Gartner L M, Lee K S, Moscioni A D
J Pediatr. 1983 Sep;103(3):464-71. doi: 10.1016/s0022-3476(83)80429-6.
The hypothesis that the etiologic mechanism of the late-onset, prolonged, unconjugated hyperbilirubinemia of the breast-fed infant, known as the breast milk jaundice syndrome, results from exaggeration of intestinal bilirubin absorption has been investigated in an adult rat model, which permits quantitative measurement of the enterohepatic circulation of bilirubin. After instillation of unconjugated bilirubin in buffer into the duodenum, 25% of the dose was absorbed and appeared in bile. Administration of bilirubin in human milk or cow milk formula resulted in a marked reduction in absorption to 2%. Administration of bilirubin in milk from mothers of infants with breast milk jaundice syndrome not only failed entirely to prevent the absorption of bilirubin, but enhanced late absorption, to produce a total absorption of 60% of the bilirubin dose. Thus, although normal milk significantly retarded intestinal bilirubin absorption and diminished the bilirubin load to the liver, milk from mothers of infants with breast milk jaundice syndrome appeared to enhance the enterohepatic circulation of bilirubin and to increase the total hepatic bilirubin load. This exaggeration of the enterohepatic circulation of bilirubin may be related to the increased concentrations in these milks of long-chain nonesterified fatty acids.
