Mechanism of development of bronze baby syndrome in neonates treated with phototherapy.

Comparisons of serum concentrations of unknown pigment and photobilirubin IX alpha , the two main bilirubin photoproducts, were made during phototherapy in infants with and without bronze baby syndrome who were treated similarly. The serum concentrations of unknown pigment estimated by high-pressure liquid chromatography in infants with the bronze baby syndrome were significantly increased in comparison with those in the control hyperbilirubinemic neonates during phototherapy. However, there was no difference in the serum concentrations of photobilirubin IX alpha between infants with bronze baby syndrome and the control groups. The unknown pigment separated from bilirubin photoproducts obtained from experiments in vitro by high-pressure liquid chromatography was gradually decomposed into brown products that showed the absorption spectrum similar to that of the serum of infants with bronze baby syndrome. This fact is probably due to reduction in hepatic excretory function of bilirubin photoproducts, especially in known pigment, because its main excretory pathway is the biliary route. The pigment accumulated in the body may be polymerized and forms bilifuscin-like substances following a free radical reaction. It is concluded that the brown pigment is formed via unknown pigment.