Three Cases of a Rare Congenital Abnormality of the Retinal Pigment Epithelium: Torpedo Maculopathy

2002 ◽  
Vol 216 (3) ◽  
pp. 226-227 ◽  
Author(s):  
Michela Rigotti ◽  
Silvia Babighian ◽  
Elisabetta Carcereri De Prati ◽  
Giorgio Marchini
Keyword(s):  
Retinal Pigment Epithelium ◽  
Congenital Abnormality ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Rare Congenital Abnormality ◽  
Torpedo Maculopathy

CASE OF TORPEDO MACULOPATHY WITH TWO DISTINCT ZONES OF THE RETINAL PIGMENT EPITHELIUM

2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Daniel A. Brill ◽  
Xihui Lin ◽  
Armando L. Garcia ◽  
Andrew C. Hou ◽  
Kim H. Le
Keyword(s):  
Retinal Pigment Epithelium ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Torpedo Maculopathy

Torpedo maculopathy: A case series – insights into basic pathology

2020 ◽  
pp. 112067212090531
Author(s):  
Doaa Kerwat ◽  
Omer Jamall ◽  
Serafeim Antonakis ◽  
Goncalo C Almeida
Keyword(s):  
Retinal Pigment Epithelium ◽  
Single Case ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Case Series ◽  
Fluid Accumulation ◽  
Benign Pathology ◽  
Intraretinal Fluid ◽  
Retinal Disorder ◽  
Torpedo Maculopathy

Torpedo maculopathy is a benign retinal disorder whose pathophysiological origins are currently poorly understood. A number of theories have been postulated, with stable developmental anomalies of the retinal pigment epithelium taking the forefront. Four clinical cases are outlined of patients with macular torpedo lesions, with differing clinical presentation. In all four cases, this reveals very thin retinal pigment epithelium and outer retina associated with the lesion. In a single case, the oldest patient of the group, there is the additional finding of subretinal and intraretinal fluid accumulation. The contrast between this case and the other cases suggests that while initially this benign pathology might start with structurally normal retina with no fluid accumulation, dysgenetic changes in the retinal pigment epithelium might lead to secondary accumulation of fluid over time. Whether indeed this disorder might be progressive in nature, or whether in fact it is a static, non-progressive developmental abnormality as formerly thought, requires further elucidation.

Multimodal imaging of torpedo maculopathy including adaptive optics

2019 ◽  
Vol 30 (2) ◽  
pp. NP27-NP31 ◽  
Author(s):  
Juliette Hugo ◽  
Marie Beylerian ◽  
Eric Denion ◽  
Aurore Aziz ◽  
Pierre Gascon ◽  
...  
Keyword(s):  
Optical Coherence Tomography ◽  
Retinal Pigment Epithelium ◽  
Fluorescein Angiography ◽  
Adaptive Optics ◽  
Multimodal Imaging ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Optical Coherence ◽  
Cone Mosaic ◽  
Torpedo Maculopathy

Purpose: The etiology of torpedo maculopathy remains unknown, but it has been recently suggested that it could represent a persistent defect in the development of the retinal pigment epithelium. As retinal pigment epithelium and photoreceptors form a functional unit, an alteration of photoreceptor distribution or function is predictable. The aim of this study is to describe multimodal imaging, including adaptive optics, in three cases of torpedo maculopathy, and discuss its pathogenesis. Methods: Multimodal imaging is presented, including fundus photographs, optical coherence tomography, adaptive optics, autofluorescence, fluorescein angiography, and ultra-widefield retinal imaging in three cases of torpedo maculopathy. Results: An oval-shaped well-delimited chorioretinal lesion both hypopigmented centrally and with a hyperpigmented border in the temporal macula, consistent with torpedo maculopathy, was observed in three patients. Optical coherence tomography showed a preservation of the inner retina, a mild atrophy of the outer retina, an alteration of the ellipsoid zone and of the retinal pigment epithelium layer, and a neurosensory detachment. These lesions were hypoautofluorescent with a hyperautofluorescent border. Fluorescein angiography showed a hyperfluorescence by window effect. Adaptive optics imaging showed an alteration of the cone mosaic within the lesions, with a lower cone density and a higher spacing between cones. Conclusion: The alteration of the cone mosaic suggested by adaptive optics in torpedo maculopathy has never been described and could be explained by the alteration of the retinal pigment epithelium. Our results support the existing hypothesis on the pathogenesis of torpedo maculopathy that a persistent defect in the development of the retinal pigment epithelium may be responsible for this clinical entity.

High-voltage electron microscopy of subretinal scar formation

1992 ◽  
Vol 50 (1) ◽  
pp. 486-487
Author(s):  
G.E. Korte ◽  
M. Marko ◽  
G. Hageman
Keyword(s):  
Electron Microscopy ◽  
Monoclonal Antibody ◽  
Retinal Pigment Epithelium ◽  
Glial Cells ◽  
High Voltage ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Sodium Iodate ◽  
High Voltage Electron Microscopy ◽  
Voltage Electron

Sodium iodate iv. damages the retinal pigment epithelium (RPE) in rabbits. Where RPE does not regenerate (e.g., 1,2) Muller glial cells (MC) forma subretinal scar that replaces RPE. The MC response was studied by HVEM in 3D computer reconstructions of serial thick sections, made using the STEREC0N program (3), and the HVEM at the NYS Dept. of Health in Albany, NY. Tissue was processed for HVEM or immunofluorescence localization of a monoclonal antibody recognizing MG microvilli (4).

scholarly journals 4-(Phenylsulfanyl) Butan-2-One Attenuates the Inflammatory Response Induced by Amyloid-β Oligomers in Retinal Pigment Epithelium Cells

Marine Drugs ◽  
2020 ◽  
Vol 19 (1) ◽  
pp. 1
Author(s):  
Peeraporn Varinthra ◽  
Shun-Ping Huang ◽  
Supin Chompoopong ◽  
Zhi-Hong Wen ◽  
Ingrid Y. Liu
Keyword(s):  
Retinal Pigment Epithelium ◽  
Inflammatory Response ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Amyloid Β ◽  
Age Related Macular Degeneration ◽  
Epithelial Cell Line ◽  
Age Related ◽  
Tnf Α ◽  
Cox 2

Age-related macular degeneration (AMD) is a progressive eye disease that causes irreversible impairment of central vision, and effective treatment is not yet available. Extracellular accumulation of amyloid-beta (Aβ) in drusen that lie under the retinal pigment epithelium (RPE) has been reported as one of the early signs of AMD and was found in more than 60% of Alzheimer’s disease (AD) patients. Extracellular deposition of Aβ can induce the expression of inflammatory cytokines such as IL-1β, TNF-α, COX-2, and iNOS in RPE cells. Thus, finding a compound that can effectively reduce the inflammatory response may help the treatment of AMD. In this research, we investigated the anti-inflammatory effect of the coral-derived compound 4-(phenylsulfanyl) butan-2-one (4-PSB-2) on Aβ1-42 oligomer (oAβ1-42) added to the human adult retinal pigment epithelial cell line (ARPE-19). Our results demonstrated that 4-PSB-2 can decrease the elevated expressions of TNF-α, COX-2, and iNOS via NF-κB signaling in ARPE-19 cells treated with oAβ1-42 without causing any cytotoxicity or notable side effects. This study suggests that 4-PSB-2 is a promising drug candidate for attenuation of AMD.

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