Liver function assessment in Glucose-6-Phosphate Dehydrogenase deficient neonates in Benin

Abstract

Background: Glucose-6-phosphate dehydrogenase (G6PD) deficiency is one of the major underlying causes of jaundice in neonates. However, the exact cause of the hyperbilirubinemia is still unknown. This study was aimed to assess liver function in G6PD deficient neonates. Methods: This study was carried out as a pre-posttest design study with a control group. A total of 410 neonates aged ≤7 days were included in the study. Intra-erythrocyte G6PD activity was determined by quantitative enzymatic method. Plasma glucose, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activity, direct and total bilirubin, calcium (Ca2+) and magnesium (Mg2+) levels were measured using ELITech reagents. Hematological analyses were performed using an automatic hematological analyzer. Results: Of the 410 neonates, 101 (24.63%) were G6PD-deficient with no significant difference between gender (male, 49 (11.95%); female, 52 (12.68%). G6PD activity level was significantly (p ˂0.001) decreased in G6PD-deficient male (2.06 ± 0.82 U/g Hb vs 16.63 ± 5.13 U/g Hb) and in female (5.42 ± 1.28 vs 19.73 ± 2.71 U/g Hb) compared to G6PD-normal controls. Blood glucose showed no variation, but conjugated bilirubin (p =0.03) and total bilirubin (p =0.01) levels were significantly increased in G6PD-deficient than in G6PD-normal controls. Calcium level was significantly (p =0.03) higher in G6PD-deficient while Magnesium level did not vary. Serum AST (p =0.01) and ALT (p =0.03) levels were significantly increased in G6PD-deficient neonates compared to G6PD-normal controls. AST and ALT levels in erythrocytes showed no changes. Conclusion: Results suggest that hyperbilirubinemia in G6PD deficient neonates may be caused by liver malfunction