April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Retinal Glial Cells Activation in Diabetics with and without Retinopathy: An in Vivo Study
Author Affiliations & Notes
  • Edoardo Midena
    Ophthalmology, University of Padova, Padova, Italy
    Fondazione GB Bietti-IRCCS, Roma, Italy
  • Ferdinando Martini
    Ophthalmology, University of Padova, Padova, Italy
  • Angela Rediu
    Ophthalmology, University of Padova, Padova, Italy
  • Margherita Casciano
    Ophthalmology, University of Padova, Padova, Italy
  • Stela Vujosevic
    Fondazione GB Bietti-IRCCS, Roma, Italy
  • Footnotes
    Commercial Relationships  Edoardo Midena, None; Ferdinando Martini, None; Angela Rediu, None; Margherita Casciano, None; Stela Vujosevic, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 1272. doi:
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      Edoardo Midena, Ferdinando Martini, Angela Rediu, Margherita Casciano, Stela Vujosevic; Retinal Glial Cells Activation in Diabetics with and without Retinopathy: An in Vivo Study. Invest. Ophthalmol. Vis. Sci. 2011;52(14):1272.

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

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Abstract

Purpose: : To evaluate if retinal glial cells activation may be detected in vivo in eyes without and with nonproliferative diabetic retinopathy.

Methods: : Eighty-eight subjects were enrolled: 58 subjects were affected by diabetes mellitus and 30 normals served as controls. Proliferative diabetic retinopathy, previous laser photocoagulation, intraocular surgery or intravitreal injection, and refractive error > 6 diopters were the main exclusion criteria. One eye of each subject was used for statistical analysis. Thirty patients had no diabetic retinopathy (no DR group) , 28 patients had non proliferative DR without macular edema (DR group). Full ophthalmic examination, stereoscopic fundus photography, and spectral domain-OCT (SD-OCT; RS-3000, Nidek, Japan) were performed in all eyes. After automatic segmentation (layering) of 5 retinal layers by SD-OCT, the thickness of these layers was automatically calculated in the foveal and pericentral area, and values compared among groups. The thickness of selected, more specific layers (inner limiting membrane, inner plexiform and nuclear layers, outer plexiform layer) was also manually quantified. All measurements were performed twice by two independent graders.

Results: : No statistically significant differences were found for age among all groups, and for diabetes duration among diabetics. In the no DR and DR groups, using automatic layering, the mean thickness of inner retina was significantly reduced compared to controls (p<.001), no change was detected in the outer retina, both in the fovea and pericentral area. A significant increase of inner limiting membrane, inner plexiform and nuclear layers was found in DR eyes vs controls (p<0.001), versus a significant decrease of retinal ganglion cell and retinal nerve fiber layers. The inter-grader agreement was at least substantial for all measurement.

Conclusions: : Increased thickness of retinal layers mainly corresponding to retinal glial cells , even before the appearance of clinically detectable retinopathy, confirms in vivo early glial cells activation in diabetic retina.Glial activation may be detected by spectral domain OCT using targetted analysis. These data strongly suggests a very early reactive and degenerative processs both in neural and glial cells of diabetic retina .

Keywords: diabetic retinopathy • Muller cells • glia 
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