Donor glucose-6-phosphate dehydrogenase deficiency decreases blood quality for transfusion.

Sarah Gehrke, Eldad A Hod, Steven L Spitalnik, James C Zimring, Yelena Ginzburg, Beth H Shaz, Debra Kessler, Chaitanya Divgi, Joseph Schwartz, Tiffany Thomas, Travis Nemkov, Richard O Francis, Julie A Reisz, Francesca La Carpia, Francesca Rapido, Arif Sheikh, Esther Coronel, Randy Yeh, Mark Soffing, Andrew Eisenberger, Angelo D'Alessandro

Journal: The Journal of clinical investigation 2021;130(5):2270-2285

PMID: 31961822

Abstract

BACKGROUNDGlucose-6-phosphate dehydrogenase (G6PD) deficiency decreases the ability of red blood cells (RBCs) to withstand oxidative stress. Refrigerated storage of RBCs induces oxidative stress. We hypothesized that G6PD-deficient donor RBCs would have inferior storage quality for transfusion as compared with G6PD-normal RBCs.METHODSMale volunteers were screened for G6PD deficiency; 27 control and 10 G6PD-deficient volunteers each donated 1 RBC unit. After 42 days of refrigerated storage, autologous 51-chromium 24-hour posttransfusion RBC recovery (PTR) studies were performed. Metabolomics analyses of these RBC units were also performed.RESULTSThe mean 24-hour PTR for G6PD-deficient subjects was 78.5% ± 8.4% (mean ± SD), which was significantly lower than that for G6PD-normal RBCs (85.3% ± 3.2%; P = 0.0009). None of the G6PD-normal volunteers (0/27) and 3 G6PD-deficient volunteers (3/10) had PTR results below 75%, a key FDA acceptability criterion for stored donor RBCs. As expected, fresh G6PD-deficient RBCs demonstrated defects in the oxidative phase of the pentose phosphate pathway. During refrigerated storage, G6PD-deficient RBCs demonstrated increased glycolysis, impaired glutathione homeostasis, and increased purine oxidation, as compared with G6PD-normal RBCs. In addition, there were significant correlations between PTR and specific metabolites in these pathways.CONCLUSIONBased on current FDA criteria, RBCs from G6PD-deficient donors would not meet the requirements for storage quality. Metabolomics assessment identified markers of PTR and G6PD deficiency (e.g., pyruvate/lactate ratios), along with potential compensatory pathways that could be leveraged to ameliorate the metabolic needs of G6PD-deficient RBCs.TRIAL REGISTRATIONClinicalTrials.gov NCT04081272.FUNDINGThe Harold Amos Medical Faculty Development Program, Robert Wood Johnson Foundation grant 71590, the National Blood Foundation, NIH grant UL1 TR000040, the Webb-Waring Early Career Award 2017 by the Boettcher Foundation, and National Heart, Lung, and Blood Institute grants R01HL14644 and R01HL148151.

Address: Department of Pathology and Cell Biology, Columbia University Vagelos College of Physicians and Surgeons and NewYork-Presbyterian Hospital, New York, New York, USA.; University of Colorado Denver-Anschutz Medical Campus, Aurora, Colorado, USA.; Department of Medicine and.; Department of Nuclear Medicine, Columbia University Vagelos College of Physicians and Surgeons and NewYork-Presbyterian Hospital, New York, New York, USA.; Division of Nuclear Medicine and Molecular Imaging, Icahn School of Medicine at Mount Sinai Hospital, New York, New York, USA.; Department of Anesthesia and Critical Care Medicine, Montpellier University Hospital Gui de Chauliac, Montpellier, France.; New York Blood Center, New York, New York, USA.; Division of Hematology Oncology, Icahn School of Medicine at Mount Sinai Hospital, New York, New York, USA.; Carter Immunology Center, University of Virginia School of Medicine, Charlottesville, Virginia, USA.
Bant logo

© Copyright 2026, Nutrition Evidence

NED wishes to thank the following organisations for their support:

We use cookies to improve your experience and analyze site traffic with Google Analytics. By continuing to use our site, you agree to our use of cookies. Learn more.