Background: Glucose-6-phosphate dehydrogenase deficiency is an enzymopathy characterized by insufficient production of reduced glutathione (GSH), a molecule known for its antioxidant role. This lack of GSH leads to a ...Background: Glucose-6-phosphate dehydrogenase deficiency is an enzymopathy characterized by insufficient production of reduced glutathione (GSH), a molecule known for its antioxidant role. This lack of GSH leads to a deficit in the elimination of peroxide ions from the red blood cells, causing thereby hemolytic accidents, which can be fatal if not properly managed. In neonates, the clinical picture is most often that of neonatal jaundice. Objectives: This study aimed to determine the place of G6PD deficiency as a cause of neonatal jaundice at Essos Hospital Centre. Methods: We conducted a prospective descriptive study over three months. Blood samples taken from newborns aged 0 to 28 days were analyzed in the medical analysis laboratory of the Essos Hospital Centre in Yaoundé. We carried out a determination of the enzymatic activity of G6PD, a blood count and the determination of the bilirubin level. The results obtained were analysed using R statistical software version 4.1.1. Linear regression analyses were used to assess correlations between the variables of interest. Results: Sixty-nine icteric neonates constituted our study population, with a total of 40 boys (58%) and 29 girls (42%) with a sex ratio of 1.37 in favour of boys. The prevalence of G6PD deficiency in icteric children was 50.72%. The mean hemoglobin was 15.3 ± 3.08 g/dL and the mean red blood cell count was 4.52 ± 1.01 × 10<sup>6</sup>/mm<sup>3</sup>. The mean total bilirubin was 122 ± 48.3 mg/L with a maximum of 308 mg/L and the mean free bilirubin was 104 ± 46.6 mg/L with a maximum of 292 mg/L. Furthermore, after linear regression analysis, we obtained a positive and significant correlation between G6PD enzymatic activity and hemoglobin level (r = 0.33;p ≤ 0.001), G6PD red blood cell level (r = 0.26;p Conclusion: Neonatal jaundice in G6PD-deficient children is a real public health problem and the prevention of hemolysis in children requires an early diagnosis of the enzyme disorder and good follow-up of the children.展开更多
文摘Background: Glucose-6-phosphate dehydrogenase deficiency is an enzymopathy characterized by insufficient production of reduced glutathione (GSH), a molecule known for its antioxidant role. This lack of GSH leads to a deficit in the elimination of peroxide ions from the red blood cells, causing thereby hemolytic accidents, which can be fatal if not properly managed. In neonates, the clinical picture is most often that of neonatal jaundice. Objectives: This study aimed to determine the place of G6PD deficiency as a cause of neonatal jaundice at Essos Hospital Centre. Methods: We conducted a prospective descriptive study over three months. Blood samples taken from newborns aged 0 to 28 days were analyzed in the medical analysis laboratory of the Essos Hospital Centre in Yaoundé. We carried out a determination of the enzymatic activity of G6PD, a blood count and the determination of the bilirubin level. The results obtained were analysed using R statistical software version 4.1.1. Linear regression analyses were used to assess correlations between the variables of interest. Results: Sixty-nine icteric neonates constituted our study population, with a total of 40 boys (58%) and 29 girls (42%) with a sex ratio of 1.37 in favour of boys. The prevalence of G6PD deficiency in icteric children was 50.72%. The mean hemoglobin was 15.3 ± 3.08 g/dL and the mean red blood cell count was 4.52 ± 1.01 × 10<sup>6</sup>/mm<sup>3</sup>. The mean total bilirubin was 122 ± 48.3 mg/L with a maximum of 308 mg/L and the mean free bilirubin was 104 ± 46.6 mg/L with a maximum of 292 mg/L. Furthermore, after linear regression analysis, we obtained a positive and significant correlation between G6PD enzymatic activity and hemoglobin level (r = 0.33;p ≤ 0.001), G6PD red blood cell level (r = 0.26;p Conclusion: Neonatal jaundice in G6PD-deficient children is a real public health problem and the prevention of hemolysis in children requires an early diagnosis of the enzyme disorder and good follow-up of the children.
