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Breast Milk Jaundice Clinical Presentation

  • Author: Prashant G Deshpande, MD; Chief Editor: Ted Rosenkrantz, MD  more...
Updated: Dec 31, 2015


Aspects of history may include the following:

  • Physiologic jaundice usually manifests after the first 24 hours of life. This can be accentuated by breastfeeding, which, in the first few days of life, may be associated with suboptimal milk and suboptimal caloric intake, especially if milk production is delayed. This is known as breastfeeding jaundice. Jaundice that manifests before the first 24 hours of life should always be considered pathologic until proven otherwise. In this situation, a full diagnostic workup with emphasis on infection and hemolysis should be undertaken.
  • True breast milk jaundice (BMJ) manifests after the first 4-7 days of life. A second peak in serum bilirubin level is noted by age 14 days.
  • In clinical practice, differentiating between physiologic jaundice from breast milk jaundice is important so that the duration of hyperbilirubinemia can be predicted. Identifying the infants who become dehydrated secondary to inadequate breastfeeding is also important. These babies need to be identified early and given breastfeeding support and formula supplementation as necessary. Depending on serum bilirubin concentration, neonates with hyperbilirubinemia may become sleepy and feed poorly.


The following physical findings may be noted:

  • Clinical jaundice is usually first noticed in the sclera and the face. Then it progresses caudally to reach the abdomen and extremities. Gentle pressure on the skin helps to reveal the extent of jaundice, especially in darker-skinned babies; however, clinical observation is not an accurate measure of the severity of the hyperbilirubinemia.
  • A rough correlation is observed between blood levels and the extent of jaundice (face, approximately 5 mg/dL; mid abdomen, approximately 15 mg/dL; soles, 20 mg/dL). Therefore, clinical decisions should always be based on serum levels of bilirubin. Skin should have normal perfusion and turgor and show no petechiae.
  • Neurologic examination, including neonatal reflexes, should be normal, although the infant may be sleepy. Muscle tone and reflexes (eg, Moro reflex, grasp, rooting) should be normal.
  • Evaluate hydration status by an assessment of the percentage of birth weight that may have been lost, observation of mucous membranes, fontanelle, and skin turgor.


The following causes may be noted:

  • Supplementation of breastfeeding with dextrose 5% in water (D5W) can actually increase the prevalence or degree of 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.[8] This may be comparable to what is observed in patients with Gilbert syndrome.[9] 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 whites 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.[10]
  • 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.[11]
  • A 2011 study has shown 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 with exclusively or partially formula fed neonates.[12]
  • The organic anion transporters (OATPs) are a family of multispecific pumps that mediate the Na- independent uptake of bile salts and broad range of organic compounds. In humans, 3 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 3-fold increased risk for development of neonatal jaundice (peak serum bilirubin level of 20 mg/dL) when adjusted for covariates.[13, 14] When the combination of the OATP-2 gene polymorphism with the variant UGT1A1 gene at nucleotide 211 further increased the risk to 22-fold (95% 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).
  • In a 2012 study, researchers measured antioxidant properties of breast milk. Bilirubin is a known antioxidant in vitro. It is suggested that there is a homeostasis maintained by the external sources such as breast milk and internal production of antioxidants like bilirubin in the body. In this study, in the breast milk of mothers of newborns with prolonged jaundice, oxidative stress was found to be increased and the protective antioxidant capacity was found to be decreased. The exact clinical significance of this finding is not known.[15]
Contributor Information and Disclosures

Prashant G Deshpande, MD Attending Pediatrician, Department of Pediatrics, Christ Hospital Medical Center and Hope Children's Hospital; Assistant Clinical Professor of Pediatrics, Midwestern University

Prashant G Deshpande, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Telemedicine Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Brian S Carter, MD, FAAP Professor of Pediatrics, University of Missouri-Kansas City School of Medicine; Attending Physician, Division of Neonatology, Children's Mercy Hospital and Clinics; Faculty, Children's Mercy Bioethics Center

Brian S Carter, MD, FAAP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Pediatric Society, American Society for Bioethics and Humanities, American Society of Law, Medicine & Ethics, Society for Pediatric Research, National Hospice and Palliative Care Organization

Disclosure: Nothing to disclose.

Chief Editor

Ted Rosenkrantz, MD Professor, Departments of Pediatrics and Obstetrics/Gynecology, Division of Neonatal-Perinatal Medicine, University of Connecticut School of Medicine

Ted Rosenkrantz, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric Society, Eastern Society for Pediatric Research, American Medical Association, Connecticut State Medical Society, Society for Pediatric Research

Disclosure: Nothing to disclose.

Additional Contributors

Oussama Itani, MD, FAAP, FACN Clinical Associate Professor of Pediatrics and Human Development, Michigan State University; Medical Director, Department of Neonatology, Borgess Medical Center

Oussama Itani, MD, FAAP, FACN is a member of the following medical societies: American Academy of Pediatrics, American Association for Physician Leadership, American Heart Association, American College of Nutrition

Disclosure: Nothing to disclose.


The authors and editors of Medscape Drugs & Diseases gratefully acknowledge the contributions of previous author Timothy Ramer, MD, to the development and writing of this article.

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The graph represents indications for phototherapy and exchange transfusion in infants (with a birthweight of 3500 g) in 108 neonatal ICUs. The left panel shows the range of indications for phototherapy, whereas the right panel shows the indications for exchange transfusion. Numbers on the vertical axes are serum bilirubin concentrations in mg/dL (lateral) and mmol/L (middle). In the left panel, the solid line refers to the current recommendation of the American Academy of Pediatrics (AAP) for low-risk infants, the line consisting of long dashes (- - - - -) represents the level at which the AAP recommends phototherapy for infants at intermediate risk, and the line with short dashes (-----) represents the suggested intervention level for infants at high risk. In the right panel, the dotted line (......) represents the AAP suggested intervention level for exchange transfusion in infants considered at low risk, the line consisting of dash-dot-dash (-.-.-.-.) represents the suggested intervention level for exchange transfusion in infants at intermediate risk, and the line consisting of dash-dot-dot-dash (-..-..-..-) represents the suggested intervention level for infants at high risk. Intensive phototherapy is always recommended while preparations for exchange transfusion are in progress. The box-and-whisker plots show the following values: lower error bar = 10th percentile; lower box margin = 25th percentile; line transecting box = median; upper box margin = 75th percentile; upper error bar = 90th percentile; and lower and upper diamonds = 5th and 95th percentiles, respectively.
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