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Prevalence of Glucose-6-phosphate Dehydrogenase Deficiency Among Children Aged 0-5 Years Infected with Plasmodium falciparum in Katsina State, Nigeria

Received: 22 August 2016    Accepted: 8 September 2016    Published: 15 November 2016
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Abstract

About 96 million people having Glucose-6-phosphate dehydrogenase (G6PD) deficiency worldwide are known to reside in malaria endemic countries and this G6PD-deficiency has been shown to protect against malaria infection, a disease which affect mostly children less than 5 years of age. This study was prompted by the paucity of scientific information on G6PD deficiency for malaria-infected children in Nigeria and so it was designed to determine the prevalence of G6PD deficiency among children (aged 0-5 years) infected with Plasmodium falciparum in Katsina State, a North-western region of Nigeria. A total of 200 blood samples were collected from children with Plasmodium falciparum malaria attending the six selected hospitals located across the three senatorial zones of the state from March 2015 to May 2015. Children’s inform consent was obtained, their socio-demographic information and clinical presentations were also taken with the aid of structured questionnaire. G6PD deficiency was detected qualitatively using G6PD screening test. Thirty two (16%) samples were G6PD deficient and were significantly associated (p<0.05) with malaria. Higher prevalence was observed among male children (62.5%) compared with their female counterpart (37.5%). Prevalence rates of 31.25%, 25.00%, 18.75% and 12.50% were seen in children of 1, 2, 3, 4 and 5 years old respectively. These conditions reach life-threatening scenarios for all G6PD deficiency patients with different genetic variants. Hence, individuals that are required to use antimalaria drugs should be screened very carefully for their tendency to have G6PD deficiency. For effective control and treatment, either a reliable test for detecting G6PD deficiency or an anti-malaria drug that can be safely given to G6PD deficiency patients is required. The need for training paediatricians on routine screening of children for G6PD deficiency in developing countries in order to avoid cases of drug-induced anaemia associated with malaria treatment need to be taken into consideration.

Published in Advances in Biochemistry (Volume 4, Issue 6)
DOI 10.11648/j.ab.20160406.11
Page(s) 66-73
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This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

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Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Glucose-6-Phosphate Dehydrogenase Deficiency (G6PD), Plasmodium Falciparum, Malaria, Children, Katsina State, Nigeria

