What are the causes of breast milk jaundice?

Updated: Dec 07, 2017
  • Author: Prashant G Deshpande, MD; Chief Editor: Muhammad Aslam, MD  more...
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Note the following causes of breast milk jaundice:

  • Delayed milk production and poor feeding lead to decreased caloric intake, dehydration, and increased enterohepatic circulation, resulting in higher serum bilirubin concentration.

  • The biochemical cause of breast milk jaundice remains under investigation. Some research reported that lipoprotein lipase, found in some breast milk, produces nonesterified long-chain fatty acids, which competitively inhibit glucuronyl transferase conjugating activity.

  • Glucuronidase has also been found in some breast milk, which results in jaundice.

  • Decreased uridine diphosphate-glucuronyl transferase (UGT1A1) activity may be associated with prolonged hyperbilirubinemia in breast milk jaundice. [14]  This may be comparable to what is observed in patients with Gilbert syndrome. [15]  Genetic polymorphisms of the UGT1A1 promoter, specifically the T-3279G and the thymidine-adenine (TA)7 dinucleotide repeat TATAA box variants, were found to be commonly inherited in white individuals with high allele frequency. These variant promoters reduce the transcriptional UGT1A1 activity. Similarly, mutations in the coding region of the UGT1A1 (eg, G211A, C686A, C1091T, T1456G) have been described in East Asian populations; these mutations reduce the activity of the enzyme and are a cause of Gilbert syndrome. [16]

  • The G211A mutation in exon 1 (Gly71Arg) is most common, with an allele frequency of 13%. Coexpression of these polymorphism in the promoter and in the coding region are common and further impair the enzyme activity. [17]

  • A study showed that neonates with nucleotide 211GA or AA variation in UGT1A1 genotypes had higher peak serum bilirubin levels than those with GG. This effect was more pronounced in the exclusively breast fed infants compared to exclusively or partially formula fed neonates. [18]

  • The organic anion transporters (OATPs) are a family of multispecific pumps that mediate the sodium independent uptake of bile salts and broad range of organic compounds. In humans, three liver-specific OATPs have been identified: OATP-A, OATP-2, and OATP-8. Unconjugated bilirubin is transported in the liver by OATP-2. A genetic polymorphism for OATP-2 (also known as OATP-C) at nucleotide 388 has been shown to correlate with three-fold increased risk for development of neonatal jaundice (peak serum bilirubin level of 20 mg/dL) when adjusted for covariates. [19, 20]  The combination of the OATP-2 gene polymorphism with the variant UGT1A1 gene at nucleotide 211 further increased the risk to 22-fold (95% confidence interval [CI], 5.5-88). When these genetic variants were combined with breast milk feeding, the risk for marked neonatal hyperbilirubinemia increased further to 88-fold (95% CI, 12.5-642.5).

  • Bilirubin is a known antioxidant. [21] It has been suggested that there is a homeostasis maintained by external sources such as breast milk and internal production of antioxidants such as bilirubin in the body. In a study by Uras et al, the breast milk of mothers of newborns with prolonged jaundice was found to have increased oxidative stress, whereas there was a reduction in the protective antioxidant capacity. [22] The exact clinical significance of this finding is not known.

  • Breastfeeding women in populations with a high prevalence of glucose-6-phosphate dehydrogenase (G6PD) deficiency should avoid consumption of fava beans as well as ingestion of quinine-containing sodas. [23] The presence of these pro-oxidant items in breast milk may induce G6PD crises in the breastfed children, leading to jaundice and/or hemolytic anemia. [23]

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