title: Influence of antenatal steroids and sex on maturation of the epidermal barrier in the preterm infant.
abstract: BACKGROUND
  The epidermal barrier is well developed in term infants but defective in the immature infant with important clinical consequences. The development of the barrier shares similarities with production of pulmonary surfactant. Studies in the rat have shown that barrier maturation is accelerated by antenatal steroids, both structurally and functionally. Females have a more mature barrier than males at the same gestational age. These factors have not been studied in the human.
  
  
  OBJECTIVE
  To examine the influence of antenatal steroids and sex on maturation of the epidermal barrier in the preterm infant.
  
  
  METHODS
  A total of 137 infants born before 34 weeks gestation, 80 boys and 57 girls, were studied: 87 had been exposed to antenatal steroids, and 50 had not; 99 were studied prospectively, and 38 had been studied previously.
  
  
  METHODS
  Barrier function was measured as transepidermal water loss from abdominal skin by evaporimetry. Measurements were made within the first 48 hours and corrected to a standard relative humidity of 50% (TEWL(50)).
  
  
  RESULTS
  The relation between TEWL(50) and gestation was exponential with very high levels in the most immature infants. No influence of antenatal steroids or sex could be shown. When infants who were optimally exposed to antenatal steroids were considered alone, no effect could be shown.
  
  
  CONCLUSIONS
  Epidermal maturation in the preterm infant does not appear to be influenced by antenatal steroids or sex, suggesting that the mechanism of maturation differs from that of the rat.
authors.affiliation: Academic Division of Child Health, Nottingham City Hospital, University of Nottingham, Hucknall Road, Nottingham NG5 1PB, UK.
authors.forename: A
authors.initials: A
authors.lastname: Jain
authors.forename: N
authors.initials: N
authors.lastname: Rutter
authors.forename: P H
authors.initials: PH
authors.lastname: Cartlidge
mesh_terms: D003907:Dexamethasone / Q000627:therapeutic use*; D004817:Epidermis / Q000187:drug effects / Q000254:growth & development*; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use*; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature / Q000502:physiology*; D008297:Male; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011446:Prospective Studies; D012189:Retrospective Studies; D012723:Sex; D014870:Water Loss, Insensible / Q000502:physiology
chemical_list: D005938:Glucocorticoids; D003907:Dexamethasone