May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Aggressive Posterior Retinopathy of Prematurity
Author Affiliations & Notes
  • K. A. Drenser
    William Beaumont Hosp, Associated Retinal Consultants, Royal Oak, Michigan
  • A. Vinikar
    William Beaumont Hosp, Associated Retinal Consultants, Royal Oak, Michigan
  • W. Dailey
    William Beaumont Hosp, Associated Retinal Consultants, Royal Oak, Michigan
  • M. T. Trese
    William Beaumont Hosp, Associated Retinal Consultants, Royal Oak, Michigan
  • A. Capone, Jr.
    William Beaumont Hosp, Associated Retinal Consultants, Royal Oak, Michigan
  • Footnotes
    Commercial Relationships  K.A. Drenser, None; A. Vinikar, None; W. Dailey, None; M.T. Trese, None; A. Capone, None.
  • Footnotes
    Support  Margaret Walters Research Grant; ROPARD
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 1388. doi:https://doi.org/
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    • Get Citation

      K. A. Drenser, A. Vinikar, W. Dailey, M. T. Trese, A. Capone, Jr.; Aggressive Posterior Retinopathy of Prematurity. Invest. Ophthalmol. Vis. Sci. 2008;49(13):1388. doi: https://doi.org/.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : We evaluated 17 infants with aggressive posterior retinopathy of prematurity (APROP) for mutations in the FZD4 gene and compared them to 31 eyes which developed classic ROP requiring treatment.

Methods: : Children with pediatric vitreoretinopathies, including ROP, were entered into a database. The database includes clinical presentation, family history, fundus photos, OCT, and peripheral blood. Infants diagnosed with ROP were selected for this subgroup analysis. A total of 48 infants with ROP were included and 17 of these infants had APROP with zone 1 disease requiring treatment by ETROP criteria. The genomic DNA was obtained from peripheral blood. Genetic analysis was performed using PCR and direct sequencing of the coding regions of the FZD4 gene.

Results: : A total of 48 infants with stage 3 or greater ROP underwent genetic analysis. Seventeen of these children were identified as having APROP. Two of 17 (12%) infants with APROP were found to have a compound heterozygous mutation in the FZD4 gene (P33S; P168S). One infant, out of 31 (3%), with classic ROP was found to have this same compound mutation. This equals an odds ratio of 4.41 for this mutation and the development of APROP.

Conclusions: : The compound heterozygous mutation in the FZD4 gene may be a predisposing factor to the development of a more aggressive form of ROP.

Keywords: retinopathy of prematurity • genetics 
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