Neonatal jaundice causes
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Causes
Intrinsic causes of hemolysis
- Membrane conditions
- Systemic contitions
- Enzyme conditions
- Glucose-6-phosphate dehydrogenase deficiency (also called G6PD deficiency)
- Pyruvate kinase deficiency
- Globin synthesis defect
Extrinsic causes of hemolysis
- Alloimmunity (The neonatal or cord blood gives a positive direct Coombs test and the maternal blood gives a positive indirect Coombs test)
Non-hemolytic causes
Hepatic causes
- Infections
- Metabolic
- Drugs
- Total parenteral nutrition
- Idiopathic
Post-hepatic
- Biliary atresia
- Bile duct obstruction
Breast milk jaundice
Whereas breast feeding jaundice is a mechanical problem, breast milk jaundice is more of a biochemical problem. The term applies to jaundice in a newborn baby.
Very rarely, "breast milk jaundice" occurs during the second or third week of life.
- First, at birth, the gut is sterile, and normal gut flora takes time to establish. The bacteria in the adult gut convert conjugatedbilirubin to stercobilinogen which is then oxidized to stercobilin and excreted in the stool. In the absence of sufficient bacteria, the bilirubin is de-conjugated by brush border β-glucuronidase and reabsorbed. This process of re-absorption is calledenterohepatic circulation. It has been suggested that bilirubin uptake in the gut (enterohepatic circulation) is increased in breast fed babies, possibly as the result of increased levels of epidermal growth factor (EGF) in breast milk.[1]
- Second, the breast-milk of some women contains a metabolite of progesterone called 3-alpha-20-beta pregnanediol. This substance inhibits the action of the enzyme uridine diphosphoglucuronic acid (UDPGA) glucuronyl transferase responsible for conjugation and subsequent excretion of bilirubin. In the newborn liver, activity of glucuronyl transferase is only at 0.1-1% of adult levels, so conjugation of bilirubin is already reduced. Further inhibition of bilirubin conjugation leads to increased levels of bilirubin in the blood [2] [citation needed]. However, these results have not been supported by subsequent studies.[3]
- Third, an enzyme in breast milk called lipoprotein lipase produces increased concentration of nonesterified free fatty acids that inhibit hepatic glucuronyl transferase, which again leads to decreased conjugation and subsequent excretion of bilirubin [4] [citation needed].
Despite the advantages of breast feeding, there is a strong association of breast feeding with neonatal hyperbilirubinemia and thus risk ofkernicterus, though this is uncommon. Serum bilirubin levels may reach as high as 30 mg/dL. Jaundice should be managed either with phototherapy or with exchange blood transfusion as is needed. Breast feeds however need not be discontinued. The child should be kept well hydrated and extra feeds given.
Neither condition is a reason to stop nursing, though caregivers may advise IV or other fluid administration to ensure the baby is not dehydrated.
References
- ↑ Kumral, A (2009). "Breast milk jaundice correlates with high levels of epidermal growth factor". Pediatr Res. 66: 218–21. Unknown parameter
|coauthors=ignored (help) - ↑ Arias, IM (1964). "Prolonged neonatal unconjugated hyperbilirubinemia associated with breast feeding and a steroid, pregnane-3(alpha), 20(beta)-diol in maternal milk that inhibits glucuronide formation in vitro". J Clin Invest. 43: 2037–47. Unknown parameter
|coauthors=ignored (help) - ↑ Murphy, J F (1981). "Pregnanediols and breast-milk jaundice". Arch Dis Child. 56: 474–76. Unknown parameter
|coauthors=ignored (help) - ↑ Poland, R L (1980). "High milk lipase activity associated with breastmilk jaundice". Pediatr Res. 14: 1328–31. Unknown parameter
|coauthors=ignored (help)