Onset of Jaundice in G-6-PD Deficient Neonates
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《印第安小儿科》
Department of Neonatology,Shaare Zedek Medical Center, Faculty of Medicine of the Hebrew University, Jerusalem;
Faculty of Health Sciences, Ben Gurion University of the Negev,
We read the letter by Drs. Murki and Dutta, in which they report on umbilical cord blood serum total bilirubin (STB) levels in glucose-6-phosphate dehydrogenase (G-6-PD)-deficient and-normal neonates, with great interest(1). In their study, cord blood bilirubin levels were similar in the G-6-PD deficient and control neonates, suggesting that, in the Indian neonates studied, G-6-PD deficiency associated neonatal jaundice did not commence in utero. The authors conclude that their data negates that of a previous study of ours that jaundice in G-6-PD deficient infants commences most likely in utero(2).
We would like to point out significant differences in concept, design and conclusions between our study and the present one which renders them not directly comparable. Because of technical and logistic problems, we could not study umbilical cord blood samples as did Drs. Murki and Dutta. Umbilical blood sampling would undoubtedly have been a more accurate method of reflecting the in utero status. Instead, we sampled neonates within 3 hours of delivery. Accordingly, we stated our objective as determining whether the onset of jaundice was in the perinatal period, either in utero or in the immediate post-natal period. We believed that our methodology was reflective of the in utero status, but we could not, and did not, categorically state so. We found that in blood sampled within three hours of delivery, STB concentrations were significantly higher in G-6-PD deficient neonates than in controls (2.9 ± 0.7 mg/dL vs. 2.6 ± 0.6 mg/dL, P = 0.003). In the G-6-PD deficient group, significantly more neonates with an early STB value > mean developed subsequent hyper-bilirubinemia. than those with STB values < mean. Despite the larger number of control neonates, similar analysis in that group did not reach statistical significance.
Many reasons may plausibly explain these differences in findings. One possibility is that our study was performed on Sephardic Jewish neonates with the G-6-PD Mediterranean mutation, while different mutations in the Indian population may have been responsible, in part, for differences between the population groups.
Diverse environmental factors, possibly interacting with varying genetic factors, may also have had an effect on the bilirubin levels.
We stand by our conclusions that G-6-PD deficiency associated neonatal hyper-bilirubinemia, in the population we studied, commences in the immediate perinatal period. Others(3-6) have also demonstrated higher umbilical cord blood or first day STB concentrations in G-6-PD deficient neonates. The fact that Drs. Murki and Dutta obtained different results is interesting and worthy of further study. However, we do not concur that their results negate those of our study or our conclusions; rather, they add interest to the subject and should stimulate further studies of this nature.
References
1. Murki S, Dutta S. Onset of bilirubin rise in G-6PD deficient neonates-prenatal or postnatal? Indian Pediatr 2005; 42: 1053.
2. Kaplan M, Algur N, Hammerman C. Onset of jaundice in glucose-6-phosphate dehydrogenase-deficient neonates. Pediatrics 2001; 108: 956-959.
3. Valaes T, Karaklis A, Stravrakakis D, Bavela-Stravrakakis K, Perakis A, Doxiadis SA. Incidence and mechanism of neonatal jaundice related to glucose-6-phosphate dehydrogenase deficiency. Pediatr Res 1969; 3: 448-458.
4. Brown WR, Boon WH. Hyperbilirubinemia and kernicterus in glucose-6-phosphate dehydrogenase deficient infants in Singapore. Pediatrics 1968; 41: 1055-1062.
5. Lu TC, Wei H, Blackwell RQ. Increased incidence of severe hyperbilirubinemia among newborn Chinese infants with G-6-PD deficiency. Pediatrics 1966; 37: 994-999.
6. Tan KL. Glucose-6-phosphate dehydrogenase status and neonatal jaundice. Arch Dis Child 1981; 56: 874-877.(Michael Kaplan)
Faculty of Health Sciences, Ben Gurion University of the Negev,
We read the letter by Drs. Murki and Dutta, in which they report on umbilical cord blood serum total bilirubin (STB) levels in glucose-6-phosphate dehydrogenase (G-6-PD)-deficient and-normal neonates, with great interest(1). In their study, cord blood bilirubin levels were similar in the G-6-PD deficient and control neonates, suggesting that, in the Indian neonates studied, G-6-PD deficiency associated neonatal jaundice did not commence in utero. The authors conclude that their data negates that of a previous study of ours that jaundice in G-6-PD deficient infants commences most likely in utero(2).
We would like to point out significant differences in concept, design and conclusions between our study and the present one which renders them not directly comparable. Because of technical and logistic problems, we could not study umbilical cord blood samples as did Drs. Murki and Dutta. Umbilical blood sampling would undoubtedly have been a more accurate method of reflecting the in utero status. Instead, we sampled neonates within 3 hours of delivery. Accordingly, we stated our objective as determining whether the onset of jaundice was in the perinatal period, either in utero or in the immediate post-natal period. We believed that our methodology was reflective of the in utero status, but we could not, and did not, categorically state so. We found that in blood sampled within three hours of delivery, STB concentrations were significantly higher in G-6-PD deficient neonates than in controls (2.9 ± 0.7 mg/dL vs. 2.6 ± 0.6 mg/dL, P = 0.003). In the G-6-PD deficient group, significantly more neonates with an early STB value > mean developed subsequent hyper-bilirubinemia. than those with STB values < mean. Despite the larger number of control neonates, similar analysis in that group did not reach statistical significance.
Many reasons may plausibly explain these differences in findings. One possibility is that our study was performed on Sephardic Jewish neonates with the G-6-PD Mediterranean mutation, while different mutations in the Indian population may have been responsible, in part, for differences between the population groups.
Diverse environmental factors, possibly interacting with varying genetic factors, may also have had an effect on the bilirubin levels.
We stand by our conclusions that G-6-PD deficiency associated neonatal hyper-bilirubinemia, in the population we studied, commences in the immediate perinatal period. Others(3-6) have also demonstrated higher umbilical cord blood or first day STB concentrations in G-6-PD deficient neonates. The fact that Drs. Murki and Dutta obtained different results is interesting and worthy of further study. However, we do not concur that their results negate those of our study or our conclusions; rather, they add interest to the subject and should stimulate further studies of this nature.
References
1. Murki S, Dutta S. Onset of bilirubin rise in G-6PD deficient neonates-prenatal or postnatal? Indian Pediatr 2005; 42: 1053.
2. Kaplan M, Algur N, Hammerman C. Onset of jaundice in glucose-6-phosphate dehydrogenase-deficient neonates. Pediatrics 2001; 108: 956-959.
3. Valaes T, Karaklis A, Stravrakakis D, Bavela-Stravrakakis K, Perakis A, Doxiadis SA. Incidence and mechanism of neonatal jaundice related to glucose-6-phosphate dehydrogenase deficiency. Pediatr Res 1969; 3: 448-458.
4. Brown WR, Boon WH. Hyperbilirubinemia and kernicterus in glucose-6-phosphate dehydrogenase deficient infants in Singapore. Pediatrics 1968; 41: 1055-1062.
5. Lu TC, Wei H, Blackwell RQ. Increased incidence of severe hyperbilirubinemia among newborn Chinese infants with G-6-PD deficiency. Pediatrics 1966; 37: 994-999.
6. Tan KL. Glucose-6-phosphate dehydrogenase status and neonatal jaundice. Arch Dis Child 1981; 56: 874-877.(Michael Kaplan)