title: Antenatal corticosteroid therapy and risk of osteoporosis.
abstract: OBJECTIVE
  To assess the risk of maternal osteoporosis associated with antenatal corticosteroid administration for neonatal respiratory distress syndrome prophylaxis.
  
  
  METHODS
  Prospective longitudinal study.
  
  
  METHODS
  Maternity unit of Chelsea and Westminster Hospital, London.
  
  
  METHODS
  Fourteen pregnant women who received dexamethasone therapy for fetal lung maturation in anticipation of delivery before 34 completed weeks of gestation.
  
  
  METHODS
  Blood samples were collected before dexamethasone administration, 24 hours and 48 hours after the course of dexamethasone, and within 24 hours of delivery. Serum levels of carboxy terminal pro-peptide of type I pro-collagen (PICP) were measured to monitor the rate of bone formation, and serum levels of cross-linked carboxy terminal telopeptide (ICTP) were measured as a marker of bone resorption.
  
  
  METHODS
  Changes in the markers of bone turnover following dexamethasone administration.
  
  
  RESULTS
  Serum PICP levels dropped 24 hours after dexamethasone therapy (P = 0.001), but partially recovered by 48 hours (P = 0.014) to reach higher than pre-therapy levels at delivery (P = 0.044). Although there were no corresponding changes in the serum levels of ICTP after 24 and 48 hours of therapy, levels increased from pretherapy to delivery (P = 0.006).
  
  
  CONCLUSIONS
  Antenatal corticosteroid therapy leads to a transient suppression of, followed by an increase in, bone formation without any significant alteration in the pattern of bone resorption expected during pregnancy.
authors.affiliation: Section of Obstetrics and Gynaecology, Imperial College School of Medicine at Chelsea and Westminster Hospital, London, UK.
authors.forename: O
authors.initials: O
authors.lastname: Ogueh
authors.forename: G
authors.initials: G
authors.lastname: Khastgir
authors.forename: J W
authors.initials: JW
authors.lastname: Studd
authors.forename: J
authors.initials: J
authors.lastname: Jones
authors.forename: J
authors.initials: J
authors.lastname: Alaghband-Zadeh
authors.forename: M R
authors.initials: MR
authors.lastname: Johnson
mesh_terms: D015415:Biomarkers / Q000097:blood; D016723:Bone Remodeling; D003094:Collagen; D024042:Collagen Type I; D003432:Cross-Linking Reagents; D003907:Dexamethasone / Q000009:adverse effects; D005260:Female; D005325:Fetal Organ Maturity; D005938:Glucocorticoids / Q000009:adverse effects*; D006801:Humans; D007231:Infant, Newborn; D008137:Longitudinal Studies; D008168:Lung / Q000196:embryology*; D007752:Obstetric Labor, Premature; D010024:Osteoporosis / Q000139:chemically induced*; D010446:Peptide Fragments / Q000097:blood; D010455:Peptides; D011247:Pregnancy; D011295:Prenatal Care; D011347:Procollagen / Q000097:blood; D011446:Prospective Studies; D012127:Respiratory Distress Syndrome, Newborn / Q000517:prevention & control*; D012307:Risk Factors
chemical_list: D015415:Biomarkers; D024042:Collagen Type I; D003432:Cross-Linking Reagents; D005938:Glucocorticoids; D010446:Peptide Fragments; D010455:Peptides; D011347:Procollagen; C052929:collagen type I trimeric cross-linked peptide; D003907:Dexamethasone; D003094:Collagen