title: Serum activin A, inhibin A, and follistatin concentrations in preeclampsia or small for gestational age pregnancies.
abstract: OBJECTIVE
  To determine whether maternal serum activin A, inhibin A, and follistatin concentrations in idiopathic small for gestational age (SGA) pregnancies are similar to those in normal pregnancies or elevated as in preeclampsia.
  
  
  METHODS
  Maternal serum activin A, inhibin A, and follistatin concentrations were determined in 1) nulliparous women with idiopathic SGA (birth weight <10th percentile; n = 18), preeclampsia (systolic blood pressure > or =140 mmHg or diastolic blood pressure > or =90 mmHg plus proteinuria > or =2+ or >0.3 g/24h; n = 22), and normotensive controls, matched for gestational age at sampling (n = 22), and 2) a longitudinal series of samples collected at five intervals throughout pregnancy from nulliparous women with idiopathic SGA (n = 19), preeclampsia (n = 22), preeclampsia plus SGA (n = 15), or who had uncomplicated pregnancies (n = 20).
  
  
  RESULTS
  Serum concentrations of activin A and inhibin A were similar in idiopathic SGA pregnancies to controls. In preeclampsia, activin A and inhibin A levels were markedly increased compared with controls or women with idiopathic SGA (P <.001), particularly in those with early-onset disease. Follistatin concentrations were only modestly (<twofold) elevated in preeclampsia (P <.001). In the longitudinal study, serum activin A or inhibin A concentrations were increased in women who later developed preeclampsia, whereas in women with idiopathic SGA pregnancy, a small overall increase in activin A levels was observed.
  
  
  CONCLUSIONS
  In contrast to women with preeclampsia, normotensive women with SGA pregnancies do not have markedly elevated circulating levels of activin A and inhibin A. These data support the hypothesis that increased serum activin A concentrations in preeclampsia may be a manifestation of maternal disease rather than just a marker of abnormal placentation.
authors.affiliation: Liggins Institute and Division of Pharmacology and Clinical Pharmacology, University of Auckland, Faculty of Medical and Health Sciences, New Zealand. j.keelan@auckland.ac.nz
authors.forename: Jeffrey A
authors.initials: JA
authors.lastname: Keelan
authors.forename: Rennae
authors.initials: R
authors.lastname: Taylor
authors.forename: Jean-Claude
authors.initials: JC
authors.lastname: Schellenberg
authors.forename: Nigel P
authors.initials: NP
authors.lastname: Groome
authors.forename: Murray D
authors.initials: MD
authors.lastname: Mitchell
authors.forename: Robyn A
authors.initials: RA
authors.lastname: North
mesh_terms: D028341:Activins / Q000097:blood*; D000328:Adult; D001794:Blood Pressure; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D005260:Female; D005317:Fetal Growth Retardation / Q000097:blood*; D038681:Follistatin; D006801:Humans; D007231:Infant, Newborn; D007236:Infant, Small for Gestational Age / Q000097:blood; D028322:Inhibin-beta Subunits / Q000097:blood*; D007265:Inhibins / Q000097:blood*; D008137:Longitudinal Studies; D011225:Pre-Eclampsia / Q000097:blood*; D011247:Pregnancy
chemical_list: D038681:Follistatin; C422405:activin A; C422362:inhibin A; D028341:Activins; D007265:Inhibins; D028322:Inhibin-beta Subunits