Choroidal Thickness in Geographic Atrophy Secondary to Age-Related Macular Degeneration

2015 ◽  
Vol 56 (2) ◽  
pp. 875-882 ◽  
Author(s):  
M. Lindner ◽  
A. Bezatis ◽  
J. Czauderna ◽  
E. Becker ◽  
C. K. Brinkmann ◽  
...  
Keyword(s):  
Macular Degeneration ◽  
Choroidal Thickness ◽  
Geographic Atrophy ◽  
Age Related Macular Degeneration ◽  
Age Related

Choroidal Thickness in Eyes With Central Geographic Atrophy Secondary to Stargardt Disease and Age-Related Macular Degeneration

2015 ◽  
Vol 46 (8) ◽  
pp. 814-822 ◽  
Author(s):  
Renata Portella Nunes ◽  
Potyra R. Rosa ◽  
Andrea Giani ◽  
Raquel Goldhardt ◽  
Benjamin Thomas ◽  
...  
Keyword(s):  
Macular Degeneration ◽  
Choroidal Thickness ◽  
Geographic Atrophy ◽  
Age Related Macular Degeneration ◽  
Stargardt Disease ◽  
Age Related

Association Between Subfoveal Choroidal Thickness, Reticular Pseudodrusen, and Geographic Atrophy in Age-Related Macular Degeneration

2015 ◽  
Vol 46 (5) ◽  
pp. 513-521 ◽  
Author(s):  
Mariana R. Thorell ◽  
Raquel Goldhardt ◽  
Renata Portella Nunes ◽  
Carlos Alexandre de Amorim Garcia Filho ◽  
Ashkan M. Abbey ◽  
...  
Keyword(s):  
Macular Degeneration ◽  
Choroidal Thickness ◽  
Geographic Atrophy ◽  
Age Related Macular Degeneration ◽  
Subfoveal Choroidal Thickness ◽  
Reticular Pseudodrusen ◽  
Age Related

scholarly journals A Review of Completed and Ongoing Complement Inhibitor Trials for Geographic Atrophy Secondary to Age-Related Macular Degeneration

2021 ◽  
Vol 10 (12) ◽  
pp. 2580
Author(s):  
Omar A. Halawa ◽  
Jonathan B. Lin ◽  
Joan W. Miller ◽  
Demetrios G. Vavvas
Keyword(s):  
Macular Degeneration ◽  
Geographic Atrophy ◽  
Age Related Macular Degeneration ◽  
Western World ◽  
Complement Factor ◽  
Complement Protein ◽  
Pivotal Phase ◽  
Complement Inhibition ◽  
Exudative Amd ◽  
Age Related

Age-related macular degeneration (AMD) is a leading cause of irreversible blindness among older adults in the Western world. While therapies exist for patients with exudative AMD, there are currently no approved therapies for non-exudative AMD and its advanced form of geographic atrophy (GA). The discovery of genetic variants in complement protein loci with increased susceptibility to AMD has led to the investigation of the role of complement inhibition in AMD with a focus on GA. Here, we review completed and ongoing clinical trials evaluating the safety and efficacy of these studies. Overall, complement inhibition in GA has yielded mixed results. The inhibition of complement factor D has failed pivotal phase 3 trials. Studies of C3 and C5 inhibition meeting their primary endpoint are limited by high rates of discontinuation and withdrawal in the treatment arm and higher risks of conversion to exudative AMD. Studies evaluating other complement members (CFB, CFH, CFI and inhibitors of membrane attack complex—CD59) are ongoing and could offer other viable strategies.

scholarly journals Outer retinal tubulation formation and clinical course of advanced age-related macular degeneration

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Alessandro Arrigo ◽  
Emanuela Aragona ◽  
Ottavia Battaglia ◽  
Andrea Saladino ◽  
Alessia Amato ◽  
...  
Keyword(s):  
Macular Degeneration ◽  
Müller Cells ◽  
Geographic Atrophy ◽  
Age Related Macular Degeneration ◽  
Advanced Age ◽  
Age Related ◽  
Dry Amd ◽  
Foveal Sparing ◽  
Wet Amd

AbstractOuter retinal tubulations (ORT) are a relatively new finding characterizing outer retinal atrophy. The main aim of the present study was to describe ORT development in advanced age-related macular degeneration (AMD) and to assess its relationship with disease’s severity. Patients with advanced AMD characterized either by macular neovascularization or geographic atrophy, showing signs of outer retinal disruption or retinal pigment epithelium atrophy on structural optical coherence tomography (OCT) at the inclusion examination were prospectively recruited. All the patients underwent complete ophthalmologic evaluation, structural OCT scans and fundus autofluorescence imaging. The planned follow-up was of 3-years. Main outcome measures were ORT prevalence, mechanism of ORT formation, mean time needed for complete ORT formation, best-corrected visual acuity (BCVA), definitely decreased autofluorescence (DDAF) area, questionably decreased autofluorescence (QDAF) area, retinal layer thickness, foveal sparing, number of intravitreal injections. We also assessed the possible role of external limiting membrane (ELM) and Müller cells in ORT pathogenesis. Seventy eyes (70 patients) were included; 43 showed dry AMD evolving to geographic atrophy, while 27 displayed the features of wet AMD. Baseline BCVA was 0.5 ± 0.5 LogMAR, decreasing to 0.9 ± 0.5 LogMAR at the 3-year follow-up (p < 0.01). We detected completely formed ORT in 26/70 eyes (37%), subdivided as follows: 20 eyes (77%) wet AMD and 6 eyes (23%) dry AMD (p < 0.01). ORT took 18 ± 8 months (range 3–35 months) to develop fully. We described the steps leading to ORT development, characterized by progressive involvement of, and damage to the photoreceptors, the ELM and the RPE. Eyes displaying ORT were associated with a smaller QDAF area, less retinal layers damage and lower rate of foveal sparing than eyes free of ORT (p < 0.01). We also described pigment accumulations simulating ORT, which were detected in 16/70 eyes (23%), associated with a greater loss of foveal sparing, increased DDAF area and smaller QDAF area at the 3-year follow-up (p < 0.01). In conclusion, this study provided a description of the steps leading to ORT development in AMD. ELM and Müller cells showed a role in ORT pathogenesis. Furthermore, we described a subtype of pigment hypertrophy mimicking ORT, evaluating its clinical utility.

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