September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Treatment of Diabetic Macular Edema with Aflibercept in Eyes with Previous Nonresponse to Ranibizumab and/or Bevacizumab
Author Affiliations & Notes
  • Rachel Sadowsky
    University of Minnesota, Minnetonka, Minnesota, United States
  • Polly Quiram
    VitreoRetinal Surgery, PA, Minneapolis, Minnesota, United States
  • Footnotes
    Commercial Relationships   Rachel Sadowsky, None; Polly Quiram, None
  • Footnotes
    Support  2015 VitreoRetinal Surgery Foundation Research Award
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 2104. doi:
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      Rachel Sadowsky, Polly Quiram; Treatment of Diabetic Macular Edema with Aflibercept in Eyes with Previous Nonresponse to Ranibizumab and/or Bevacizumab. Invest. Ophthalmol. Vis. Sci. 2016;57(12):2104.

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

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Purpose : Diabetic Macular Edema (DME) is a vascular endothelial growth factor (VEGF) driven process that can be effectively treated with intravitreal injections of anti-VEGF agents bevacizumab and ranibizumab. In a subset of patients, DME persists and visual loss occurs despite active treatment with these anti-VEGF agents. The Food and Drug Administration recently approved aflibercept, now a third commonly used intravitreous anti-VEGF agent. This retrospective chart review identified patients with persistent DME as “nonresponders,” and tested the hypothesis that treatment with aflibercept improves functional and structural outcomes in patients that were otherwise resistant to prior anti-VEGF therapies.

Methods : The design of this study is a single center, retrospective chart review. Consecutive eyes previously receiving intravitreal bevacizumab (1.25mg) or ranibizumab (0.3mg) for chronic DME and later switched to aflibercept (2mg) were identified. Inclusion criteria included "nonresponding" eyes previously receiving 6 or more injections of ranibizumab and/or bevacizumab for DME. Exclusion criteria included eyes receiving less than 6 previous intravitreal injections of anti-VEGF agents. Eyes with less than 6 month follow up were excluded. Primary outcomes include mean change in visual acuity (VA) and mean change in central subfield foveal thickness (CSFT) by SD-OCT following initiation of aflibercept therapy.

Results : In this study, 58 eyes deemed "nonresponders" were identified for analysis. Prior to treatment with aflibercept, 53% of eyes were treated primarily with bevacizumab, and 47% with ranibizumab. The mean number of total injections before aflibercept was 16 (range 6-49). Of eyes with chronic DME, 58% previously received focal laser (mean 2.7; range 1-8). At initiation of aflibercept therapy, mean VA was 20/60 and CSFT was 417 ±117mm. Following a single dose of aflibercept, mean VA improved to 20/50 (p=0.015) and CSFT improved to 351 ± 88mm (p=0.011). Following 3 treatments of aflibercept, mean VA improved to 20/40 (p=0.16) and CSFT improved to 364 ± 119mm (p=0.03).

Conclusions : This study has identified eyes with chronic DME that are nonresponsive to intravitreal bevacizumab and ranibizumab. The novel mechanism of aflibercept appears to benefit eyes with chronic DME. Additional analysis will determine the long-term (1 year) benefit of aflibercept in eyes with chronic DME.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.


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