TREATMENT FOR MALARIA PATIENTS IN PAKISTAN AND THE PREDOMINANCE OF GLUCOSE-6-PHOSPHATE DEHYDROGENASE (G6PD) DEFICIENCY

Syed Waqad Ali; Marium Raziq; Muhammad Muzammil Khan; Sania Tanvir; Syed Jamal Hyder Zaidi; Sidra Abid Syed; Bullo Saifullah; Shahzad  Nasim

doi:10.34016/pjbt.2024.21.01.866

Authors

Syed Waqad Ali Sir Syed University of Engineering & Technology, Biomedical Engineering Department, Karachi
Marium Raziq Sir Syed University of Engineering & Technology, Biomedical Engineering Department, Karachi
Muhammad Muzammil Khan Sir Syed University of Engineering & Technology, Biomedical Engineering Department, Karachi
Sania Tanvir 1Sir SyeUniversity of Engineering & Technology, Biomedical Engineering Department, Karachi
Syed Jamal Hyder Zaidi IQRA University, Karachi
Sidra Abid Syed Sir Syed University of Engineering & Technology, Biomedical Engineering Department, Karachi
Bullo Saifullah The Begum Nusrat Bhutto Women University
Shahzad Nasim Begum Nusrat Bhutto Women University, Faculty of Management Information Science and Technology, Sukkur, Pakistan

DOI:

https://doi.org/10.34016/pjbt.2024.21.01.866

Keywords:

G6PD deficiency, malaria control, Plasmodium Falciparum

Abstract

Even though it predisposes carriers to hemolysis, glucose-6-phosphate dehydrogenase (G6PD) deficiency is linked with malaria endemicity. This fact supports the malaria prevention theory. The objective of this paper to determine whether and how much there is a protective relationship between malaria and G6PD deficiency. Twelve databases were searched for studies describing any G6PD connection in malaria patients. 38 of the 50 included papers qualified for the review. Results indicated that there was no harmful association between G6PD deficiency and uncomplicated falciparum malaria in Even though it puts carriers at risk for hemolysis, glucose-6-phosphate dehydrogenase (G6PD) deficiency is widespread in areas of Pakistan where malaria is also prevalent. This data supports the malaria protection hypothesis. Pakistan's annual malaria burden is estimated to be 1.5 million cases. The government needs to execute a successful malaria control and eradication program, given the prevailing circumstances. Destroying Plasmodium falciparum gametocytes and eradicating Plasmodium vivax hypnozoite reservoirs are possible with primaquine. However, when using this medication, those who lack the enzyme glucose-6-phosphate (G6PD) experience hemolysis. The distribution of malaria and G6PD deficiency in Pakistan must be mapped to create an effective medication to suppress the disease. No significant reports of G6PD deficiency (G6PDd) in malaria patients have come from Pakistan. This review article seeks to establish the existence and magnitude of a protective connection between malaria and G6PD deficiency

Metrics

Metrics Loading ...

References

Ali, N., Anwar, M., Ayyub, M., Bhatti, F. A., Nadeem, M., & Nadeem, A. (2005). Frequency of glucose-6-phosphate dehydrogenase deficiency in some ethnic groups of Pakistan. Journal of the College of Physicians and Surgeons--Pakistan: JCPSP, 15(3), 137–141.

Allison, C., & Clyde, D. F. (1961). Malaria in African children with deficient erythrocyte glucose-6- phosphatedehydrogenase. British Medical Journal, 5236, 1346–1349. DOI: https://doi.org/10.1136/bmj.1.5236.1346

Alving, A. S., Tarlov, A. R., Brewer, G., Carson, P. E., Keller-Meyer, R. W., & Long, W. K. (1960). Glucose-6-phosphate dehydrogenase deficiency: some biological implications. Transactions of the Association of American Physicians, 73, 80–92.

Azadbakht, M., Hosseinimehr, S. J., Shokrzadeh, M., Habibi, E., & Ahmadi, A. (2011). Diospyros lotus L. fruit extract protects G6PD-deficient erythrocytes from hemolytic injury in vitro and in vivo: prevention of favism disorder. European Review for Medical and Pharmacological Sciences, 15(11), 1270–1281.

