April 2009
Volume 50, Issue 13
ARVO Annual Meeting Abstract  |   April 2009
Ocular Toxoplasmosis and Asymmetric Diabetic Retinopathy
Author Affiliations & Notes
  • B. A. Schlaen
    Ophthalmology, Hospital Universitario Austral, Derqui-Pilar, Argentina
  • M. J. Saravia
    Ophthalmology, Hospital Universitario Austral, Derqui-Pilar, Argentina
  • Footnotes
    Commercial Relationships  B.A. Schlaen, None; M.J. Saravia, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 6017. doi:
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      B. A. Schlaen, M. J. Saravia; Ocular Toxoplasmosis and Asymmetric Diabetic Retinopathy. Invest. Ophthalmol. Vis. Sci. 2009;50(13):6017.

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

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Purpose: : To show a case of severe impairment of diabetic retinopathy after an episode of ocular toxoplasmosis.

Methods: : A 60 years old male patient was admitted in our service, complaining of loss of vision and floaters in OS of 4 months’ duration. He told that his symptoms partially relieved at time of presentation in our institution. He had a history of 25 years of diabetes. He brought a positive result of antibodies against toxoplasma. He also brought color fundus photographs and a fluorescein angiography taken one month previous to consultation which revealed 2 foci of juxtapapillary retinitis along with optic disk neovascularization in OS and a non proliferative diabetic retinopathy in OD. At examination, best corrected visual acuity was of 20/20 in OD and 20/60 in OS. At biomicroscopy, OD examination was normal, whereas traces of aqueous cells and 1+ vitritis were observed in OS. Intraocular pressure was of 15 mmHg in OD and 16 mmHg in OS. Fundus examination revealed no changes in OD, while in OS, optic disk neovascularization had a severe impairment and retinochoroidal scars were observed instead of both foci of retinitis. Vitrectomy with endolaser panretinal photocoagulation with previous intravitreal bevacizumab was offered. Patient refused treatment and had not return for follow up.

Results: : There are several factors that appear to lead to asymmetric development of diabetic retinopathy: carotid disease, cataract surgery, endophthalmitis, choriorretinal scarring, complete posterior vitreous detachment, amblyopia, unilateral elevated intraocular pressure, optic atrophy, retinal pigment epithelial atrophy, high myopia, concurrent retinal vascular disease, vitreous loss, radiation, unilateral recurrent panuveitis, retinitis pigmentosa and others. Although there is a report that Fuchs syndrome appears to be protective against the development of diabetic retinopathy, intraocular inflammation is associated in most cases to an impairment of diabetic retinopathy. This is probably related to the fact that both conditions share some biochemical mechanisms such as an increase of VEGF and other proinflammatory cytokines.

Conclusions: : Ocular toxoplasmosis can accelerate diabetic retinopathy development.

Keywords: toxoplasmosis • diabetic retinopathy • neovascularization 

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