Subject(s)
Calcium-Binding Proteins/genetics , Extracellular Matrix Proteins/genetics , Gene Expression Regulation , RNA/genetics , Retinal Detachment/genetics , Subretinal Fluid/metabolism , Calcium-Binding Proteins/biosynthesis , Extracellular Matrix Proteins/biosynthesis , Humans , Ophthalmoscopy , Retinal Detachment/diagnosis , Retinal Detachment/metabolism , Subretinal Fluid/diagnostic imagingABSTRACT
PURPOSE: To report spectral domain optical coherence tomography (OCT) and angiographic findings in exudative retinal detachment complicating central serous chorioretinopathy. DESIGN: interventional case report. METHODS: 33-year old man with bilateral nonrhegmatogenous retinal detachment, misdiagnosed as uveitis, iatrogenically treated with systemic corticosteroids. RESULTS: Discontinuation of corticotherapy led to anatomic and visual improvement. Fluorescein angiography demonstrated multiple leakage points; indocyanine green angiography disclosed large hyperfluorescent patches in the choroid and OCT demonstrated retinal detachment with dense subretinal deposits. CONCLUSION: The recognition of this atypical presentation with a combination of opthalmoscopic, angiographic and OCT findings may avoid inappropriate diagnosis and treatment with corticosteroids.
Subject(s)
Adrenal Cortex Hormones/adverse effects , Central Serous Chorioretinopathy/complications , Central Serous Chorioretinopathy/diagnosis , Fluorescein Angiography , Retinal Detachment/etiology , Tomography, Optical Coherence , Adrenal Cortex Hormones/administration & dosage , Adult , Central Serous Chorioretinopathy/physiopathology , Coloring Agents , Diagnostic Errors , Drug Administration Schedule , Exudates and Transudates/metabolism , Humans , Indocyanine Green , Male , Retinal Detachment/metabolism , Uveitis/diagnosis , Uveomeningoencephalitic Syndrome/diagnosis , Uveomeningoencephalitic Syndrome/drug therapyABSTRACT
Proliferative vitreoretinopathy (PVR) is characterized by severe glial remodeling. Glial activation and proliferation that occur in brain diseases are modulated by endothelin-1 (ET-1) and its receptor B (ETR-B). Because retinal astrocytes contain ET-1 and express ETR-B, we studied the changes of these molecules in an experimental mouse model of PVR and in human PVR. Both ET-1 and ETR-B immunoreactivities increased in mouse retina after induction of PVR with dispase. Epi- and subretinal outgrowths also displayed these immunoreactivities in both human and experimental PVR. Additionally, myofibroblasts and other membranous cell types showed both ET-1 and ETR-B immunoreactivities. In early stages of experimentally induced PVR, prepro-ET-1 and ETR-B mRNA levels increased in the retina. These mRNA levels also increased after retinal detachment (RD) produced by subretinal injection. Treatment of mice with tezosentan, an antagonist of endothelinergic receptors, reduced the histopathological hallmarks of dispase-induced PVR: retinal folding, epiretinal outgrowth, and gliosis. Our findings in human and in dispase-induced PVR support the involvement of endothelinergic pathways in retinal glial activation and the phenotypic transformations that underlie the growth of membranes in this pathology. Elucidating these pathways further will help to develop pharmacological treatments to prevent PVR. In addition, the presence of ET-1 and ETR-B in human fibrous membranes suggests that similar treatments could be helpful after PVR has been established.