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American Journal of Public Health Research. 2014, 2(2), 51-55
DOI: 10.12691/AJPHR-2-2-3
Original Research

Glucose-6-Phosphate Dehydrogenase (G6pd) Deficiency and Sickle Cell Trait among Blood Donors in Nigeria

Omisakin C.T1, , Esan A.J1, Ogunleye A.A2, O. Ojo-Bola3, Owoseni M.F1 and Omoniyi D.P1

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

Pub. Date: March 30, 2014

Cite this paper

Omisakin C.T, Esan A.J, Ogunleye A.A, O. Ojo-Bola, Owoseni M.F and 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

Abstract

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.

Keywords

blood donors, G6PD deficiency, sickle cell trait

Copyright

Creative CommonsThis work is licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

References

[1]  Ahmed MA, Al-Ali AK, Al-Idrissi HY, Al-Sibai MH, Al-Mutairy AR, Knox-Macaulay H (1991). Sickle cell trait and G6PD deficiency in blood donors in eastern Saudi Arabia. Vox Sang; 61: 69-70.
 
[2]  Akanni1 E.O, Oseni1 B.S.A, Agbona V.O, Tijani B.A, Tosan E, Fakunle E.E and Mabayoje V.O (2010). Glucose-6-phosphate dehydrogenase deficiency in blood donors and jaundiced neonates in Osogbo, Nigeria; Journal of Medical Laboratory and Diagnosis; Vol. 1 (1) pp. 1-4.
 
[3]  Akhigbe R.E, Ige S.F, Afolabi A.O, Azeez O.M, Adegunlola G.J and Gamidele J.O (2009). Prevalence of haemoglobin variants, ABO and rhesus blood group in Ladoke Akintola University of Technology, Ogbomoso, Nigeria. Trends in Medical Research, Academic Journals Inc; 1819-3587.
 
[4]  Amoozegar HM, Mirshakeris, Paishva N (2005). Prevalence of Glucose- 6-Phosphate Dehydrogenase Deficiency among male donors in Shiraz, Southern Iran. Iran J. Med. Sci. 30 (2): 94-96.
 
[5]  Beutler E, Mitchel M (1968). Special Modification of the Fluorescent Screening method for Glucose-6-phosphate dehydrogenase deficiency Blood pp. 32: 816.
 
[6]  Bhagwat G.P, Bapat J.P (1987). Glucose 6-phosphate dehydrogenase deficiency in Bahraini blood donors; Bahraini medical bulletin, Vol. 9; No 3: 120-122.
 
[7]  Bienzle U, Effiong C, Luzzatto L (2008). Erythrocyte glucose 6-phosphate dehydrogenase deficiency (G6PD type A-) and neonatal jaundice. Acta Paediatr; 65701: 3.
 
[8]  Brandão MM, Saad ST, Cezar CL, Fontes A, Costa FF, Barjas-Castro ML (2003). Elastic properties of stored red blood cells from sickle trait donor units. Vox Sang.; 85: 213-215. Byrne KM, Leitman SF, Schechter AN, Stroncek DF (2003). Increasing oxygen tension.
 
[9]  Improves filtration of sickle trait donor blood. Br J Haematol; 122: 678-681.
 
[10]  Cheesbrough M (2002). Blood Transfusion Practice: Blood donation and Storage of blood, District Laboratory Practice in tropical countries, low-price edition by Cambridge Universal Press pp. 352-353.
 
[11]  Erhabor O, Adias T.C, Jeremiah Z.A, Hart M.L (2010). Abnormal haemoglobin variants, ABO and rhesus blood group distribution among students in the Niger Delta of Nigeria. Pathology laboratory medicine international; 2: 41-46
 
[12]  Esan A.J, Omisakin C.T, Okhuakhua O (2012). Frequency distribution of haemoglobin variants, ABO and rhesus blood groups among children in Ido-Osi Local Government, Ekiti State, Nigeria. Journal of medical laboratory science; vol. 12, No 2: 10-18.
 
