June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Change of scleral architecture in Chronic Vogt-Koyanagi-Harada disease
Author Affiliations & Notes
  • Yosuke Harada
    ophthalmology, Northwestern university, Chicago, IL
  • Pooja Bhat
    ophthalmology, University of Illinois Chicago, Chicago, IL
  • Amina Chaudhry
    ophthalmology, Northwestern university, Chicago, IL
  • Debra A Goldstein
    ophthalmology, Northwestern university, Chicago, IL
  • Footnotes
    Commercial Relationships Yosuke Harada, None; Pooja Bhat, None; Amina Chaudhry, None; Debra Goldstein, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 3126. doi:
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      Yosuke Harada, Pooja Bhat, Amina Chaudhry, Debra A Goldstein; Change of scleral architecture in Chronic Vogt-Koyanagi-Harada disease. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):3126.

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

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Abstract

Purpose: Complications of Vogt-Koyanagi-Harada disease (VKH) include cataract, glaucoma, choriodal neovascularization, subretinal fibrosis, and optic atrophy. While chronic disease has typically been described as affecting only the anterior segment (AJO. 131: 599-606, 2001), progressive choroidal thinning in chronic VKH patients has been reported (Graefes Arch Clin Exp Ophthalmol. 250: 1089-95, 2012). We have seen VKH patients with apparent changes in scleral architecture as well as retinal atrophy and choroidal thinning. The purpose of this study is to evaluate whether chronic VKH disease affects the sclera.

Methods: Chart review of patients with VKH seen by the uveitis service at Northwestern University July 2012 - September 2014. Change of scleral architecture was defined as 1) progressive stapyloma-like posterior bowing on optic coherence tomography (OCT), 2) progressive increase in axial length, or 3) change of refraction of more than -1.0 D not explicable by other etiologies.

Results: 16 patients (28 eyes) with VKH were included. 4 eyes of 4 patients were excluded for lack of follow up imaging. 8 eyes (28.6%) of 5 patients showed progressive scleral architectural changes. 5 eyes of 3 patients developed posterior architectural changes on OCT, 1 eye had posterior bowing on OCT with documented progression of axial length, 2 eyes of a bilaterally pseudophakic patient developed refractive change more than -1.5D with documented increase in axial length. All of these eyes had choroidal thinning.

Conclusions: Recently, choroidal thinning has been reported in chronic VKH patients. Our results indicate that scleral structure may also change in these patients, via a mechanisms as yet unknown. While choroidal thinning of VKH patients is reported to develop within 12 months of onset (Graefes Arch Clin Exp Ophthalmol. 250: 1089-95, 2012), scleral changes in this study continued to develop for years after onset. This suggests that scleral change may develop after choroidal thinning. The choroid is reported to play a role in regulating scleral remodeling (Progress in Retinal and Eye Research. 29: 144-68, 2010), and scleral change may be caused by impairment of scleral remodeling resulting from choroidal atrophy. Progressive scleral architectural change may be a complication of chronic VKH.

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