Physiologic - Recirculation
Physiologic jaundice
Enteric recirculation
So far these neonatal aberrations in bilirubin metabolism have been simply a matter of degree - more hemoglobin, shorter RBC life span, less BUG-T. However the area of enteric recirculation involves something unique to the newborn. The neonate and fetus have an enzyme, beta-glucuronidase, in the duodenum and jejunum which unconjugates the excreted conjugated bilirubin turning it back into lipid-soluble unconjugated bilirubin which then is reabsorbed into the portal circulation, the so-called enterohepatic recirculation of bilirubin.In fetal life, this recirculation helps in excretion of bilirubin by bringing more bilirubin into contact with the placenta, the organ of bilirubin clearance for the fetus. Contributing factors are a high level of bilirubin in meconium (as much as 80-180 mg), the lack of enteric bacterial flora preventing conversion of bilirubin to nonreabsorbable urobilinoids, the lack of stooling which allows continued exposure of the bilirubin in meconium to the beta-glucuronidase and the presence of primarily BMG which is more easily unconjugated than BDG. Confirming the role of the enterohepatic recirculation in the etiology of physiologic jaundice is the fact that oral administration to the neonate of non-reabsorbable substances such as agar or activated charcoal, which bind bilirubin, increases stool bilirubin content and leads to decreased serum bilirubin levels. Conversely, conditions in which there is delayed passage of meconium, such as meconium plug syndrome, Hirschprung's disease or meconium ileus are associated with hyperbilirubinemia.Once feedings are begun postnatally, stooling occurs, leading to elimination of the bilirubin-laden meconium. Also feedings lead to establishment of the normal GI tract bacterial flora, which both degrade the beta-glucuronidase and begin converting bilirubin to urobilinoids which are excreted in the stool.Return to top of page