Beutler, E. (1994). G6PD deficiency. Blood, 84(11). DOI: https://doi.org/10.1182/blood.V84.11.3613.bloodjournal84113613

Beutler, E. (1996). G6PD: population genetics and clinical manifestations. Blood Reviews, 10(1), 45–52. DOI: https://doi.org/10.1016/S0268-960X(96)90019-3

Bouma, M. J., Goris, M., Akhtar, T., Khan, N., Khan, N., & Kita, E. (1995). Prevalence and clinical presentation of glucose-6-phosphate dehydrogenase deficiency in Pakistani Pathan and Afghan refugee communities in Pakistan; implications for the use of primaquine in regional malaria control programmes Trans R Soc Trop Med Hyg. Trans R Soc Trop Med Hyg, 89, 62–64. DOI: https://doi.org/10.1016/0035-9203(95)90661-4

Cappellini, M. D., & Fiorelli, G. (2008). Glucose-6-phosphate dehydrogenase deficiency. Lancet, 371(9606), 64–74. DOI: https://doi.org/10.1016/S0140-6736(08)60073-2

Clark, G., & Chaudhri, W. (1989). Some roles of freeradicals in malaria. Free Radical Biology and Medicine, 5(3), 315–321. DOI: https://doi.org/10.1016/0891-5849(89)90058-0

Friedman, M. J., & Trager, W. (1981). The biochemistry ofresistance to malaria. Science Americana, 244(3), 158–164. DOI: https://doi.org/10.1038/scientificamerican0381-154

Greene, L. S. (1993). G6PD deficiency as protection against falciparum malaria,” An epidemiologic critique of populationand experimental studies. American Journal of PhysicalAnthropology, 36(S17), 153–178. DOI: https://doi.org/10.1002/ajpa.1330360609

Hedrick, P. W. (2011). Population genetics of malaria resistance in humans. Heredity, 107(4), 283–304. DOI: https://doi.org/10.1038/hdy.2011.16

Howes, R. E., Piel, F. B., Patil, A. P., Nyangiri, O. A., Gething, P. W., Dewi, M., Hogg, M. M., Battle, K. E., Padilla, C. D., Baird, J. K., & Hay, S. I. (2012). G6PD deficiency prevalence and estimates of affected populations in malaria endemic countries: a geostatistical model-based map. PLoS Medicine, 9(11), DOI: https://doi.org/10.1371/journal.pmed.1001339

Kakar, Q., Khan, M. A., & Bile, K. M. (2010). Malaria control in Pakistan: new tools at hand but challenging epidemiological realities. La Revue de Sante de La Mediterranee Orientale [Eastern Mediterranean Health Journal], 16(Supp.), 54–60. DOI: https://doi.org/10.26719/2010.16.Supp.54

Kaplan, M., Beutler, E., Vreman, H. J., Hammerman, C., Levy-Lahad, E., & Renbaum, P. (1999). Neonatal hyperbilirubinemia in glucose-6- phosphate dehydrogenase-deficient heterozygotes. Pediatrics, 104, 68–74. DOI: https://doi.org/10.1542/peds.104.1.68

Khattak, A. A., Venkatesan, M., Nadeem, M. F., Satti, H. S., Yaqoob, A., Strauss, K., Khatoon, L., Malik, S. A., & Plowe, C. V. (2013). Prevalence and distribution of human Plasmodium infection in Pakistan. Malaria Journal, 12(1), 297. DOI: https://doi.org/10.1186/1475-2875-12-297

Khattak, M., Dawood, M., & Saleem, M. (1992). The prevalence of glucose-6-phosphate dehydrogenase deficiency in Northern Pakistan. Pak Armed Forces Med J, 42, 35–38.

Kruatrachue, M., Charoenlarp, P., Chongsuphajaisiddhi, T., & Harinasuta, C. (1962). Erythrocyte glucose-6-phosphate dehydrogenase and malaria in Thailand. Lancet, 280(7267), 1183–1186. DOI: https://doi.org/10.1016/S0140-6736(62)90956-X

Leslie, T., Briceño, M., Mayan, I., Mohammed, N., Klinkenberg, E., Sibley, C. H., Whitty, C. J. M., & Rowland, M. (2010). The impact of phenotypic and genotypic G6PD deficiency on risk of plasmodium vivax infection: a case-control study amongst Afghan refugees in Pakistan. PLoS Medicine,7(5), e1000283. DOI: https://doi.org/10.1371/journal.pmed.1000283

Luzzatto, L., & Gordon-Smith, E. C. (2001). Inherited haemolyticanaemia. In Postgraduate Haematology (pp. 120–143). Arnold.

Mehmood, A., Akhtar, M., & Niazi, M. (2010). Frequency of glucose-6-phosphate dehydrogenase deficiency in asymptomatic Pakistani population. Pak Armed Forces Med J, 60, 1–3.

