title: Antenatal glucocorticoid treatment is not associated with long-term metabolic risks in individuals born before 32 weeks of gestation.
abstract: BACKGROUND
  A single course of maternal glucocorticoid treatment is effective in reducing neonatal mortality after preterm birth. However, in animals, maternal glucocorticoid treatment is associated with lifelong hyperglycaemia and hypertension, and impaired nephrogenesis in offspring. Findings from studies in humans on this topic are highly contradictory due to a number of methodological flaws, and renal function after glucocorticoid exposure has never been assessed.
  
  
  OBJECTIVE
  To assess in individuals born <32 gestational weeks whether antenatal glucocorticoid treatment for preterm birth is associated with long-term metabolical risks, including renal function, in adulthood.
  
  
  METHODS
  Birth cohort study.
  
  
  METHODS
  Multicentre study.
  
  
  METHODS
  412 19 year olds born <32 gestational weeks from the Project On Preterm and Small-for-gestational-age infants (POPS) cohort.
  
  
  METHODS
  Maternal betamethasone 12 mg administered twice with a 24 h interval.
  
  
  METHODS
  Body composition, insulin resistance, the serum lipid profile, blood pressure and estimated renal function.
  
  
  RESULTS
  We did not find any long-term adverse effects of antenatal betamethasone, with the exception of an effect on glomerular filtration rate (GFR). In 19-year-old survivors, GFR was lower after betamethasone: -5.2 ml/min (95% CI -8.9 to -1.4) per 1.73 m(2).
  
  
  CONCLUSIONS
  The reduction in neonatal mortality associated with a single course of maternal betamethasone is not accompanied by long-term metabolical risks in survivors of preterm birth. The only adverse effect found was lower GFR. Although this difference was not clinically relevant at 19 years, it might predict an increased risk of chronic renal failure in prematurely born individuals who were exposed antenatally to betamethasone.
authors.affiliation: Department of Pediatrics, Leiden University Medical Center, Leiden, The Netherlands. m.j.j.finken@lumc.nl
authors.forename: M J J
authors.initials: MJ
authors.lastname: Finken
authors.forename: M G
authors.initials: MG
authors.lastname: Keijzer-Veen
authors.forename: F W
authors.initials: FW
authors.lastname: Dekker
authors.forename: M
authors.initials: M
authors.lastname: Frölich
authors.forename: F J
authors.initials: FJ
authors.lastname: Walther
authors.forename: J A
authors.initials: JA
authors.lastname: Romijn
authors.forename: B J
authors.initials: BJ
authors.lastname: van der Heijden
authors.forename: J M
authors.initials: JM
authors.lastname: Wit
mesh_terms: D001623:Betamethasone / Q000009:adverse effects* / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects; D001823:Body Composition / Q000187:drug effects; D005260:Female; D005500:Follow-Up Studies; D005865:Gestational Age; D005919:Glomerular Filtration Rate / Q000187:drug effects; D005938:Glucocorticoids / Q000009:adverse effects* / Q000627:therapeutic use; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature; D007333:Insulin Resistance; D008055:Lipids / Q000097:blood; D008297:Male; D011247:Pregnancy; D011295:Prenatal Care / Q000379:methods; D011297:Prenatal Exposure Delayed Effects; D055815:Young Adult
chemical_list: D005938:Glucocorticoids; D008055:Lipids; D001623:Betamethasone