title: Asymmetrical fetal growth is not associated with altered trophoblast apoptotic activity in idiopathic intrauterine growth retardation.
abstract: OBJECTIVE
  To investigate whether there is difference in trophoblast apoptosis between infants with asymmetrical idiopathic intrauterine growth retardation (IUGR) and those with symmetrical fetal growth appropriate for gestational age (AGA).
  
  
  METHODS
  Data and placentas from 52 singleton term pregnancies with idiopathic IUGR, from which a subgroup of 33 (63.4%) infants with asymmetrical growth and malnutrition was identified using the ponderal index served as a study group. The control group included 60 (86.9%) infants with symmetrical growth, identified by the same criterion among 69 normal singleton pregnancies with AGA. IUGR was defined by birthweight less than the 10th percentile of standard values. Ponderal index value was considered as the measurement of fetal growth proportionality.
  
  
  RESULTS
  The proportion of fetal thinness up to ponderal index value was greater in the IUGR group than control (χ(2) = 9.2; P = 0.002). There was no statistically significant difference in the cytotrophoblast proliferation (t = 0.88; P = 0.373), trophoblast expression of the Bcl-2 anti-apoptotic factor (z = 0.66; P = 0.505), total trophoblast apoptotic index (t = 0.45; P = 0.651), as in cytotrophoblast (t = 0.01; P = 0.988) and syncytiotrophoblast apoptotic index (t = 0.34; P = 0.730) between the idiopathic asymmetrical IUGR and control group.
  
  
  CONCLUSIONS
  Asymmetry of fetal growth is a result of rather long-term placental nutritive insufficiency in which trophoblasts have a central role. Although being crucial for its functioning, the proliferative and apoptotic trophoblast activity remains unaltered in the placentas from pregnancies with idiopathic IUGR and asymmetrical fetal growth. The results obtained in this study indicate that placental nutritive insufficiency may develop without any deviation in the physiological trophoblast regeneration via apoptosis.
authors.affiliation: Clinical Hospital Center Split, Split, Croatia.
authors.forename: Damir
authors.initials: D
authors.lastname: Roje
authors.forename: Sandra
authors.initials: S
authors.lastname: Zekic Tomas
authors.forename: Vesna
authors.initials: V
authors.lastname: Capkun
authors.forename: Jelena
authors.initials: J
authors.lastname: Marusic
authors.forename: Jasminka
authors.initials: J
authors.lastname: Resic
authors.forename: Ivana
authors.initials: I
authors.lastname: Kuzmic Prusac
mesh_terms: D000328:Adult; D017209:Apoptosis; D001724:Birth Weight; D049109:Cell Proliferation; D005260:Female; D047109:Fetal Development / Q000502:physiology*; D005317:Fetal Growth Retardation / Q000503:physiopathology*; D005865:Gestational Age; D006801:Humans; D007231:Infant, Newborn; D019394:Ki-67 Antigen / Q000032:analysis; D008297:Male; D011247:Pregnancy; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000032:analysis; D014327:Trophoblasts / Q000737:chemistry / Q000502:physiology*; D055815:Young Adult
chemical_list: D019394:Ki-67 Antigen; D019253:Proto-Oncogene Proteins c-bcl-2
keywords: apoptosis; fetal growth retardation; infant; placenta; thinness