Fetal cocaine exposure and neonatal bilirubinemia

Abstract To assess the effect of fetal exposure to cocaine on neonatal serum bilirubin values, we compared 17 infants whose cocaine exposure was confirmed by urine toxicology studies, with no evidence of other drug exposure by history or urinalysis, with 31 sequentially born healthy term infants without evidence of maternal drug use. The mean (±SD) bilirubin concentration in control infants was 110 ± 32 μmol/L (6.5 ± 1.9 mg/dl) at 30.5 ± 5.4 hours of age, compared with 55 ± 26 μmol/L (3.2 ± 1.5 mg/dl) at 30.8 ± 5.3 hours in cocaine-exposed infants ( p 5 -3-ketosteroid isomerase (KSI), glutathione- S -transferase (GST), and BGT. Cocaine was a weak inducer of GST but a strong inducer of KSI, a member of the GST family of enzymes that is closely associated with bilirubin transport (ligandin) in liver, and a moderately strong inducer of BGT. Neither drug increased cytochrome P-450 levels, and only clofibrate induced peroxisomal β-oxidase. We conclude that cocaine appears to induce bilirubin metabolizing pathways, resulting in a lower risk of neonatal hyperbilirubinemia. (J P EDIATR 1994;125:613-6)