Glucose-6-phosphate dehydrogenase deficiency and homozygous sickle cell disease in Congo.
G6PD genotypes were determined in Brazzaville (Congo) on 188 HbSS patients (109 females, 79 males) and 210 controls (115 females and 95 males) with HbAA. DNA samples were analyzed by the polymerase chain reaction (PCR). The frequencies of G6PD B, A+ and A- alleles were 56.9, 20.8 and, 22.2% in the patients versus 56.3, 21.2 and, 22.5% in the controls, respectively. The prevalence of G6PD genotypes in HbSS did not differ (p > 0.05) from that found in the controls. Prevalence of G6PD deficiency did not change when patients were stratified by age, suggesting that there is no advantage of the association of G6PD deficiency with HbSS. Red blood cell count, mean corpuscular volume and mean corpuscular hemoglobin were not modified by the G6PD genotypes, while Hb level was lower in HbSS with G6PD A-. Our study suggests that in Congo, G6PD deficiency does not offer any biological advantage to sicklers.
INSERM U474, Hôpital Henri-Mondor, Créteil, France.
J C
JC
Bouanga
R
R
Mouélé
C
C
Préhu
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H
Wajcman
J
J
Feingold
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F
Galactéros
D000293:Adolescent; D000328:Adult; D000367:Age Factors; D000755:Anemia, Sickle Cell / Q000097:blood / Q000150:complications* / Q000453:epidemiology; D002648:Child; D002675:Child, Preschool; D003223:Congo / Q000453:epidemiology; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D005955:Glucosephosphate Dehydrogenase Deficiency / Q000150:complications* / Q000453:epidemiology / Q000235:genetics*; D006441:Hemoglobin A; D006720:Homozygote; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D010641:Phenotype; D016133:Polymerase Chain Reaction / Q000379:methods; D015995:Prevalence; D017678:Sex Distribution
C028672:hemoglobin AA; D006441:Hemoglobin A