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(Investigative Ophthalmology and Visual Science. 2004;45:1712-1715.)
© 2004 by The Association for Research in Vision and Ophthalmology, Inc.
DOI:  10.1167/iovs.03-1303
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Genetic Polymorphisms and Retinopathy of Prematurity

Richard W. I. Cooke,1 Jo A. Drury,1 Roger Mountford,2 and David Clark3

1From the Department of Child Health University of Liverpool, Neonatal Unit, and the 2Regional Molecular Genetic Laboratory, Liverpool Women’s Hospital, Liverpool, United Kingdom; and the 3Department of Ophthalmology, University Hospital Aintree, Liverpool, United Kingdom.

PURPOSE. Retinopathy of prematurity (ROP) is a major problem among very preterm survivors of neonatal intensive care. Neovascularization of the retina is prominent in the proliferative stages of ROP and is under the control of several factors such as vascular endothelial growth factor (VEGF). This study was undertaken on the hypothesis that genetic polymorphisms of VEGF, transforming growth factor (TGF)-ß1, and tumor necrosis factor (TNF)-{alpha} would occur more frequently in preterm infants with progressive ROP than in those with mild or no disease.

METHODS. The frequencies of VEGF –634 G->C, VEGF *936 C->T, TNF-{alpha} –308 G->A, and TGF-ß –509 C->T were determined in DNA from 91 infants who had received treatment for threshold ROP and 97 comparison infants.

RESULTS. The frequencies of the VEGF *936 C->T, TNF-{alpha} –308 G->A and TGF-ß –509 C->T polymorphisms were similar in both groups. The distribution of alleles at VEGF –634 was significantly different between the two groups (P = 0.03). Homozygotes for the G allele, associated with higher VEGF production were twice as likely to have threshold ROP.

CONCLUSIONS. The progression of ROP to threshold ROP in very preterm infants may be influenced by genetic differences in VEGF production. Future efforts at prevention of threshold ROP may be directed toward blocking excess production of VEGF.




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