References
[1] L. Luzzatto, and E. C. Gordon-Smith,“Inherited haemolytic anaemia,”Postgraduate Haematology, 4th ed., London: Arnold, 2001, pp. 120–143.
[2] R. E. Howes, F. B. Piel andA. P. Patil,“G6PD deficiency prevalence and estimate of affected populations in malaria endemic countries,” A geostatistical model-based map. PLoS, Med., 2012, vol. 9, e1001339.
[3] C. Ruwende, S. C. Khoo and R. W. Snow,“Natural selection of hemi- and heterozygotes for G6PD deficiency in Africa by resistance to severe malaria,”Nature, 1995, vol. 376, pp. 246-249.
[4] F. P. Mockenhaupt, O. Müller and B. Mark,“Haemolysis risk in methylene blue treatment of G6PD-sufficient and G6PD-deficient West-African children with uncomplicated falciparum malaria,” A synopsis of four RCTs. Pharmacoepidemiol Drug Saf., 2003, vol. 4, pp. 376–385.
[5] T. G. Clark, A. E. Fry andS. Auburn,“Allelic heterogeneity of G6PD deficiency in West Africa and severe malaria susceptibility,” European Journal of Human Genetics, 2009, vol. 17, pp. 1080–5.
[6] E. Beutler,“G6PD Population genetics and clinical manifestation,”Blood Reviews, 1996, vol. 10, pp. 45-52.
[7] L. Luzzatto,“Glucose-6-phosphate dehydrogenase deficiency from genotype to phenotype, Haematologica, 2006, vol. 91, pp. 1303–1306
[8] T. Z. Lui, T. F. Lin, I. J. Hung, J. S. Wei and D. T. Y. Chiu, “Enhanced Susceptibility of Erythrocytes Deficient in Glucose-6-Phosphate Dehydrogenase in Alloxan, GSH-induced decrease in Red Cell Deformability,” Life Science, 1994, vol. 55, pp. 155-160.
[9] S. Udomsak, K. Srivucha, T. Sombat, W. Polsat, C. Kobsiri, Y. M. Hla, M. Pannamas, J. W. Nicholas, R. Victor, M. B. Gary, and L. Sornchai, “Clinical Trial of Oral Artesunate with or without High Dose Primaquine for the Treatment of vivax malaria in Thailand,” American Journal of Tropical Medical Hygiene, 2003, vol. 6, pp. 14-18.
[10] P. J. Mason, J. M. Bautista and F. Gilsanz, G6PD deficiency: “The genotype phenotype association,” Blood Reviews., 2007, vol. 21, pp. 267-83.
[11] M. D. Cappellini and G. Fiorelli, “Glucose-6-phosphate dehydrogenase deficiency,”Lancet, 2008, vol. 371 pp. 64-74.
[12] World Health Organisation Working Group,“Glucose-6-phosphate dehydrogenase deficiency,”WHO Bull. World Health Organ., 1989, vol. 67, pp. 601-11.
[13] D. R. Miller and R. l. Baehner, “Blood Diseases of Infancy and Childhood,” 7thed., Mosby, St., Louis: MO, 1995, pp. 866-923.
[14] I. Z. Isaac, A. S. Mainasara, O. Erhabor, S. T. Omojuyigbe, M. K. Dallatu andL. S. Bilbis, “Glucose-6-phosphate dehydrogenase deficiency among children attending the Emergency Paediatric Unit of Usmanu Danfodiyo University Teaching Hospital, Sokoto, Nigeria,” International Journal of General Medicine, 2013, vol. 6, pp. 557-562.
[15] E. O. Akanni, B. S. A. Oseni and V. O. Agbona, “Glucose-6-phosphate dehydrogenase deficiency in blood donors and jaundiced neonates in Oshogbo, Nigeria,” Journal of Medical Laboratory Diagnostics, 2010, vol. 1 pp. 1– 4.
[16] D. Egesie, D. E. Joseph, I. Isiguzoro and U. G. Egesie,“Glucose-6-phosphate dehy¬drogenase activity and deficiency in a population of Nigerian male residents in Jos,”Nigerian Journal of Physiological Science, 2008, vol. 1–2, pp. 9–11.
[17] K. Iwai, A. Hirono and H. Matsuoka, “Distribution of glucose-6-phosphate dehydrogenase mutations in Southeast Asia,”Human Genetics, 2001, vol. 6 pp. 445–449.
[18] C. Louicharoen and I. Nuchprayoon, “G6PD Viangchan (871G. A) is the most common G6PD-deficient variant in the Cambodian population, Journal of Human Genetics, 2005, vol. 9, pp. 448–452.
[19] S. Sukumar, M. B. Mukherjee, R. B. Colah and D. Mohanty,“Molecular basis of G6PD deficiency in India,”Blood Cells Molecular Disease, 2004, vol. 2, pp. 141–145.
[20] A. Al-Riyami and G. J. Ebrahim,“Genetic blood disorders survey in the sultan¬ate of Oman,”Journal of Tropical Paediatrics, 2003, vol. 49, Suppl. 1, i1–i20.
[21] E. A. Usanga and R. Ameen, “Glucose-6-phosphate dehydrogenase deficiency in Kuwait, Syria, Egypt, Iran, Jordan and Lebanon,”Human Heredity, 2000, vol. 3, pp. 158–161.
[22] M. B. Compri, S. T. Saad andA. S. Ramalho, “Genetic-epidemiological and molecular investigation of G6PD deficiency in a Brazilian community,”Cad. SaudePublica, 2000, vol. 2, pp. 335–342. Portuguese.
