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Published on: September 6, 2019
Risk of hyperbilirubinemia in breast-fed infants
Pi-Feng Chang1, Yu-Cheng Lin, Kevin Liu
1Department of Pediatrics, Far Eastern Memorial Hospital, Pan-Chiao, Taipei, Taiwan.
Insights
Exclusively breast-fed infants with UGT1A1 gene variants, G6PD deficiency, or born via vaginal delivery face higher risks of hyperbilirubinemia. Early identification of these risk factors is crucial for managing infant jaundice.
Area of Science:
- Neonatal Medicine
- Pediatric Gastroenterology
- Genetics
Background:
- Hyperbilirubinemia is a common condition in newborns.
- Breastfeeding is encouraged, but certain genetic and delivery factors may increase jaundice risk.
Purpose of the Study:
- To identify risk factors for hyperbilirubinemia in exclusively breast-fed infants.
- To investigate the impact of specific genetic variants and delivery modes on neonatal jaundice.
Main Methods:
- Prospective study of 252 exclusively breast-fed term infants.
- Assessed birth weight, sex, delivery mode, G6PD deficiency, UGT1A1, and SLCO1B1 gene variants.
- Hyperbilirubinemia defined as serum bilirubin ≥15.0 mg/dL at 3 days old.
Main Results:
- 23.4% of infants developed hyperbilirubinemia.
- Significant risk factors included UGT1A1 variant nucleotide 211 (OR 2.48), G6PD deficiency (OR 12.24), and vaginal delivery (OR 3.55).
Conclusions:
- Breast-fed neonates with UGT1A1 variants, G6PD deficiency, or born via vaginal delivery are at increased risk.
- These findings aid in predicting and managing hyperbilirubinemia in breast-fed infants.
Objective:
To investigate the risk factors for hyperbilirubinemia in infants who are exclusively breast-fed.
Study Design:
A prospective study was conducted to investigate the effects of birth body weight, sex, mode of delivery, glucose-6-phosphate dehydrogenase (G6PD) deficiency, variant UDP-glucuronosyltransferase 1A1 (UGT1A1) gene, and hepatic solute carrier organic anion transporter 1B1 (SLCO1B1) gene on hyperbilirubinemia in neonates who were breast-fed. Hyperbilirubinemia was diagnosed when a full term neonate had a bilirubin level ≧15.0 mg/dL (256.5 μM) in serum at 3 days old. The polymerase chain reaction-restriction fragment length polymorphism method was used as a means of detecting the known variant sites in the UGT1A1 and SLCO1B1 gene.
Results:
Of 252 infants born at term who were exclusively breast-fed, 59 (23.4%) had hyperbilirubinemia. The significant risk factors were a variant nucleotide 211 in UGT1A1 (2.48; 95% CI, 1.29 to 4.76; P = .006), G6PD deficiency (12.24; 95% CI, 1.08 to 138.62; P < .05), and vaginal delivery (3.55; 95% CI, 1.64 to 7.66; P < .001).
Conclusion:
Breast-fed neonates who are 211 variants in the UGT1A1, G6PD deficiency, and vaginal delivery are at high-risk for hyperbilirubinemia.
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