Assessment of glucose-6-phosphate dehydrogenase activity using CareStart G6PD rapid diagnostic test and associated genetic variants in Plasmodium vivax malaria endemic setting in Mauritania.

Oum Kelthoum Mamadou Djigo,Mohamed Abdallahi Bollahi,Leonardo Basco,Mohamed Salem Ould Ahmedou Salem,Rachida Tahar,Hervé Bogreau,Moina Hasni Ebou,Ali Ould Mohamed Salem Boukhary

doi:10.1371/journal.pone.0220977

Abstract

BackgroundPrimaquine is recommended by the World Health Organization (WHO) for radical treatment of Plasmodium vivax malaria. This drug is known to provoke acute hemolytic anemia in individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency. Due to lack of data on G6PD deficiency, the use of primaquine has been limited in Africa. In the present study, G6PD deficiency was investigated in blood donors of various ethnic groups living in Nouakchott, a P. vivax endemic area in Mauritania.Methodology/Principal findingsVenous blood samples from 443 healthy blood donors recruited at the National Transfusion Center in Nouakchott were screened for G6PD activity using the CareStart G6PD deficiency rapid diagnostic test. G6PD allelic variants were investigated using DiaPlexC G6PD genotyping kit that detects African (A-) and Mediterranean (B-) variants. Overall, 50 of 443 (11.3%) individuals (49 [11.8%] men and 1 [3.7%] woman) were phenotypically deficient. Amongst men, Black Africans had the highest prevalence of G6PD deficiency (15 of 100 [15%]) and White Moors the lowest (10 of 168, [5.9%]). The most commonly observed G6PD allelic variants among 44 tested G6PD-deficient men were the African variant A- (202A/376G) in 14 (31.8%), the Mediterranean variant B- (563T) in 13 (29.5%), and the Betica-Selma A- (376G/968C) allelic variant in 6 (13.6%). The Santamaria A- variant (376G/542T) and A variant (376G) were observed in only one and two individuals, respectively. None of the expected variants was observed in 8 (18.2%) of the tested phenotypically G6PD-deficient men.ConclusionThis is the first published data on G6PD deficiency in Mauritanians. The prevalence of phenotypic G6PD deficiency was relatively high (11.3%). It was mostly associated with either African or Mediterranean variants, in agreement with diverse Arab and Black African origins of the Mauritanian population.

Highlights

Malaria remains a major public health burden in Mauritania with two-thirds of the population at risk
In the northern Saharan zone of the country, including Nouakchott, the capital city, malaria is predominantly caused by Plasmodium vivax [1, 2], whereas in the southern Sahelian zone, almost all malaria cases are due to Plasmodium falciparum [3, 4]
All ethnic groups in Mauritania were represented in the study population (168 white Moors, 173 black Moors, 100 Black Africans, and 2 mixed ethnic origins)

Summary

Introduction

Malaria remains a major public health burden in Mauritania with two-thirds of the population at risk. Radical cure of P. vivax malaria requires the elimination of both the blood stage parasites and hypnozoites. Tafenoquine (Krintafel), another 8-aminoquinoline with a hypnozoicidal activity, has recently been approved by the United States Food and Drug Administration [6]. Despite their effectiveness in eliminating hypnozoites, 8-aminoquinolines may cause dose-dependent oxidant hemolysis in glucose-6-phosphate dehydrogenase (G6PD) deficient individuals [7, 8]. Primaquine is recommended by the World Health Organization (WHO) for radical treatment of Plasmodium vivax malaria. This drug is known to provoke acute hemolytic anemia in individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency. G6PD deficiency was investigated in blood donors of various ethnic groups living in Nouakchott, a P. vivax endemic area in Mauritania

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