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Glucose-6-phosphate dehydrogenase deficiency in the newborn: its prevalence and relation to neonatal jaundice
V S Tanphaichitr1, P Pung-amritt, S Yodthong
1Department of Pediatrics, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand.
Insights
Glucose-6-phosphate dehydrogenase (G6PD) deficiency affects 12.08% of Thai males, increasing neonatal jaundice risk. While G6PD deficiency is linked to higher jaundice incidence, key bilirubin levels and onset were similar between deficient and normal groups.
Area of Science:
- Medical Genetics
- Neonatology
- Public Health
Background:
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency is common in Thailand, posing risks for neonatal hyperbilirubinemia.
- Understanding the prevalence and impact of G6PD deficiency on neonatal jaundice is crucial for early diagnosis and management.
Purpose of the Study:
- To investigate the prevalence of G6PD deficiency in Thai male newborns.
- To determine the association between G6PD deficiency and the incidence and characteristics of neonatal jaundice.
Main Methods:
- Quantitative red blood cell (RBC) G6PD assay performed on cord blood from 505 male neonates.
- Jaundice observation, bilirubin level determination, and workup for other causes in G6PD deficient and normal groups.
- Follow-up questionnaires to assess outcomes and associated conditions.
Main Results:
- Prevalence of G6PD deficiency was 12.08% (61/505 males).
- Neonatal jaundice occurred in 49.15% of G6PD deficient infants versus 23.68% in G6PD normal infants.
- No statistically significant differences were found in jaundice onset, peak bilirubin levels, or hospitalization duration between groups, though ABO incompatibility was more frequent in the G6PD deficient group.
Conclusions:
- G6PD deficiency is prevalent in Thai male newborns and is associated with a higher incidence of neonatal jaundice.
- Despite increased incidence, G6PD deficiency did not significantly alter the severity or timing of jaundice markers compared to G6PD normal neonates.
- Further research may explore specific management strategies for jaundiced neonates with G6PD deficiency in high-prevalence regions.
Abstract:
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is prevalent in Thailand. This condition can cause acute hemolysis during oxidative stress and also severe hyperbilirubinemia in the newborn in some populations. Our aim was to study the prevalence of G6PD deficiency in relation to neonatal jaundice. We performed quantitative red blood cell (RBC) G6PD assay in the cord blood of 505 male subjects. Observation of jaundice and determination of bilirubin level as well as work up for other causes of jaundice were made in the G6PD deficiency group compared to a G6PD normal group. Questionnaires were also sent for further follow up to both groups. The results of the study were as follows: Sixty-one of 505 male (12.08%) had RBC G6PD deficiency (Group I). The rest (444 cases) had normal G6PD (Group II). In Group I, 49.15% developed neonatal jaundice, of which 28.82% were physiologic and 20.33% were pathologic jaundice. In group II, 23.68% developed jaundice; 16.51% were physiologic and 7.17% were pathologic jaundice, respectively. Onset of jaundice, date of peak bilirubin and peak bilirubin level in Group I and Group II were not statistically different. ABO incompatibility was associated with Group I in 17.24% and with Group II in 9.09%. Hospitalization day in Groups I and II were not statistically different. Other associated diseases were found in both groups, ie infection, congenital malformation, respiratory distress syndrome, but there was no significant difference in terms of jaundice. Phototherapy was required in 18.64% and 10.28% in Group I and II with a duration of 3.91 +/- 1.24 and 3.21 +/- 1.75 days, respectively. One case in Group I who was also premature received one exchange blood transfusion due to severe sepsis but he did not survive. One case in Group II who had polycythemia was successfully treated by partial exchange transfusion with plasma.