders
Fatal Outcome
Female
Genetic Diseases, Inborn
Humans
Induction Chemotherapy
Leukemia, Myeloid, Acute
Platelet Transfusion