Bronze Baby Syndrome: New Insights on Bilirubin-Photosensitization of Copper-Porphyrins

Abstract

“Bronze” baby syndrome (BBS) was first described in 1972 by Kopelman et al.,^l who observed a newborn infant with a grey-brown discoloration following phototherapy for unconjugated hyperbilirubinemia. Subsequent reports^2–6 described the clinical aspects of this syndrome while other papers attempted to clarify the biochemical mechanisms leading to the onset of BBS.^7–9 In 1982, we were able to demonstrate that a large amount of porphyrins is present in sera of BBS patients.⁸ These porphyrins were identified as Cu²⁺-uro, Cu²⁺-copro, and Cu²⁺-protoporphyrin.⁹ In addition, large amounts of serum porphyrins and serum copper were detected in sera of adult and pediatric patients with cholestatic disorders.^10,11 On the basis of these observations and “in vitro” studies showing that, after visible light-irradiation, synthetically prepared Cu²⁺-porphyrins added to cord blood serum exhibited spectral changes closely similar to those found upon irradiation of BBS serum, we have suggested that Cu²⁺-porphyrins undergo photodestruction sensitized by bilirubin yielding photoproducts having generalized absorption in the near-UV and red spectral regions, hence responsible for the brown discoloration.⁹