Background And Objective: Prevalence of hemoglobinophaty S and glucose-6-phosphate dehydrogenase (G6PD) deficiency are very increased in certain zones of Western Africa due to the positive pressure exerted by malaria on these congenital defects. In Maresme, a region of East Catalonia, there is a numerous community of African people, coming from areas of Western Africa where sickle cell trait and G6PD deficiency are frequent. The aim of our study was to know the prevalence of both disturbances in this population.
Population And Method: We studied 204 individuals of black ethnical background who were migrant Africans. They attended the Immigrant Attention Unit or Outside Surgery Department of Consorcio Sanitario de Mataró for any medical or surgical problems but not for anemia. The G6PD deficiency was determined by a quantitative assay and 2 screening techniques. The identification of abnormal hemoglobins was done by electrophoresis.
Results: We studied 141 males (69%) and 63 females (31%). Mean age was 30.8 years (range: 1-70). The studied population came from Gambia, Senegal, Equatorial Guinea, Guinea Bissau, Mali, Somalia, Guinea Conakry, Nigeria, Ghana, Ivory Coast, Sierra Leone, Liberia and Mauritania, and were members of the Sarankhole, Mande, Fulani, Peul, Djola, Bambara, Pare and Ibo ethnic groups (according to the frequency order). We found abnormal hemoglobins in 44 subjects (21.5%): 36 hemoglobin S carriers, 7 hemoglobin C carriers and one hemoglobin C homozygous. Moreover, we identified G6PD deficiency in 31 subjects. According to these results, the prevalence of hemoglobinophaty S in these people is 17.6%; the prevalence of hemoglobinophaty C is 3.9%, and the prevalence of G6PD deficiency is 15.2%. The association of abnormal hemoglobins and G6PD deficiency was found only in a 3% of the cases (2.5% hemoglobinophaty S and 0.5% hemoglobinophaty C).
Conclusions: This results demonstrate a high prevalence of hemoglobinopathies and G6PD deficiency in this population. The morbidity and mortality of sickle cell disease and the complications due to G6PD deficiency, besides the easy detection using electrophoresis and G6PD determination, make it necessary to standardize these tests in areas with high density of black people.
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http://dx.doi.org/10.1157/13123035 | DOI Listing |
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a well-known red blood cell enzymopathy and a cause of intravascular hemolysis. This case report presents a child with underlying G6PD deficiency who experienced an acute episode of extensive intravascular hemolysis induced by a scrub typhus infection. The key takeaway from this report is that scrub typhus infection can trigger extensive hemolysis in patients with even "mild" G6PD deficiency, and normal G6PD levels found during the acute phase of hemolysis do not rule out the possibility of underlying G6PD deficiency.
View Article and Find Full Text PDFPurpose: To develop an algorithm using routine clinical laboratory measurements to identify people at risk for systematic underestimation of glycated hemoglobin (HbA1c) due to p.Val68Met glucose-6-phosphate dehydrogenase (G6PD) deficiency.
Methods: We analyzed 122,307 participants of self-identified Black race across four large cohorts with blood glucose, HbA1c, and red cell distribution width measurements from a single blood draw.
Int J Hematol
January 2025
Children's Medical Center, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, People's Republic of China.
Objective: G6PD deficiency is a potentially life-threatening condition in neonates presenting with hyperbilirubinemia. This study aims to identify clinical and laboratory predictors of G6PD deficiency in neonates presenting with hyperbilirubinemia.
Methods: This was a retrospective study of 227 term neonates admitted to Heyuan People's Hospital from January 2019 to October 2023.
Lancet Infect Dis
January 2025
Institut Pasteur, Université Paris Cité, G5 Épidémiologie et Analyse des Maladies Infectieuses, Paris, France. Electronic address:
Background: Plasmodium vivax forms dormant liver stages (hypnozoites) that can reactivate weeks to months after primary infection. Radical cure requires a combination of antimalarial drugs to kill both the blood-stage and liver-stage parasites. Hypnozoiticidal efficacy of the liver-stage drugs primaquine and tafenoquine cannot be estimated directly because hypnozoites are undetectable.
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