Moiz, B., Nasir, A., Moatter, T., Naqvi, Z. A., & Khurshid, M. (2009). Population study of 1311 C/T polymorphism of Glucose 6 Phosphate Dehydrogenase gene in Pakistan - an analysis of 715 Xchromosomes. BMC Genet, 10. DOI: https://doi.org/10.1186/1471-2156-10-41

Moiz, B., Nasir, A., Moatter, T., Naqvi, Z. A., & Khurshid, M. (2011). Molecular characterization of glucose-6-phosphate dehydrogenase deficiency in Pakistani population: Molecular Characterization of Glucose-6-Phosphate Dehydrogenase Deficiency in Pakistan. International Journal of Laboratory Hematology, 33(6), 570–578. DOI: https://doi.org/10.1111/j.1751-553X.2011.01325.x

Moiz, Bushra. (2013). A review of G6PD deficiency in Pakistani perspective. JPMA. The Journal of the Pakistan Medical Association, 63(4), 501–503.

Ninokata, R., Kimura, U., Samakkarn, W., & Settheetham-Ishida, T. (2006). Coexistence of five G6PD variants indicatesethnic complexity of Phuket islanders, Southern Thailand. Journal Human Genetics, 51(5), 424–428. DOI: https://doi.org/10.1007/s10038-006-0380-y

Nkhoma, E. T., Poole, C., Vannappagari, V., Hall, S. A., & Beutler, E. (2009). The global prevalence of glucose-6-phosphate dehydrogenase deficiency: a systematic review and meta-analysis. Blood Cells, Molecules & Diseases, 42(3), 267–278. DOI: https://doi.org/10.1016/j.bcmd.2008.12.005

Rehman, H., Khan, M. A., Hameed, A., Roghani, M. T., & Ahmad, A. (1995). Erythrocyte glucose 6 phosphate dehydrogenase deficiency and neonatal jaundice. JPMA. The Journal of the Pakistan Medical Association, 45(10), 259–260.

Riskin, A., Gery, N., Kugelman, A., Hemo, M., Spevak, I., & Bader, D. (2012). Glucose-6-phosphate dehydrogenase deficiency and borderline deficiency: association with neonatal hyperbilirubinemia. The Journal of Pediatrics, 161(2), 191-6. e1. DOI: https://doi.org/10.1016/j.jpeds.2012.02.018

Ronald, A. R., Underwood, B. A., & Woodward, T. E. (1968). Glucose-6-phosphate dehydrogenase deficiency in Pakistani males. Transactions of the Royal Society of Tropical Medicine and Hygiene, 62(4), 531–533. DOI: https://doi.org/10.1016/0035-9203(68)90139-9

Ruwende, S. C., & Khoo, R. W. (1995). Natural selection ofhemi- and heterozygotes for G6PD deficiency in Africa byresistance to severe malaria. Nature, 376, 246–249. DOI: https://doi.org/10.1038/376246a0

Saha, N., Ramzan, M., Tay, J. S., Low, P. S., Basair, J. B., & Khan, F. M. (1994). Molecular characterisation of red cell glucose-6-phosphate dehydrogenase deficiency in north-west Pakistan. Human Heredity, 44(2), DOI: https://doi.org/10.1159/000154196

Saleem A Glucose-6-phosphate dehydrogenase deficiency and hemolytic anemia. (1966). J Pak Med Assoc, 16, 3–9.

Shah, S. S., Diakite, S. A. S., Traore, K., Diakite, M., Kwiatkowski, D. P., Rockett, K. A., Wellems, T. E., & Fairhurst, R. M. (2012). A novel cytofluorometric assay for the detection and quantification of glucose-6-phosphate dehydrogenase deficiency. Scientific Reports, 2, 299. DOI: https://doi.org/10.1038/srep00299

Stern, M. A., Kynoch, P. A., & Lehmann, H. (1968). Beta-thalassaemia, glucose-6- phosphate-dehydrogenase deficiency, and haemoglobin DPunjab in Pathans. Lancet, 1, 1284–1285. DOI: https://doi.org/10.1016/S0140-6736(68)92296-4

Tikmani, S. S., Warraich, H. J., Abbasi, F., Rizvi, A., Darmstadt, G. L., & Zaidi, A. K. (2010). Incidence of neonatal hyperbilirubinemia: a populationbased prospective study in Pakistan. Trop Med Int Health, 15, 502–507. DOI: https://doi.org/10.1111/j.1365-3156.2010.02496.x

Toncheva, D., & Tzoneva, M. (1985). Prenatal selection and fetal development disturbances occurring in carriers of G6PDdeficiency. Human Genetics, 69(1). DOI: https://doi.org/10.1007/BF00295536

Youngster, I., Arcavi, L., Schechmaster, R., Akayzen, Y., Poplisti, H., & Shimonov, J. (2010). Medications and glucoses-6-phosphate dehydrogenase deficiency: an evidence-based review. Drug Saf, 33, 713–726 DOI: https://doi.org/10.2165/11536520-000000000-00000