Bilirubin Metabolism in the Fetus.

Although the kinetics of fetal erythropoiesis and the life span of fetal erythrocytes have not been accurately determined, thus precluding a quantitative appraisal of bilirubin production in the fetus, there is convincing evidence that this pigment is formed during intrauterine life. Supporting this are the presence of bilirubin in meconium (2), in fetal plasma (3) and the fetal gall bladder (4), and the elevated mean bilirubin concentrations in fetal and cord blood as compared to those in maternal blood (3, 5). On the other hand, in fetal liver the enzymatic apparatus for glucuronide formation is functionally deficient (6), which is believed to interfere with pigment excretion in the fetal bile (7). Despite this "immaturity" of the fetal liver, bilirubin levels in cord blood are surprisingly low (8), even in instances of erythroblastosis in which manifest hemolysis had occurred in utero (9). Shortly after birth, however, the level of unconjugated bilirubin in the neonatal serum rises steeply, reaching peak values during the first week of life (8). These observations suggest that during intrauterine life fetal bile pigment is disposed of by mechanisms other than biliary excretion, and they point to the placenta as a likely route of elimination (10). Previous investigations found human and rat placenta to lack the enzymatic mechanism for glucuronide formation (10), indicating that in fetal bile pigment metabolism, the placenta does