All Posts tagged ARMD

Age-Related Macular Degeneration (AMD) is one of the leading causes of visual impairment in individuals over the age of 55 years in developed countries.¹ The neovascular form of AMD, with vascular endothelial growth factor (VEGF) as one of the key factors, causes severe and irreversible vision loss, frequently resulting in legal blindness.^2,3 In recent years, VEGF inhibition by anti-VEGF antibodies has significantly improved visual outcomes in patients with neovascular AMD. However, in many patients with neovascular AMD anti-VEGF needs to be continuously administered over many years to persistently suppress disease activity and maintain visual function.

The need for long-term treatment with anti-VEGF agents has also become evident in the extension studies, where long-term outcomes 7-8 years after initiation of intensive ranibizumab therapy suggest that many patients require long-term treatment with anti-VEGF agents.⁴ However, despite the beneficial effect of anti-VEGF therapy, long-term side effects are not clarified yet and are a matter of ongoing controversy. There is evidence that repeated long-term anti-VEGF treatment may accelerate atrophy of different ocular tissues. Retinal pigment epithelium atrophy,⁵ as well as scleral thinning, has been reported.⁶ In the last years, several studies have investigated the effect of intravitreal anti-VEGF injections on the peripapillary retinal nerve fiber layer (RNFL). There exists some controversy regarding the effect of anti-VEGF agents on retinal ganglion cells (RGCs). In mice, some reports suggest severe damage to RGCs after local treatment with VEGF binding agents,⁷ while another report did not find any changes within the retinal ganglion cell layer (RGCL) after VEGF receptor blockade in mice.⁸ Because most studies have analyzed peripapillary optical coherence tomography (OCT) scans, these reports have focused on RNFL change after antiVEGF treatment. However, several studies focusing on glaucoma patients have shown that RGCL thickness changes may be a more sensitive marker for global and regional visual field sensitivities.^9,10

In the present study, we investigated RNFL and RGCL changes in the macular area in eyes receiving long-term intravitreal anti-VEGF treatment for neovascular AMD using spectral-domain optical coherence tomography (Spectralis SDOCT; Heidelberg Engineering, Heidelberg, Germany) and automated segmentation of macular scans.

Full Paper: Retinal Ganglion Cell Layer Change in Patients Treated With Anti–Vascular Endothelial Growth Factor for Neovascular Age-related Macular Degeneration
(1.1M PDF)

Age-related Macular Degeneration (AMD) and cataract are common causes of vision loss in our aging population. Recent advances in the treatment of wet AMD have succeeded to either stabilize or improve vision in a large proportion of cases.^1–4 It is therefore not uncommon for wet AMD patients to develop visually significant cataracts. However, there is concern about proceeding with cataract surgery in patients with wet AMD, as there may be a risk of exacerbating choroidal neovascularization (CNV) or progressing geographic atrophy.

There is little evidence in the current literature to aid the decision to proceed with cataract surgery in patients undergoing active treatment for wet AMD. Concern exists that intraocular pressure fluctuations and increased inflammatory mediators associated with uncomplicated cataract surgery may disrupt or further stimulate delicate neovascular vessels. Adverse events related to worsening wet AMD may lead to poorer visual outcome or increased AMD treatment demands, requiring further cost and clinic visits for the patient.

Our study aims to evaluate the visual outcomes and possible complications of cataract surgery in patients with wet AMD. This is the first study to include a control arm and an examination of specific optical coherence tomography (OCT) features.

Full Paper: The Effects of Cataract Surgery on Patients With Wet Macular Degeneration
(464K PDF)

Age-related macular degeneration (AMD) is a complex disorder triggered by a wide range of environmental and genetic risk factors.^1-3 Numerous common variants are known markers of AMD including several complement pathway genes: complement factor H (CFH),^4-8 complement factor I,⁹ complement component 2, complement factor B,^7,10 and complement 3.¹¹

We previously reported the association of a rare CFH variant with AMD, R1210C, which is the strongest genetic risk factor to date, with an odds ratio (OR) of 20.^12,13 The R1210C variant is also known to be associated with inherited forms of atypical hemolytic uremic syndrome and primary glomerulonephritis.^14-21 In addition to linking 2 clinically unrelated conditions, such as AMD and atypical hemolytic uremic syndrome,the R1210C finding suggests that compromised function of the factorH protein is involved in AMD pathogenesis as a causal factor and not merely as an associated factor.¹²

In that initial report, the R1210C rare variant was associated with an earlier age at diagnosis of advanced AMD.¹² This variant is also significantly associated with progression from early or intermediate AMD to advanced stages in a multigene prediction model.^22,23 However, the fundus phenotype typically related to the variant is still to be determined. This knowledge is needed to better understand the manifestations of this rare CFH mutation and to help detect and characterize this phenotype in clinical practice. Identification of such high-risk individuals will be important for screening, potential new therapeutic strategies, and personalized medicine. Therefore, the objective of this study, conducted from 2012 to 2014, was to determine specific fundus features of a white population carrying the CFH R1210C rare variant.

Full Paper: Phenotypic Characterization of Complement Factor H R1210C Rare Genetic Variant in Age-Related Macular Degeneration
(461K PDF)