title: Erythroid apoptosis in idiopathic neonatal jaundice.
abstract: OBJECTIVE
  The objectives of this study were to evaluate the contribution of erythroid apoptosis to neonatal idiopathic pathologic jaundice and to determine whether a measurement of the erythroid apoptosis value at birth could predict the development of hyperbilirubinemia during the first 15 days of life.
  
  
  METHODS
  Three groups were defined: group 1 (n = 101), healthy newborns whose erythroid apoptosis value and serum total bilirubin levels were detected from birth to day 15; group 2 (n = 24), newborns who were hospitalized for jaundice (serum total bilirubin level: > 12.9 mg/dL) without any identifiable pathologic cause; and group 3 (control group, n = 24), healthy newborns whose serum total bilirubin levels were < or = 12.9 mg/dL. Erythroid apoptosis value was assessed by flow cytometry using an annexin-V fluorescein isothiocyanate kit.
  
  
  RESULTS
  In group 1, there was no correlation between the erythroid apoptosis value and serum total bilirubin levels obtained at birth and at the fourth and 15th days of life; the erythrocyte apoptosis value obtained at birth was not significantly different between the neonates whose serum total bilirubin levels were > 12.9 and < or = 12.9 mg/dL and who had prolonged and nonprolonged jaundice during follow-up. The erythroid apoptosis value differed significantly between the newborns in groups 2 and 3. There was no significant correlation between the erythroid apoptosis value and serum total bilirubin levels of the infants in groups 2 and 3.
  
  
  CONCLUSIONS
  The erythroid apoptosis value obtained at birth could not predict the development of hyperbilirubinemia in neonates, but it was increased significantly in jaundiced neonates whose serum total bilirubin levels were > 12.9 mg/dL. In these infants, increase in the erythroid apoptosis value may be a result of the toxic effect of bilirubin or of a protective mechanism of neonates to increase heme turnover and bilirubin production to diminish oxidative stress.
authors.affiliation: Dokuz Eylül University Faculty of Medicine, Department of Pediatric Neonatology, 35340 Balcova, Izmir, Turkey.
authors.forename: Hasan
authors.initials: H
authors.lastname: Ozkan
authors.forename: Hale
authors.initials: H
authors.lastname: Oren
authors.forename: Mansur
authors.initials: M
authors.lastname: Tatli
authors.forename: Halil
authors.initials: H
authors.lastname: Ateş
authors.forename: Abdullah
authors.initials: A
authors.lastname: Kumral
authors.forename: Nuray
authors.initials: N
authors.lastname: Duman
mesh_terms: D017209:Apoptosis; D001663:Bilirubin / Q000097:blood; D004912:Erythrocytes / Q000473:pathology; D041905:Erythroid Cells / Q000473:pathology*; D005260:Female; D005312:Fetal Blood / Q000166:cytology; D006400:Hematocrit; D006801:Humans; D051556:Hyperbilirubinemia, Neonatal / Q000097:blood; D007231:Infant, Newborn; D007567:Jaundice, Neonatal / Q000097:blood*; D008297:Male
chemical_list: D001663:Bilirubin