June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Weight Gain Acceleration and Risk of Retinopathy of Prematurity
Author Affiliations & Notes
  • Sila Bal
    Ophthalmology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States
  • Gui-Shuang Ying
    Ophthalmology, University of Pennsylvania, Philadelphia, Pennsylvania, United States
  • Lauren Tomlinson
    Ophthalmology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States
  • Gil Binenbaum
    Ophthalmology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States
  • Footnotes
    Commercial Relationships   Sila Bal, None; Gui-Shuang Ying, None; Lauren Tomlinson, None; Gil Binenbaum, None
  • Footnotes
    Support  NIH 1R01EY021137-01A1
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 5536. doi:
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      Sila Bal, Gui-Shuang Ying, Lauren Tomlinson, Gil Binenbaum; Weight Gain Acceleration and Risk of Retinopathy of Prematurity. Invest. Ophthalmol. Vis. Sci. 2017;58(8):5536.

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

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Purpose : Slow weight gain in early life, a surrogate for low serum IGF-1, is associated with the subsequent development of retinopathy of prematurity (ROP). While early low IGF-1 inhibits retinal vessel growth, a later rise in IGF-1 is thought to activate VEGF, causing neovascular ROP. A fast rise in IGF-1 is represented by fast weight acceleration. Therefore, we evaluated the hypothesis that faster weight gain acceleration later in postnatal life is associated with a higher, rather than lower, risk of severe ROP.

Methods : Secondary analysis of the G-ROP Study, a retrospective cohort of infants undergoing ROP exams at 30 hospitals in North America between 2006-12. Infants with inadequate weight data were excluded. Weight gain rate during PMA weeks 29-33 (WGR-29-33) and weight gain acceleration during weeks 34-38 (WGA-34-38) were determined with linear regression of daily weight measurements and changes in daily weight measurements, respectively. The primary outcome was association between WGA-34-38 (grouped into tertiles) and severe (Type 1 or 2) ROP. Confounding was considered for well-established ROP risk factors: birth weight (BW), gestational age (GA), and WGR-29-33. There was significant interaction between WGR and WGA with respect to ROP, so stratified analysis of WGR-29-33 tertiles was performed. BW and GA were controlled for with multivariable logistic regression.

Results : 6835 infants were studied, mean(SD) BW 1086(357) g, GA 27.9(2.5) wks. 868(12.7%) had severe ROP (19% in the lowest WGR-29-33 tertile, 12.4% middle, 6.9% highest). In the lowest WGR-29-33 tertile (<12 g/day), there was no association between WGA-34-38 and severe ROP. In the middle WGR-29-33 tertile (12-24 g/day), the middle WGA-34-38 tertile (-0.25 to +0.55 g/day*day) had the highest risk of ROP (adjusted OR compared to lowest tertile, 1.4 (95%CI 0.98-1.94)). The same effect was seen in the highest WGR 29-33 tertile (>24 g/day), with the middle WGA-34-38 tertile at highest ROP risk (adjusted OR=1.6 (1.02-2.6)). Generally, risk of severe ROP increased with increasing WGA-34-38, up until about the 80th percentile of WGA (Figure).

Conclusions : The effect of WGA on ROP depends on WGR earlier in postnatal development. Very low WGR-29-33 is associated with severe ROP regardless of subsequent WGA. But if WGR-29-33 is moderate or high, subsequent rapid rises in weight gain rate are associated with increasing risk of severe ROP.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.



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