{"title":"CD36 immunization causing platelet transfusion refractoriness: narrative review","authors":"Mia J. Sullivan, J. P. Botero","doi":"10.21037/aob-21-36","DOIUrl":null,"url":null,"abstract":"Objective: This narrative review aims to describe the clinical and laboratory approach to patients with platelet transfusion refractoriness (PTR) from CD36 immunization. Background: The most common cause of PTR is non-immune and within the immune-mediated causes, antibodies against CD36 are rare but clinically significant. CD36 deficiency is more common in African, African American, Chinese and Japanese populations. Immune-mediated PTR from CD36 antibodies almost exclusively affects individuals with type I deficiency, affecting both platelets and monocytes. Methods: We describe a general approach to identify and manage patients with CD36 immunization as the cause of PTR. An overview of cases reported in the literature with emphasis in the clinical characteristics and outcomes is presented. Conclusions: Approaching patients systematically, with post-transfusion counts, antibody screening and confirmatory testing to identify the antigen(s) involved is key in selecting the platelet units that are most likely to provide an adequate transfusion yield. Due to the high frequency of CD36 in the general population, CD36 negative platelet units are not readily available, and procurement of these units relies on related donors or units from reference blood banks around the world. Even when CD36 negative platelet units are available, other immune and non-immune mediated causes of PTR can be present simultaneously making platelet transfusions of little clinical utility. Additional interventions to increase transfusion yield such as administration of polyvalent immunoglobulin and addition of immunosuppression have also been described. The management of patients with PTR from CD36 antibodies remains challenging despite wider access to testing and antigen negative platelet units.","PeriodicalId":72211,"journal":{"name":"Annals of blood","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Annals of blood","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.21037/aob-21-36","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: This narrative review aims to describe the clinical and laboratory approach to patients with platelet transfusion refractoriness (PTR) from CD36 immunization. Background: The most common cause of PTR is non-immune and within the immune-mediated causes, antibodies against CD36 are rare but clinically significant. CD36 deficiency is more common in African, African American, Chinese and Japanese populations. Immune-mediated PTR from CD36 antibodies almost exclusively affects individuals with type I deficiency, affecting both platelets and monocytes. Methods: We describe a general approach to identify and manage patients with CD36 immunization as the cause of PTR. An overview of cases reported in the literature with emphasis in the clinical characteristics and outcomes is presented. Conclusions: Approaching patients systematically, with post-transfusion counts, antibody screening and confirmatory testing to identify the antigen(s) involved is key in selecting the platelet units that are most likely to provide an adequate transfusion yield. Due to the high frequency of CD36 in the general population, CD36 negative platelet units are not readily available, and procurement of these units relies on related donors or units from reference blood banks around the world. Even when CD36 negative platelet units are available, other immune and non-immune mediated causes of PTR can be present simultaneously making platelet transfusions of little clinical utility. Additional interventions to increase transfusion yield such as administration of polyvalent immunoglobulin and addition of immunosuppression have also been described. The management of patients with PTR from CD36 antibodies remains challenging despite wider access to testing and antigen negative platelet units.