Fluorescence Lifetime Patterns of Retinal Pigment Epithelium Atrophy in Patients with Stargardt Disease and Age-Related Macular Degeneration

2019 ◽  
Vol 243 (3) ◽  
pp. 195-206
Author(s):  
Yasmin Solberg ◽  
Chantal Dysli ◽  
Pascal Escher ◽  
Lisa Berger ◽  
Sebastian Wolf ◽  
...  
2021 ◽  
Author(s):  
Martin Hammer ◽  
Juliane Jakob-Girbig ◽  
Linda Schwanengel ◽  
Christine A. Curcio ◽  
Somar Hasan ◽  
...  

AbstractPurposeTo observe changes of the retinal pigment epithelium (RPE) on the transition from dysmorphia to atrophy in age related macular degeneration (AMD) by fluorescence lifetime imaging ophthalmoscopy (FLIO).MethodsMultimodal imaging including color fundus photography (CFP), optical coherence tomography (OCT), fundus autofluorescence (FAF) imaging, and FLIO was performed in 40 eyes of 37 patients with intermediate AMD and no evidence for geographic atrophy or macular neovascularization) (mean age: 74.2±7.0 years). Twenty-three eyes were followed for 28.3±18.3 months. Seven eyes had a second follow up after 46.6±9.0 months. Thickened RPE on OCT, hyperpigmentation on CFP, and migrated RPE, seen as hyperreflective foci (HRF) on OCT, were identified. Fluorescence lifetimes in two spectral channels (SSC: 500-560 nm, LSC: 560-720 nm) as well as emission spectrum intensity ratio (ESIR) of the lesions were measured by FLIO.ResultsAs hyperpigmented areas form and RPE migrates into the retina, FAF lifetimes lengthen and ESRI of RPE cells increase. Thickened RPE showed lifetimes of 256±49 ps (SSC) and 336±35 ps (LSC) and an ESIR of 0.552±0.079. For hyperpigmentation, these values were 317±68 ps (p<0.001), 377±56 ps (p<0.001), and 0.609±0.081 (p=0.001), respectively, and for HRF 337±79 ps (p<0.001), 414±50 ps (p<0.001), and 0.654±0.075 (p<0.001).ConclusionsIn the process of RPE degeneration, comprising different steps of dysmorphia, hyperpigmentation, and migration, lengthening of FAF lifetimes and a hypsochromic shift of emission spectra can be observed by FLIO. Thus, FLIO might provide early biomarkers for AMD progression and contribute to our understanding of RPE pathology.


2017 ◽  
Vol 17 (2) ◽  
pp. 9-13
Author(s):  
Lita Jekabsone ◽  
Anete Kursite ◽  
Oskars Gertners ◽  
Guna Laganovska

Abstract Introduction.Age-related macular degeneration is the leading cause of visual impairment in developed world. The reason for using intravitreal injections of anti-vascular endothelial growth factor (VEGF) is to prevent choroidal neovascularization which is the main pathogenic mechanism for exudative age-related macular degeneration. Although injections may improve visual acuity, there are evidence showing association of anti-VEGF injections with progression of retinal pigment epithelium (RPE) atrophy. Aim of the Study.The purpose of this study was to investigate the intravitreal anti-vascular endothelial growth factor impact on retinal pigment epithelium atrophy development and progression. Material and methods.A single-centre retrospective study was conducted. Total 51 eyes of 39 patients with exudative age-related macular degeneration undergoing intravitreal anti-vascular endothelial growth factor therapy for 48 months. Heidelberg Spectralis Optical Coherence Tomography and fundus autofluorescence were used for evaluation of retinal pigment epithelium atrophy area and retinal thickness. Measurements were made manually. Best-corrected visual acuity (BCVA) measurements were taken from patient medical histories. For statistical analysis, IBM Statistical Package for the Social Sciences, version 23.0 was used. Results.The average age of patients was 81.6 ± 6.7 years. After first year of intravitreal anti-VEGF therapy, retinal pigment epithelium atrophy area enlarged from baseline (from 1.91 ± 2.3 mm2 to 2.74 ± 2.3mm2, p < 0.001). The mean number of intravitreal anti- VEGF injections received in 48 months was 15.47 ± 5.14. There was a statistically significant correlation between total number of intravitreal injections and RPE atrophy (R = 0.757, p < 0.001). After first year of anti-VEGF therapy best-corrected visual acuity (decimals) was statistically improved from baseline (0.32 ± 0.26 to 0.37 ± 0.24, p = 0.04). However, despite significant improvement at first year, the further treatment contributed BCVA reduction. Conclusions.Retinal pigment epithelium atrophy is a frequent finding in eyes with exudative age-related macular degeneration before and after anti-VEGF therapy. Our data show statistically significant association between total number of intravitreal anti-VEGF injections and retinal pigment epithelium atrophy area enlargement. Also there was statistically significant best-corrected visual acuity improvement after first year of anti-VEGF therapy.


2021 ◽  
Vol 22 (16) ◽  
pp. 8387
Author(s):  
Alexa Klettner ◽  
Johann Roider

(1) Background: Inflammation is a major pathomechanism in the development and progression of age-related macular degeneration (AMD). The retinal pigment epithelium (RPE) may contribute to retinal inflammation via activation of its Toll-like receptors (TLR). TLR are pattern recognition receptors that detect the pathogen- or danger-associated molecular pattern. The involvement of TLR activation in AMD is so far not understood. (2) Methods: We performed a systematic literature research, consulting the National Library of Medicine (PubMed). (3) Results: We identified 106 studies, of which 54 were included in this review. Based on these studies, the current status of TLR in AMD, the effects of TLR in RPE activation and of the interaction of TLR activated RPE with monocytic cells are given, and the potential of TLR activation in RPE as part of the AMD development is discussed. (4) Conclusion: The activation of TLR2, -3, and -4 induces a profound pro-inflammatory response in the RPE that may contribute to (long-term) inflammation by induction of pro-inflammatory cytokines, reducing RPE function and causing RPE cell degeneration, thereby potentially constantly providing new TLR ligands, which could perpetuate and, in the long run, exacerbate the inflammatory response, which may contribute to AMD development. Furthermore, the combined activation of RPE and microglia may exacerbate neurotoxic effects.


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