Document Detail


Postnatal head growth deficit among premature infants parallels retinopathy of prematurity and insulin-like growth factor-1 deficit.
MedLine Citation:
PMID:  16740833     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
Chatarina Löfqvist; Eva Engström; Jon Sigurdsson; Anna-Lena Hård; Aimon Niklasson; Uwe Ewald; Gerd Holmström; Lois E H Smith; Ann Hellström
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Pediatrics     Volume:  117     ISSN:  1098-4275     ISO Abbreviation:  Pediatrics     Publication Date:  2006 Jun 
Date Detail:
Created Date:  2006-06-02     Completed Date:  2006-06-26     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0376422     Medline TA:  Pediatrics     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1930-8     Citation Subset:  AIM; IM    
Affiliation:
Pediatric Growth Research Center, Institute for Clinical Sciences, Department of Pediatrics, Sahlgrenska Academy of Göteborg University, Göteborg, Sweden.
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MeSH Terms
Descriptor/Qualifier:
Female
Growth Disorders / blood,  etiology*
Head / growth & development*
Humans
Infant, Newborn
Insulin-Like Growth Factor I / analysis,  deficiency*
Male
Prospective Studies
Retinal Vessels / growth & development*
Retinopathy of Prematurity / blood,  etiology*
Grant Support
ID/Acronym/Agency:
EY008670/EY/NEI NIH HHS; EY14811/EY/NEI NIH HHS
Chemical
Reg. No./Substance:
67763-96-6/Insulin-Like Growth Factor I
Comments/Corrections
Comment In:
Pediatrics. 2006 Jun;117(6):2287-9   [PMID:  16740879 ]

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