1Haematology and Blood Transfusion Department, Federal Medical Centre, Ido – Ekiti, Nigeria
2Ondo State Hospital Management board, Okiti pupa, Nigeria
3Medical Microbiology Department, Federal Medical Centre, Ido – Ekiti, Nigeria
American Journal of Public Health Research.
2014,
Vol. 2 No. 2, 51-55
DOI: 10.12691/ajphr-2-2-3
Copyright © 2014 Science and Education PublishingCite this paper: Omisakin C.T, Esan A.J, Ogunleye A.A, O. Ojo-Bola, Owoseni M.F, Omoniyi D.P. Glucose-6-Phosphate Dehydrogenase (G6pd) Deficiency and Sickle Cell Trait among Blood Donors in Nigeria.
American Journal of Public Health Research. 2014; 2(2):51-55. doi: 10.12691/ajphr-2-2-3.
Correspondence to: Omisakin C.T, Haematology and Blood Transfusion Department, Federal Medical Centre, Ido – Ekiti, Nigeria. Email:
christopheromisakin@gmail.comAbstract
This study is being aimed to determine the prevalence of glucose-6-phosphate dehydrogenase deficiency and sickle cell trait among blood donors. Blood donation from glucose-6-phosphate dehydrogenase (G6PD)-deficient and sickle cell trait (SCT) donors might alter the quality of the donated blood during processing, storage or in the recipient′s circulatory system. It has been proposed that several biochemical changes and depletion in the antioxidant defense system occur on storage of G6PD-deficient blood. Red blood cells collected from sickle cell trait donors frequently occlude white blood cells reduction filters; the main cause of this filtration failure is haemoglobin polymerization. A total of 314 blood donor samples were collected from prospective and healthy blood donors after proper screening. Glucose-6-Phosphate dehydrogenase was determined using two standard methods; methaemoglobin reduction test and fluorescent spots test; haemoglobin variants were determined using cellulose acetate electrophoresis at alkaline PH 8.6. Out of the 314 blood donors, 80 (25.5%) were G6PD deficient, 104 haemoglobin variants AS, AC and SC were 82 (78.8%), 21 (20.2%) and 1 (1.0%) respectively. Commercial blood donors had highest G6PD deficient and highest haemoglobin variants. Age group 25-34 had highest G6PD deficient prevalence while age group 15-24 had highest haemoglobin variants. Transfusion with G6PD-deficient blood carries a potential risk of hemolytic complications, especially if it is used for exchanged blood transfusion in neonates. On the other hand, the blood donated from SCT donors, apart from its undesired effects if transfused to sickle cell disease patients, also leads to WBC filtration failure.
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