ArticleTransfusion2025
Management challenge of a rare concomitant platelet glycoprotein IV/CD36 and IIb/IIIa deficiencies: Case illustration.
Article in Transfusion, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Development and clinical application of a low-cost high-resolution melting curve assay for CD36 gene variant screening in a chinese population.Molecular biology reports · 2025Article
- Management challenge of a rare concomitant platelet glycoprotein IV/CD36 and IIb/IIIa deficiencies: Case illustration.Transfusion · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
INTRODUCTION/
backgroundPlatelet membrane glycoproteins (GPs) serve several functions, the most significant of which is their role in primary hemostasis. Among these, GP IIb/IIIa is the primary fibrinogen receptor and is essential for platelet aggregation. Its deficiency or dysfunction impairs platelet aggregation, leading to Glanzmann thrombasthenia, a rare autosomal recessive bleeding disorder. In contrast, platelet GP IV (CD36) has a limited role in primary hemostasis. While also rare, CD36 deficiency has a disproportionately higher prevalence in individuals of East Asian, African, and Arabian descent. Patients with platelet GP deficiencies can develop antibodies against the missing GPs, leading to immune-mediated platelet transfusion refractoriness (PTR). Consequently, they are unresponsive to platelet transfusions when mostly needed. CASE PRESENTATION: Here we present the case of an Egyptian male with a lifelong history of an incompletely characterized bleeding disorder who presented for pre-surgical evaluation. We diagnosed the patient with Type I Glanzmann thrombasthenia. Further evaluation revealed anti-CD36 antibodies, leading to the discovery of a concurrent platelet CD36 deficiency. The dual GP deficiency significantly complicated his management, as finding crossmatch-compatible platelets was challenging due to the rarity of CD36-deficient blood donors in the United States. DISCUSSION/
conclusionAwareness of coexisting platelet disorders and their ramifications is limited, mostly because these are stochastically rare (~1 in 100 million for the present case). This case highlights the importance of thoroughly evaluating platelet glycoprotein deficiencies, particularly in individuals with severe bleeding disorders and from ethnic backgrounds with a predisposition to specific platelet disorders. Such an approach can prevent future platelet antibody formation or reduce bleeding risk with pre-existing antibodies.
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Registered trials
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