[23] S. Castro, R. Weber, V. Dadalt, V. Tavares and R. Giugliani, “Prevalence of G6PD deficiency in newborns in the south of Brazil,”Journal of Medical Screening, 2006, vol. 2, pp. 85–86.
[24] M. S. Santana, M. V. G. de Lacerda, M. D. G. V. Barbosa, W. D. Alecrim and M. D. G. C. Alecrim, “Glucose-6-phosphate dehydrogenase deficiency in an endemic area for malaria in Manaus,” A cross-sectional survey in the Brazilian Amazon, PLoS One, 2009, vol. 4, e5259.
[25] U. Dauda, S. U. Gulumbe, M. Yakubu and L. K. Ibrahim “Monetering of Infectious Diseases in Katsina and Daura Zones of Katsina State,” A Clustering Analysis, Nigerian Journal of Basic and Applied Science, 2011, vol. 19, (1), pp. 31-42.
[26] B. McConell, “Malria Laboratory Diagnosis” 2011.
[27] F. L. Black, F. M. Salzano and Z. Layrisse,“Restriction and persistence of polymorphisms of HLA and other genetic traits in the Parakana Indians of Brazil,”American Journal of Physical Anthropology, 1980, vol. 52, pp. 119–132.
[28] P. Phompradit, J. Kuesap, W. Chaijaroenkul, R. Rueangweerayut, Y. Hongkaew, R. Yamnuan, and K. Na-Bangchang, “Prevalence and distribution of glucose-6-phosphate dehydrogenase (G6PD) variants in Thai and Burmese populations in malaria endemic areas of Thailand,” Malaria Journal, 2011, Vol. 10, pp. 368.
[29] S. A. Tishkoff, R. Varkonyi and N. Cahinhinan, “Haplotype diversity and linkage disequilibrium at human G6PD,” Recent origin of alleles that confer malarial resistance, Science, 2001, vol. 293, pp. 455-62.
[30] R. Munyanganizi, F. Cotton and F. Vertongen, “Red blood cell disorders in Rwandese neonates,” Screening for sickle cell disease and glucose-6-phosphate dehydrogenase deficiency, Journal of Medical Screening, 2006, vol. 3, pp. 129–131.
[31] A. Guindo, R. M. Fairhurst and O. K. Doumbo,“X-linked G6PD deficiency protects hemizygous males but not heterozygous females against severe malaria,”PLoS Med., 2010, vol. 4, e66.
[32] A. Motulsky, and I. Campbell-Kraut, “Proceedings of the conference on genetic polymorphisms and geographic variations in disease,” Grune and Stratton, New York, 1961, pp. 159-180.
[33] M. Siniscalco and L. Bernini, “Favism and thalassaemia in Sardinia and their relationship to malaria,” Nature, 1961, Vol. 190, pp. 1179-1180.
[34] M. Ganczakowski, M. Town, and D. Bowden, “Multiple glucose 6-phosphate dehydrogenase-deficient variants correlate with malaria endemicity in the Vanuatu archipelago (southwestern Pacific),” American journal of human genetics, 1995, Vol. 56 (1), pp. 294-301.
[35] S. Sukumar, “Glucose-6-phosphate dehydrogenase deficiency,” An overview, Immunohaematol Bull, 2000, Vol. 31, pp. 1-12.
[36] A. C. Allison, and D. F. Clyde, “Malaria in African children with deficient erythrocyte glucose-6-phosphate dehydrogenase,” British Medical Journal, 1961, 1 (5236), PP. 1346-1349.
[37] Kruatrachue, M., Charoenlarp, P., Chongsuphajaisiddhi, T. and Harinasuta, C. (1962): Erythrocyte glucose-6-phosphate dehydrogenase and malaria in Thailand. Lancet, 2 (7267): 1183-1186.
[38] Ninokata, R. Kimura, U. Samakkarn, W. Settheetham-Ishida, and T. Ishida, “Coexistence of five G6PD variants indicates ethnic complexity of Phuket islanders, Southern Thailand,” Journal Human Genetics, 2006, Vol. 51 (5), pp. 424-428.
[39] I. Clark, G. Chaudhri, and W. Cowden, “Some roles of free radicals in malaria,” Free Radical Biology and Medicine, 1989, Vol. 6 (3), pp. 315-321.
[40] D. Toncheva and M. Tzoneva, 1985“Prenatal selection and fetal development disturbances occurring in carriers of G6PD deficiency,”Human Genetics, 1985, Vol. 69 (1), pp. 88.
[41] L. S. Greene, “G6PD deficiency as protection against falciparum malaria,” An epidemiologic critique of population and experimental studies, American Journal of Physical Anthropology, 1993, Vol. 36, (S17), pp. 153-178.
[42] M. J. Friedman and W. Trager, “The biochemistry of resistance to malaria,”Science Americana, 1981, Vol. 244 (3), pp. 154-155, 158-164.
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    Bello Ibrahim, Abdulsalami Mohammed Sani, Bulus Timothy. (2016). Prevalence of Glucose-6-phosphate Dehydrogenase Deficiency Among Children Aged 0-5 Years Infected with Plasmodium falciparum in Katsina State, Nigeria. Advances in Biochemistry, 4(6), 66-73. https://doi.org/10.11648/j.ab.20160406.11

