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Fuchs’ heterochromic cyclitis: a post-infectious manifestation of ocular toxoplasmosis?
Fuchs’ heterochromic cyclitis: a post-infectious manifestation of ocular toxoplasmosis?
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Fuchs’ heterochromic cyclitis: a post-infectious manifestation of ocular toxoplasmosis?
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Fuchs’ heterochromic cyclitis: a post-infectious manifestation of ocular toxoplasmosis?
Fuchs’ heterochromic cyclitis: a post-infectious manifestation of ocular toxoplasmosis?
Journal Article

Fuchs’ heterochromic cyclitis: a post-infectious manifestation of ocular toxoplasmosis?

2013
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Overview
The purpose of this article is to report the development of Fuchs’ heterochromic cyclitis (FHC) secondary to toxoplasmosis chorioretinitis. The design is based on observational case series report. We report in this article six cases of typical FHC developing secondary to ocular toxoplasmosis. Intraocular immunoglobulin G production against Toxoplasma gondii was determined in the aqueous humor of five patients by calculation of the Goldmann–Witmer coefficient (GWC). The clinical examination revealed typical FHC with no active chorioretinal scar. We report on five women and one man (aged 33–64 years old; median 44.6 years) who developed FHC over a period of time ranging from 2–13 years. A positive GWC (>3) was found in four patients; of the two remaining patients one was negative and the other did not have anterior chamber paracentesis. Four patients were treated for an active ocular toxoplasmic lesion before the development of FHC with pyrimethamine, sulfadiazine and corticosteroids. Two patients had negative anti-toxoplasmic therapy for FHC (one with trimethoprim-sulfamethoxazole for 3 weeks and the other with pyrimethamine, sulfadiazine and corticosteroids for 8 weeks). One never had any treatment. All the patients had mild anterior chamber reaction with no synechia, diffuse and characteristic white stellate keratic precipitates and vitritis; five patients had posterior subcapsular cataract and heterochromia and three had elevated intraocular pressure. The findings help us to conclude that FHC can develop over a period of time after ocular toxoplasmosis. This could be a main association to search for when a Fuchs’ uveitis is found with a chorioretinal scar. Ocular inflammation does not mean reactivation of ocular toxoplasmosis. FHC could be a secondary immune reaction with a past antigenic stimulation to a previous infection, i.e., toxoplasmosis, etc.