title: Postnatal head growth deficit among premature infants parallels retinopathy of prematurity and insulin-like growth factor-1 deficit.
abstract: BACKGROUND
  We hypothesized that in premature infants, retinal vascular growth retardation between birth and postmenstrual age of approximately 30 to 32 weeks that initiates retinopathy of prematurity is paralleled by brain growth retardation.
  
  
  METHODS
  In a prospective longitudinal study, we measured postnatal head growth, retinopathy of prematurity stage, protein and energy intake, severity of illness and serum insulin-like growth factor-1 levels in 58 preterm infants (mean gestational age at birth: 27.6 weeks) from birth until postmenstrual age of approximately 40 weeks.
  
  
  RESULTS
  Premature infant head growth decelerates dramatically after birth until postmenstrual age of approximately 30 weeks. Head growth retardation coincides with retinal vascular growth suppression. Accelerated growth follows between post menstrual ages of approximately 30 to 32 weeks and approximately 40 weeks. The degree of head growth retardation up to postmenstrual age of 31 weeks corresponds to the degree of retinopathy of prematurity and to the degree of suppression of serum levels of insulin-like growth factor-1. At postmenstrual age of 31 weeks, if a child's head circumference SD is below -2.5, then the probability of also developing at least stage 3 retinopathy of prematurity increases fivefold compared with head circumference above -2.5 SD (32% vs 6%) suggesting parallel processes in brain and retina. Serum insulin-like growth factor-1 levels correlate positively with head circumference SD score and with the degree of retinopathy of prematurity.
  
  
  CONCLUSIONS
  The correlation between head and retinal growth is consistent with insulin growth factor-1 being one of the postnatal growth factors involved in this multifactorial process and also suggests that factors that contribute to retinopathy of prematurity during this critical period may also affect neurological dysfunction. Additional studies are required to establish this connection.
authors.affiliation: Pediatric Growth Research Center, Institute for Clinical Sciences, Department of Pediatrics, Sahlgrenska Academy of Göteborg University, Göteborg, Sweden.
authors.forename: Chatarina
authors.initials: C
authors.lastname: Löfqvist
authors.forename: Eva
authors.initials: E
authors.lastname: Engström
authors.forename: Jon
authors.initials: J
authors.lastname: Sigurdsson
authors.forename: Anna-Lena
authors.initials: AL
authors.lastname: Hård
authors.forename: Aimon
authors.initials: A
authors.lastname: Niklasson
authors.forename: Uwe
authors.initials: U
authors.lastname: Ewald
authors.forename: Gerd
authors.initials: G
authors.lastname: Holmström
authors.forename: Lois E H
authors.initials: LE
authors.lastname: Smith
authors.forename: Ann
authors.initials: A
authors.lastname: Hellström
mesh_terms: D005260:Female; D006130:Growth Disorders / Q000097:blood / Q000209:etiology*; D006257:Head / Q000254:growth & development*; D006801:Humans; D007231:Infant, Newborn; D007334:Insulin-Like Growth Factor I / Q000032:analysis / Q000172:deficiency*; D008297:Male; D011446:Prospective Studies; D012171:Retinal Vessels / Q000254:growth & development*; D012178:Retinopathy of Prematurity / Q000097:blood / Q000209:etiology*
chemical_list: D007334:Insulin-Like Growth Factor I