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    Bello Ibrahim; Abdulsalami Mohammed Sani; Bulus Timothy. Prevalence of Glucose-6-phosphate Dehydrogenase Deficiency Among Children Aged 0-5 Years Infected with Plasmodium falciparum in Katsina State, Nigeria. Adv. Biochem. 2016, 4(6), 66-73. doi: 10.11648/j.ab.20160406.11

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    AMA Style

    Bello Ibrahim, Abdulsalami Mohammed Sani, Bulus Timothy. Prevalence of Glucose-6-phosphate Dehydrogenase Deficiency Among Children Aged 0-5 Years Infected with Plasmodium falciparum in Katsina State, Nigeria. Adv Biochem. 2016;4(6):66-73. doi: 10.11648/j.ab.20160406.11

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  • @article{10.11648/j.ab.20160406.11,
      author = {Bello Ibrahim and Abdulsalami Mohammed Sani and Bulus Timothy},
      title = {Prevalence of Glucose-6-phosphate Dehydrogenase Deficiency Among Children Aged 0-5 Years Infected with Plasmodium falciparum in Katsina State, Nigeria},
      journal = {Advances in Biochemistry},
      volume = {4},
      number = {6},
      pages = {66-73},
      doi = {10.11648/j.ab.20160406.11},
      url = {https://doi.org/10.11648/j.ab.20160406.11},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ab.20160406.11},
      abstract = {About 96 million people having Glucose-6-phosphate dehydrogenase (G6PD) deficiency worldwide are known to reside in malaria endemic countries and this G6PD-deficiency has been shown to protect against malaria infection, a disease which affect mostly children less than 5 years of age. This study was prompted by the paucity of scientific information on G6PD deficiency for malaria-infected children in Nigeria and so it was designed to determine the prevalence of G6PD deficiency among children (aged 0-5 years) infected with Plasmodium falciparum in Katsina State, a North-western region of Nigeria. A total of 200 blood samples were collected from children with Plasmodium falciparum malaria attending the six selected hospitals located across the three senatorial zones of the state from March 2015 to May 2015. Children’s inform consent was obtained, their socio-demographic information and clinical presentations were also taken with the aid of structured questionnaire. G6PD deficiency was detected qualitatively using G6PD screening test. Thirty two (16%) samples were G6PD deficient and were significantly associated (p<0.05) with malaria. Higher prevalence was observed among male children (62.5%) compared with their female counterpart (37.5%). Prevalence rates of 31.25%, 25.00%, 18.75% and 12.50% were seen in children of 1, 2, 3, 4 and 5 years old respectively. These conditions reach life-threatening scenarios for all G6PD deficiency patients with different genetic variants. Hence, individuals that are required to use antimalaria drugs should be screened very carefully for their tendency to have G6PD deficiency. For effective control and treatment, either a reliable test for detecting G6PD deficiency or an anti-malaria drug that can be safely given to G6PD deficiency patients is required. The need for training paediatricians on routine screening of children for G6PD deficiency in developing countries in order to avoid cases of drug-induced anaemia associated with malaria treatment need to be taken into consideration.},
     year = {2016}
    }
    

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    T1  - Prevalence of Glucose-6-phosphate Dehydrogenase Deficiency Among Children Aged 0-5 Years Infected with Plasmodium falciparum in Katsina State, Nigeria
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    AB  - About 96 million people having Glucose-6-phosphate dehydrogenase (G6PD) deficiency worldwide are known to reside in malaria endemic countries and this G6PD-deficiency has been shown to protect against malaria infection, a disease which affect mostly children less than 5 years of age. This study was prompted by the paucity of scientific information on G6PD deficiency for malaria-infected children in Nigeria and so it was designed to determine the prevalence of G6PD deficiency among children (aged 0-5 years) infected with Plasmodium falciparum in Katsina State, a North-western region of Nigeria. A total of 200 blood samples were collected from children with Plasmodium falciparum malaria attending the six selected hospitals located across the three senatorial zones of the state from March 2015 to May 2015. Children’s inform consent was obtained, their socio-demographic information and clinical presentations were also taken with the aid of structured questionnaire. G6PD deficiency was detected qualitatively using G6PD screening test. Thirty two (16%) samples were G6PD deficient and were significantly associated (p<0.05) with malaria. Higher prevalence was observed among male children (62.5%) compared with their female counterpart (37.5%). Prevalence rates of 31.25%, 25.00%, 18.75% and 12.50% were seen in children of 1, 2, 3, 4 and 5 years old respectively. These conditions reach life-threatening scenarios for all G6PD deficiency patients with different genetic variants. Hence, individuals that are required to use antimalaria drugs should be screened very carefully for their tendency to have G6PD deficiency. For effective control and treatment, either a reliable test for detecting G6PD deficiency or an anti-malaria drug that can be safely given to G6PD deficiency patients is required. The need for training paediatricians on routine screening of children for G6PD deficiency in developing countries in order to avoid cases of drug-induced anaemia associated with malaria treatment need to be taken into consideration.
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Author Information
  • National Biotechnology Development Agency, Abuja, Nigeria

  • Department of Biological Sciences, Nigerian Defence Academy, Kaduna, Nigeria

  • Department of Biochemistry, Kaduna State University, Kaduna, Nigeria

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