[13]  Gagandeep Kaur, Sabita Basu, Ravneet Kaur, Paramjit Kaur, Shailja Garg (2010). Patterns of infections among blood donors in a tertiary care centre: a retrospective study. The national medical journal of India vol. 23; No 3: 147-149.
 
[14]  Huang CS, Sung YC, Huang MJ, Yang CS, Shei WS, Tang TK (1998). Content of reduced glutathione and consequences in recipients of glucose-6-phosphate dehydrogenase deficient red blood cells. Am J Hematol.; 57: 187-192.
 
[15]  Józwik M, Szczypka M, Gajewska J, Laskowska-Klita T (1997). Antioxidant defence of red blood cells and plasma in stored human blood. Clin Chim Acta.; 267: 129-142.
 
[16]  McCurdy PR, Morse EE (1975). Glucose-6-phosphate dehydrogenase deficiency and blood transfusion. Vox Sang. 28: 230-237.
 
[17]  Mimouni F, Shohat S, Reisner SH (1986). G6PD-deficient donor blood as a cause of hemolysis in two preterm infants. Isr J Med Sci.; 22: 120-122.
 
[18]  Mohammed K Alabdulaai, Khaled M Alayed, Abdulazizi F Alshakh, Shihab A Almashhadani (2010). Prevalence of glucose-6-phosphate dehydrogenase deficiency and sickle cell trait among blood donors in Riyadh. Asian journal of transfusion science. 4 (1): 31-33.
 
[19]  Kamran Moradkhani (2011). Clinical heterogeneity of G6PD deficiency: New variants and Correlation between genotype and phenotype, results of a five-year-survey; CHU Henri Mondor - Creteil Dorys 2011 Strasbourg
 
[20]  Orlina A R, Josephson A M, McDonald BJ (1970). The poststorage viability of glucose-6-phosphatase dehydrogenase-deficient erythrocytes. J Lab Clin Med.; 75: 930-936.
 
[21]  Ould Amar AK (2006). Red blood cells from donors with sickle cell trait: A safety issue for transfusion? Transfus Med.; 16: 248-253.
 
[22]  Sandip S, Praveen K, Sai SK, Gurjeewan G, Anil N (2009). Donor blood glucose 6-phosphate dehydrogenase deficiency reduces the efficacy of exchange transfusion in neonatal hyperbilirubinemia. Pediatrics; 123: 96-100.
 
[23]  Seyed HN, Amir AV (2007). The Prevalence of G6PD deficiency in blood transfusion recipent. Haematology 12: 85-88.
 
[24]  Shahriary M, Pishva N, Mohammadi T (1997). Incidence of G6PD deficiency in Fars province. Iran J Med Sci.; 22: 151.
 
[25]  Shalev O, Manny N, Sharon R (1993). Post-transfusional hemolysis in recipients of glucose-6-phosphate dehydrogenase-deficient erythrocytes. Vox Sang.; 64: 94-98.
 
[26]  Stroncek DF, Rainer T, Sharon V, Byrne KM, Noguchi CT, Klein HG, et al., 2002 Sickle Hb polymerization in RBC components from donors with sickle cell trait prevents effective WBC reduction by filtration. Transfusion; 42: 1466-1472.
 
[27]  Stroncek DF, Byrne KM, Noguchi CT, Schechter AN, Leitman SF (2004). Increasing hemoglobin oxygen saturation levels in sickle trait donor whole blood prevents hemoglobin S polymerization and allows effective white blood cell reduction by filtration. Transfusion; 44: 1293-1229.
 
[28]  Schuetz AN, Hillyer KL, Roback JD, Hillyer CD (2004). Leukoreduction filtration of blood with sickle cell trait. Transfus Med Rev.; 18: 168-176.
 
[29]  Uzoegwu P.N and Onwurah A.E 2003. Prevalence of heamoglobinopathy and malaria disease in the population of old Aguata Division, Anambra State, Nigeria. Biokemistri, 15: 57-66.