Molecular epidemiology and activity of erythrocyte G6PD variants in a homogenous Nigerian population

Ademowo, O G; Falusi, Adeyinka G.

doi:10.4314/eamj.v79i1.8924

Cited by 27 publications

(26 citation statements)

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“…This proportion of G6PD deficient individuals fall within the range reported for Nigerians from other parts of the country and collaborates with the report from a community in South Western part of Nigeria in male individuals studied (Ademowo and Falusi 2002). It may then be that the prevalence of G6PD deficiency among Nigerian males irrespective of their geographical location is relatively constant.…”

Section: Discussionsupporting

confidence: 68%

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Glucose -6- phosphate dehydrogenase (g6pd) activity and deficiency in a population of Nigerian males resident in jos

Egesie

Joseph²,

Isiguzoro³

et al. 2010

Nig. J. Phys Sci

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Summary:The activity of red blood cell Glucose 6-phosphate dehydrogenase (G6PD) in one hundred and twenty six healthy male individuals who are Nigerians residing in Jos was evaluated. The enzyme activity was determined quantitatively by spectrophotometer assay method. The activity of red cell G6PD enzyme was subnormal in 20% of the population studied. This agrees with previous report of the prevalence of G6PD deficiency in Nigerian males from the Western region of the country which is between 20 and 26%. The proportion of Nigerian males with subnormal G6PD activity is relatively constant irrespective of their geographical location.

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Section: Discussionsupporting

confidence: 68%

“…In Nigerians, the prevalence of G6PD deficiency ranges from 4 -26% with the male population having about 20 -26% (Luzzatto 2001, Ademowo 2002. This prevalence rate varies from one community to another.…”

Section: Introductionmentioning

confidence: 99%

Glucose -6- phosphate dehydrogenase (g6pd) activity and deficiency in a population of Nigerian males resident in jos

Egesie

Joseph²,

Isiguzoro³

et al. 2010

Nig. J. Phys Sci

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“…This value was lower than the frequency of 20% reported among 30 children with a mean age of 3.6 years who were brought to hospital with convulsions and falciparum malaria infection in Ibadan [20]. Similarly, the respective prevalence rates of 16.4% and 8.1% among male and female malaria patients in the present study are at variance with the respective figures of 23.9% and 4.6% among males and females reported recently by Ademowo and Falusi [11]. The prevalence of G6PD deficiency among males is four times higher than in females in the general population.…”

Section: Discussioncontrasting

confidence: 56%

“…In Nigeria, G6PD deficiency occurs in 24% of boys and 5% of girls [11]. It is also known to be a significant cause of anaemia in children, especially neonates [7].…”

Section: Introductionmentioning

confidence: 99%

Glucose-6-phosphate dehydrogenase status and severity of malarial anaemia in Nigerian children

Orimadegun

Sodeinde

2011

J Infect Dev Ctries

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Introduction: Glucose-6-phosphate dehydrogenase (G6PD) deficiency (Gd-) contributes to morbidity and mortality in sub-Saharan Africa but recent data on the interaction between Gd-and malaria among children is scarce. We hypothesised that, being a haemolytic factor, Gdmakes severe malarial anaemia (SMA) more common and even more severe. Methodology: We selected 930 children aged 0.5-12 years attending a reference hospital with microscopically proven falciparum malaria. G6PD and haemoglobin were typed by the fluorescent spot test and electrophoresis, respectively. Molecular typing by PCR and restriction enzyme digestion was also performed on 15% of randomly selected samples. Haematocrit (PCV) values, haemoglobin type, blood group, presence of sickle cell trait (HbAS), and parasite counts were compared between G6PD-normal and deficient children. Results: Prevalence of Gd-was 16.4% and 8.1% among boys and girls with malaria, respectively. Mean PCV was 22.8% in deficient children compared with 21.0% in normal children (p=0.041). In boys, 2.7% of Gd-had PCV ≤10%, as compared to 13.6% in Gd+ (p = 0.005). Similarly, 21.3% of Gd-had PCV ≤15% compared with 39.4% in Gd+ (p=0.003). No such difference was found among girls. Overall, HbAS was typed in 7.6% and was more common in Gd-(13.0%) than in Gd+ (6.8%), but the difference was not statistically significant (p=0.058). The mean parasite counts were significantly lower in Gd-(15477.5/μl) than in Gd+ (19784.4/μl; p=0.013), and it was independent from HbAS. Conclusion: Gd-males but not females were significantly less likely to develop severe malarial anaemia.

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“…[8][9][10] G6PD A-is molecularly characterized by two distinct variants within the gene: one variant is always 376 A-G (underlying G6PD A, which has 85% enzyme activity and is not considered to be a deficient variant); a second deficiencycausing mutation is 202 G-A (376G/202A; most common), 680 G-T (376G/680T), or 968 T-C (376G/968C; Betica Selma). 11 Virtually all of the second A-mutations have been found in the presence of 376 A-G, with only one exception reported so far.…”

mentioning

confidence: 99%

G6PD A- Deficiency and Severe Malaria in The Gambia: Heterozygote Advantage and Possible Homozygote Disadvantage

Sirugo

Predazzi

Bartlett

et al. 2014

The American Society of Tropical Medicine and Hygiene

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Abstract. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is frequent in Africa, because it confers resistance to Plasmodium falciparum malaria; however, the nature of the protection and the genotypes associated with it have been controversial. In 1972, Bienzle and others described protection from malaria in West African females heterozygous for G6PD A-. They determined that G6PD A-heterozygotes had lower parasite counts than A-homozygotes, hemizygous males, and normal individuals. However, other studies have reached different conclusions about the protective genotypes. DNA samples from 135 children with severe malaria and 146 children with mild malaria from The Gambia were genotyped for the G6PD A-mutation that is most frequent among Gambians (G6PD 968 T-C); there was a marked deficiency of heterozygotes and an excess of homozygotes with severe malaria, producing a strong deviation from Hardy-Weinberg equilibrium. Our results support the protective effect in G6PD A-heterozygous females and suggest that homozygotes might be more susceptible to severe malaria attacks.Glucose-6-phosphate dehydrogenase (G6PD) deficiency is widespread across Africa, because it confers resistance to Plasmodium falciparum (and possibly, P. vivax) malaria, but despite this evidence and the previous evidence that G6PD is under strong natural selection, the nature of the protection and genotypes associated with it has been controversial.

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Molecular epidemiology and activity of erythrocyte G6PD variants in a homogenous Nigerian population

Cited by 27 publications

References 0 publications

Glucose -6- phosphate dehydrogenase (g6pd) activity and deficiency in a population of Nigerian males resident in jos

Glucose -6- phosphate dehydrogenase (g6pd) activity and deficiency in a population of Nigerian males resident in jos

Glucose-6-phosphate dehydrogenase status and severity of malarial anaemia in Nigerian children

G6PD A- Deficiency and Severe Malaria in The Gambia: Heterozygote Advantage and Possible Homozygote Disadvantage

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