Abstract
Plasmodium vivax malaria is endemic in Mauritania. Individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency may develop acute hemolytic anemia when exposed to 8-aminoquinoline antimalarial drugs, which are indispensable for a complete cure. The prevalence of G6PD allelic variants was assessed in different ethno-linguistic groups present in Mauritania. A total of 996 blood samples (447 males and 549 females; 499 white Moors and 497 individuals of black African ancestry) were collected from febrile patients in 6 different study sites: Aleg, Atar, Kiffa, Kobeni, Nouakchott, and Rosso. The presence of the African-type G6PD A- (G202A, A376G, A542T, G680T, and T968C mutations) and the Mediterranean-type G6PD B- (C563T) variants was assessed by PCR followed by restriction fragment length polymorphism and/or DNA sequencing. The prevalence of African-type G6PD A- genotype was 3.6% (36/996), with 6.3% (28/447) of hemizygote (A-) males and 1.5% (8/549) of homozygous (A-A-) females. Forty of 549 (7.3%) women were heterozygous (AA-). The following genotypes were observed among hemizygous men and/or homozygous women: A376G/G202A (22/996; 2.2%), A376G/T968C Betica-Selma (12/996; 1.2%), and A376G/A542T Santamaria (2/996; 0.2%). The Mediterranean-type G6PD B- genotype was not observed. The prevalence rates of G6PD A- genotype in male (10/243; 4.1%) and heterozygous female (6/256; 2.3%) white Moors were lower (p < 0.05) than those of males (18/204; 8.8%) and heterozygous females (34/293; 11.6%) of black African ancestry. There were only a few homozygous women among both white Moors (3/256; 1.2%) and those of black African ancestry (5/293; 1.7%). The prevalence of G6PD deficiency in Mauritania was comparable to that of neighboring countries in the Maghreb. Because of the purportedly close ethnic ties between the Mauritanian white Moors and the peoples in the Maghreb, further investigations on the possible existence of the Mediterranean-type allele are required. Moreover, a surveillance system of G6PD phenotype and/or genotype screening is warranted to establish and monitor a population-based prevalence of G6PD deficiency.
Highlights
Glucose-6-phosphate dehydrogenase (G6PD) is the key enzyme of pentose phosphate pathway, the unique source of the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) in mature human erythrocytes
When mature erythrocytes are deficient in G6PD and are exposed to various exogenous trigger factors, including infections, a variety of drugs (e.g., 8-aminoquinoline antimalarial drugs, which include primaquine and tafenoquine), and vicine and convicine found in fava beans, the antioxidant defense system is unable to neutralize free radicals that accumulate in the erythrocytes, leading to lipid peroxidation and cell lysis, which may be manifested clinically by acute hemolytic anemia [? ? ]
We found a much higher prevalence of G6PD deficiency in black Moors and three minority ethnic groups than in white Moors in Mauritania, in practice, it may be argued that many of these individuals of black African ancestry may not be confronted with the potential problem of anti-hypnozoite therapy with 8-aminoquinolines because they tend to be Duffy-negative, as in the majority of black Africans elsewhere in sub-Saharan Africa, and may be naturally “resistant to P. vivax infections [? ? ? ? ]
Summary
Glucose-6-phosphate dehydrogenase (G6PD) is the key enzyme of pentose phosphate pathway, the unique source of the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) in mature human erythrocytes. When mature erythrocytes are deficient in G6PD and are exposed to various exogenous trigger factors, including infections, a variety of drugs (e.g., 8-aminoquinoline antimalarial drugs, which include primaquine and tafenoquine), and vicine and convicine found in fava beans, the antioxidant defense system is unable to neutralize free radicals that accumulate in the erythrocytes, leading to lipid peroxidation and cell lysis, which may be manifested clinically by acute hemolytic anemia [? Most G6PD mutations are clinically silent unless the G6PD-deficient individual is challenged with a trigger factor. The main clinical manifestation in such individuals is potentially fatal non-immune acute hemolytic anemia
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