Variation in Glucose-6-Phosphate Dehydrogenase activity following acute malaria
Issued Date
2022-01-01
Resource Type
ISSN
19352727
eISSN
19352735
Scopus ID
2-s2.0-85129922558
Pubmed ID
35544453
Journal Title
PLoS Neglected Tropical Diseases
Volume
16
Issue
5
Rights Holder(s)
SCOPUS
Bibliographic Citation
PLoS Neglected Tropical Diseases Vol.16 No.5 (2022)
Suggested Citation
Ley B. Variation in Glucose-6-Phosphate Dehydrogenase activity following acute malaria. PLoS Neglected Tropical Diseases Vol.16 No.5 (2022). doi:10.1371/journal.pntd.0010406 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/87426
Title
Variation in Glucose-6-Phosphate Dehydrogenase activity following acute malaria
Author(s)
Author's Affiliation
Faculty of Tropical Medicine, Mahidol University
Melbourne School of Population and Global Health
Arba Minch University
Eijkman Institute for Molecular Biology
Universitas Gadjah Mada
Menzies School of Health Research
International Centre for Diarrhoeal Disease Research Bangladesh
Nuffield Department of Medicine
Papuan Health and Community Development Foundation
Melbourne School of Population and Global Health
Arba Minch University
Eijkman Institute for Molecular Biology
Universitas Gadjah Mada
Menzies School of Health Research
International Centre for Diarrhoeal Disease Research Bangladesh
Nuffield Department of Medicine
Papuan Health and Community Development Foundation
Other Contributor(s)
Abstract
Primaquine and tafenoquine are the only licensed drugs with activity against Plasmodium vivax hypnozoites but cause haemolysis in patients with glucose–6–phosphate dehydrogenase (G6PD) deficiency. Malaria also causes haemolysis, leading to the replacement of older erythrocytes with low G6PD activity by reticulocytes and young erythrocytes with higher activity. Aim of this study was to assess the impact of acute malaria on G6PD activity. Selected patients with uncomplicated malaria were recruited in Bangladesh (n = 87), Indonesia (n = 75), and Ethiopia (n = 173); G6PD activity was measured at the initial presentation with malaria and a median of 176 days later (range 140 to 998) in the absence of malaria. Among selected participants (deficient participants preferentially enrolled in Bangladesh but not at other sites) G6PD activity fell between malaria and follow up by 79.1% (95%CI: 40.4 to 117.8) in 6 participants classified as deficient (<30% activity), 43.7% (95%CI: 34.2 to 53.1) in 39 individuals with intermediate activity (30% to <70%), and by 4.5% (95%CI: 1.4 to 7.6) in 290 G6PD normal (≥70%) participants. In Bangladesh and Indonesia G6PD activity was significantly higher during acute malaria than when the same individuals were retested during follow up (40.9% (95%CI: 33.4–48.1) and 7.4% (95%CI: 0.2 to 14.6) respectively), whereas in Ethiopia G6PD activity was 3.6% (95%CI:-1.0 to-6.1) lower during acute malaria. The change in G6PD activity was apparent in patients presenting with either P. vivax or P. falciparum infection. Overall, 66.7% (4/6) severely deficient participants and 87.2% (34/39) with intermediate deficiency had normal activities when presenting with malaria. These findings suggest that G6PD activity rises significantly and at clinically relevant levels during acute malaria. Prospective case-control studies are warranted to confirm the degree to which the predicted population attributable risks of drug induced haemolysis is lower than would be predicted from cross sectional surveys.