ISSN 2997-1036
International Journal of Hematology | Vol. 2, No. 1, January 2011 | pp. 1–8
DOI: 10.46882/2011/IJH/000013
Original Article
Title: Molecular epidemiology of Glucose-6-Phosphate Dehydrogenase variants among blood donors
Names of Authors: O. P. Gbadamosi¹, E. E. Udo², M. A. Dikko³
Authors’ Affiliations: ¹Department of Haematology and Blood Transfusion, Ladoke Akintola University of Technology, Ogbomoso, Nigeria; ²Department of Haematology, University of Calabar, Calabar, Nigeria; ³Department of Pathology, Ahmadu Bello University, Zaria, Nigeria
Abstract: Transfusing glucose-6-phosphate dehydrogenase deficient blood may compromise erythrocyte survival post-transfusion and induce acute hemolytic reactions in vulnerable recipients. This study screened 400 healthy male blood donors for glucose-6-phosphate dehydrogenase deficiency using the methemoglobin reduction test, followed by molecular genotyping via polymerase chain reaction. The overall phenotypic prevalence of deficiency was 19.5% (78 of 400 donors). Molecular analysis identified the G6PD A- variant (202G→A / 376A→G) in 84.6% of the deficient cohort, while the severe Mediterranean variant (563C→T) was absent. Donor units with glucose-6-phosphate dehydrogenase deficiency exhibited significantly higher baseline plasma hemoglobin (0.45 ± 0.12 g/dl) and lower glutathione levels after 21 days of storage at 4 °C compared to normal units (P < 0.01). These observations suggest that a significant proportion of donor blood contains enzymatically deficient red cells prone to accelerated storage lesions. Screening donor pools for this enzymopathy is highly recommended to optimize transfusion safety, particularly for neonatal and exchange transfusion recipients.
Keywords: Glucose-6-phosphate dehydrogenase, blood donors, G6PD A- variant, transfusion safety, erythrocyte storage
Manuscript Timeline: Received: October 20, 2010; Revised: November 25, 2010; Accepted: December 11, 2010; Published: January 14, 2011