BACKGROUND: Development of central serous chorioretinopathy (CSC) following the administration of corticosteroids by diverse routes is a well-known fact. We report acute visual loss after the use of systemic corticosteroids in three patients with long-standing ocular inflammatory disorders in whom CSC could initially be misinterpreted as a worsening of the primary inflammatory condition. METHODS: We analyzed the clinical findings and the fluorescein and indocyanine green (ICG) angiographic signs in those three patients. RESULTS: The first patient had birdshot chorioretinopathy with minimal functional impairment for several years without treatment. When visual acuity and fields deteriorated, systemic corticosteroids were administered resulting in improved inflammatory and functional parameters during the first 2 months. Subsequently, the visual acuity of his left eye decreased due to CSC. The second patient had Vogt-Koyanagi-Harada disease with five episodes of acute inflammation. She was treated each time with systemic corticosteroids, but thrice her visual acuity deteriorated, caused by CSC. The third patient presented with scleritis of his right eye related to relapsing polychondritis. Massive oral corticosteroids were given, soon followed by the development of CSC in the right eye. Fluorescein and ICG angiographic signs were typical for CSC in all three patients. Cyclosporine was introduced in the two first patients and cyclophosphamide in the third patient, in parallel with tapering of oral corticosteroids. Progressive regression of CSC occurred in all three patients. CONCLUSION: The potentially deleterious effects of corticosteroids, favoring CSC, are well-known. They should be borne in mind when an unexpected clinical and angiographic evolution compatible with CSC develops in an uveitis patient treated with corticosteroids.
BACKGROUND: Development of central serous chorioretinopathy (CSC) following the administration of corticosteroids by diverse routes is a well-known fact. We report acute visual loss after the use of systemic corticosteroids in three patients with long-standing ocular inflammatory disorders in whom CSC could initially be misinterpreted as a worsening of the primary inflammatory condition. METHODS: We analyzed the clinical findings and the fluorescein and indocyanine green (ICG) angiographic signs in those three patients. RESULTS: The first patient had birdshot chorioretinopathy with minimal functional impairment for several years without treatment. When visual acuity and fields deteriorated, systemic corticosteroids were administered resulting in improved inflammatory and functional parameters during the first 2 months. Subsequently, the visual acuity of his left eye decreased due to CSC. The second patient had Vogt-Koyanagi-Harada disease with five episodes of acute inflammation. She was treated each time with systemic corticosteroids, but thrice her visual acuity deteriorated, caused by CSC. The third patient presented with scleritis of his right eye related to relapsing polychondritis. Massive oral corticosteroids were given, soon followed by the development of CSC in the right eye. Fluorescein and ICG angiographic signs were typical for CSC in all three patients. Cyclosporine was introduced in the two first patients and cyclophosphamide in the third patient, in parallel with tapering of oral corticosteroids. Progressive regression of CSC occurred in all three patients. CONCLUSION: The potentially deleterious effects of corticosteroids, favoring CSC, are well-known. They should be borne in mind when an unexpected clinical and angiographic evolution compatible with CSC develops in an uveitispatient treated with corticosteroids.