Hyperbilirubinemia and urinary D-glucaric acid excretion in premature infants following antepartum dexamethasone treatment

Early corticosteroid treatment does not affect severity of unconjugated hyperbilirubinemia in extreme low birth weight preterm infants

“…Although the pattern of hyperbilirubinemia seems altered, it is unlikely that DXM caused this pattern: (i) TSB concentrations were comparable at most postnatal days and (ii) although maximal TSB concentrations were earlier reached after DXM treatment, time of occurrence of maximal TSB concentration was comparable when all DXM‐treated ELBW preterm infants were analysed in the same group (data not shown). These results contradict with in vitro data on DXM and, at least in part, with in vivo human data on foetal DXM exposure and hyperbilirubinemia as alluded in the Introduction of this paper (6,9,10).…”

“…Moreover, Nemeth et al. showed that levels of unconjugated bilirubin were about 40 μmol/L higher in the first postnatal week in 16 dexamethasone (DXM)‐treated infants compared to 18 control infants with similar gestational age (32 weeks) and birthweight (2000 g) (9). To the best of our knowledge, only one study described beneficial effects of antenatal DXM exposure on neonatal hyperbilirubinemia.…”

“…The proportion infants with maximal total serum bilirubin (TSB) >257 lmol ⁄ L significantly increased after maternal prednisolone treatment: 51% vs. 27% (prednisolone (n = 147) versus controls (n = 231), respectively; p < 0.01) (8). Moreover, Nemeth et al showed that levels of unconjugated bilirubin were about 40 lmol ⁄ L higher in the first postnatal week in 16 dexamethasone (DXM)-treated infants compared to 18 control infants with similar gestational age (32 weeks) and birthweight (2000 g) (9). To the best of our knowledge, only one study described beneficial effects of antenatal DXM exposure on neonatal hyperbilirubinemia.…”

“…In vivo human data on the effects of corticosteroid exposure and unconjugated hyperbilirubinemia are limited to maternal administration, i.e. antenatal exposure, and are not conclusive (Table 1) (7–10). In 1972, Liggins and Howie described a controlled trial of antenatal betamethasone acetate versus cortisone acetate (the latter having little glucocorticoid activity) for the prevention of respiratory distress syndrome (7).…”

The effects of antenatal corticosteroid exposure on the rate of hyperbilirubinemia in term newborns

“…Many authors have reported that betamethasone-exposed infants did not exhibit increased rates of hyperbilirubinemia 5. In another study, Nemeth et al showed that antenatal dexamethasone exposure led to further increased serum unconjugated bilirubin levels in the first week after birth versus non-exposed controls; they also reported a higher rate of hyperbilirubinemia requiring treatment 11. Pettit et al carried out a retrospective cohort study of 6675 preterm deliveries (from 32 to 37 weeks of gestation) and found an association between antenatal betamethasone exposure a neonatal hypoglycemia and hyperbilirubinemia 8.…”