June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
Contribution of Breakdown of Outer Blood-retinal Barrier (BOBRB) to Diabetic Macular Edema
Author Affiliations & Notes
  • Weiye Li
    Ophthalmology, Drexel University College of Medicine, Philadelphia, PA
  • Mansi Patel
    Ophthalmology, Drexel University College of Medicine, Philadelphia, PA
  • Behnaz Rouhani
    Ophthalmology, Drexel University College of Medicine, Philadelphia, PA
  • Raza Shah
    Ophthalmology, Drexel University College of Medicine, Philadelphia, PA
  • Fang Wang
    Ophthalmology, Tenth People's Hospital of Tongi University, Shanghai, China
  • Liumei Hu
    Ophthalmology, Tenth People's Hospital of Tongi University, Shanghai, China
  • Yaprak Unver
    Ophthalmology, Birinci Eye Hospital, Istanbul, Turkey
  • Footnotes
    Commercial Relationships Weiye Li, None; Mansi Patel, None; Behnaz Rouhani, None; Raza Shah, None; Fang Wang, None; Liumei Hu, None; Yaprak Unver, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 219. doi:https://doi.org/
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      Weiye Li, Mansi Patel, Behnaz Rouhani, Raza Shah, Fang Wang, Liumei Hu, Yaprak Unver; Contribution of Breakdown of Outer Blood-retinal Barrier (BOBRB) to Diabetic Macular Edema. Invest. Ophthalmol. Vis. Sci. 2013;54(15):219. doi: https://doi.org/.

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

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Abstract

Purpose: Despite the substantial evidence of the BOBRB as a pathogenic component of experimental diabetic retinopathy, the contribution of the BOBRB to clinical diabetic retinopathy has largely been neglected. This study has provided clinical evidence to support this concept.

Methods: A cohort study of 34 patients, 19 male and 15 female, with diabetic macular edema (DME), ranging from 43 to 82 years of age, were included in this study. All patients were evaluated by SD-OCT showing DME with subfoveal fluid, subretinal fluid (SRF), and clearly identifiable outer retina layers including the external limited membrane (ELM), photoreceptor (IS/OS), and retinal pigment epithelium (RPE). The affected eyes were also evaluated with overlay fundus photos, fundus auto fluorescence (FAF), fluorescein angiography (FA), and SD-OCT with enhanced depth imaging (EDI) to measure the underlying RPE thickness and overlaying IS/OS integrity corresponding to the area of SRF.

Results: All of the tested eyes showed an intact ELM, indicating a lack of fluid communication between the inner and outer retina. The FAs demonstrated isolated hyperfluorescent spots in the early phase with limited oozing into the subfoveal space during the late phase in only a few patients. The overlay FAF examination showed either hyper- or hypo-AF, indicating an accumulation of lipofuscin or a loss of RPE cells, respectively. By using SD-OCT with EDI, the trend of a thinning and more irregular RPE and IS/OS was observed.

Conclusions: The major hurdle for the insufficiency in detecting the role of OBRB is the difficulty to measure the OBRB- specific leakage in DME. The combination of current advances in retinal imaging studies enables us to specifically characterize the BOBRB clinically. This approach has provided evidence that dysfunction of OBRB contributes to DME formation, Therefore, these findings merit serious consideration of the BOBRB as a therapeutic target in DME.

Keywords: 499 diabetic retinopathy • 701 retinal pigment epithelium • 468 clinical research methodology  
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