ArticleTransfusion2022
Glucose-6-phosphate dehydrogenase deficiency is more prevalent in Duffy-null red blood cell transfusion in sickle cell disease.
Article in Transfusion, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Red blood cell transfusion survival in sickle cell disease is reduced by donor characteristics and recipient spleen activity.Blood advances · 2026Trial
- Post-transfusion biotin-labeled red blood cell survival studies in pediatric sickle cell disease with antibodies of uncertain significance.Transfusion · 2024Article
- Intricacies of GATA-ca, continued.Haematologica · 2022Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundResistance to malaria infection may be conferred by erythrocyte genetic variations including glucose-6-phosphate dehydrogenase (G6PD) deficiency and lack of Duffy antigens. In red blood cell (RBC) transfusion, G6PD deficiency may shorten transfusion survival. Because Duffy-null units are commonly transfused in sickle cell disease (SCD) due to antigen matching protocols, we examined whether Duffy-null donor RBC units have a higher prevalence of G6PD deficiency. MATERIALS AND
methodsPediatric patients with SCD on chronic transfusion therapy were followed prospectively for multiple transfusions. RBC unit segments were collected to measure G6PD activity and RBC genotyping. The decline in donor hemoglobin (ΔHbA) following transfusion was assessed from immediate posttransfusion estimates and HbA measurements approximately 1 month later.
resultsOf 564 evaluable RBC units, 59 (10.5%) were G6PD deficient (23 severe, 36 moderate deficiency); 202 (37.6%) units were Duffy-null. G6PD deficiency occurred in 40 (19.8%) Duffy-null units versus 15 (4.5%) Duffy-positive units (p < .0001). In univariate analysis, the fraction of Duffy-null RBC units per transfusion was associated with greater decline in HbA (p = .038); however, in multivariate analysis, severe G6PD deficiency (p = .0238) but not Duffy-null RBC (p = .0139) were associated with ΔHbA.
conclusionSelection of Duffy-null RBC units may result in shorter in vivo survival of transfused RBCs due to a higher likelihood of transfusing units from G6PD deficient donors.
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