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Article
June 1968

Neonatal Hyperbilirubinemia and Kernicterus: Experimental Support for Treatment by Exposure to Visible Light

Author Affiliations

Chicago; San Francisco
From the Department of Medicine (Neurology), University of Chicago, Chicago (Dr. Diamond). and the Department of Medicine, University of California, San Francisco (Dr. Schmid). Dr. Diamond is now at Harvard Medical School, Boston.

Arch Neurol. 1968;18(6):699-702. doi:10.1001/archneur.1968.00470360121012
Abstract

CREMER et al1 noted that in infants with neonatal icterus exposure to sunlight resulted in a prompt reduction of the serum bilirubin level; this was subsequently confirmed by other investigatiors.2 Broughton et al3 and Lucey et al4 explored the possibility of applying this observation to the treatment of uncomplicated neonatal hyperbilirubinemia.

Bilirubin is a lipid-soluble molecule which readily crosses the blood-brain barrier in either direction.5 In the plasma, bilirubin is tightly bound to albumin which greatly limits the access of the pigment to the central nervous system (CNS).5,6 Illumination of bilirubin in vitro leads to progressive decomposition of the pigment, eventually resulting in loss of its yellow color and its characteristic absorption spectrum in the visible range.7-9 Although the exact chemical structure of these decomposition products is unclear, they are known to be more polar and hence, more water-soluble than bilirubin.8-10

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