Focal Inner Retinal Hemorrhages in Patients with Drusen

Gass, Jörn‐Markus; Agarwal, Anita; Lavina, Adrian; Tawansy, K.A.

doi:10.1097/00006982-200312000-00001

Cited by 166 publications

(34 citation statements)

References 8 publications

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“…Finally, choroidal neovascularization occurs and forms retinal-choroidal anastomoses. In contrast, Gass et al [33] suggested that focal atrophy of the RPE and type 1 occult choroidal neovascularization under the RPE are the initial lesions of RAP. These lesions permit the retinal neovasculature to infiltrate into the outer retina and form chorioretinal anastomoses with the original type 1 occult choroidal vessel.…”

Section: Discussionmentioning

confidence: 94%

Characterization of a Spontaneous Retinal Neovascular Mouse Model

et al. 2014

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BackgroundVision loss due to vascular disease of the retina is a leading cause of blindness in the world. Retinal angiomatous proliferation (RAP) is a subgroup of neovascular age-related macular degeneration (AMD), whereby abnormal blood vessels develop in the retina leading to debilitating vision loss and eventual blindness. The novel mouse strain, neoretinal vascularization 2 (NRV2), shows spontaneous fundus changes associated with abnormal neovascularization. The purpose of this study is to characterize the induction of pathologic angiogenesis in this mouse model.MethodsThe NRV2 mice were examined from postnatal day 12 (p12) to 3 months. The phenotypic changes within the retina were evaluated by fundus photography, fluorescein angiography, optical coherence tomography, and immunohistochemical and electron microscopic analysis. The pathological neovascularization was imaged by confocal microscopy and reconstructed using three-dimensional image analysis software.ResultsWe found that NRV2 mice develop multifocal retinal depigmentation in the posterior fundus. Depigmented lesions developed vascular leakage observed by fluorescein angiography. The spontaneous angiogenesis arose from the retinal vascular plexus at postnatal day (p)15 and extended toward retinal pigment epithelium (RPE). By three months of age, histological analysis revealed encapsulation of the neovascular lesion by the RPE in the photoreceptor cell layer and subretinal space.ConclusionsThe NRV2 mouse strain develops early neovascular lesions within the retina, which grow downward towards the RPE beginning at p15. This retinal neovascularization model mimics early stages of human retinal angiomatous proliferation (RAP) and will likely be a useful in elucidating targeted therapeutics for patients with ocular neovascular disease.

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Section: Discussionmentioning

confidence: 94%

Characterization of a Spontaneous Retinal Neovascular Mouse Model

et al. 2014

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“…The clinical forms of exudative AMD were divided into the following six categories using fluorescein angiography, SD-OCT scans and indocyanine green angiography if required: occult, minimally classic, predominantly classic, classic and type 3 CNV and idiopathic polypoidal vasculopathy as previously described [10,11,12,13,14,15,16]. The clinical forms were classified by two senior retina specialists (M.B.…”

Section: Methodsmentioning

confidence: 99%

Intravitreal Ranibizumab in Daily Clinical Practice for Age-Related Macular Degeneration: Treatment of Exudative Age-Related Macular Degeneration in Real Life

Cazet-Supervielle

Gozlan²,

Cabasson³

et al. 2015

Ophthalmologica

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Purpose: To describe the anatomical and functional outcomes in patients with exudative age-related macular degeneration (AMD) undergoing ranibizumab therapy in real-life practice. Methods: This is a retrospective analysis of patients with exudative AMD treated with ranibizumab. Visual acuity (VA) and optic coherence tomography characteristics at baseline and at the end of the follow-up, clinical forms of the disease, delay between diagnosis and treatment as well as the number of follow-up visits and of intravitreal injections were collected. Results: One hundred and seventy-nine patients (220 eyes) were followed up during a mean of 24 months. The mean delay between diagnosis and treatment was 20.3 days (SD ±16.8). VA stabilization was observed in 46.4% of eyes, 21.7% of eyes gained ≥15 ETDRS (Early Treatment Diabetic Retinopathy Study) letters and 31.9% lost ≥15 ETDRS letters. The mean central retinal thickness decreased from 380.6 μm at baseline to 295.6 µm at the final examination. A lower baseline VA score was associated with a greater gain of letters (OR 1.04, 95% CI 1.02-1.06; p < 0.001). Conclusion: Shortening the delays in diagnosis appears to be a key point in real-life situations.

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“…It has been shown, for example, that ganglion cell neurites grow into human epiretinal membranes in association with glial cells [269,270]. There are also cases of intraretinal neovascularization which are permitted or induced by Müller cells: in patients with retinal angiomatous proliferation, a subform of exudative age-related macular degeneration, neovascularization starts in the outer plexiform layer, progresses to the subretinal space, and then anastomoses with choroidal vessels [271][272][273]. Multiple factors have been described to be involved in the formation and progression of epiretinal membranes which mediate their effects via autocrine and paracrine loops of different signaling molecules.…”

Section: Inhibitory Effects Of Müller Cellsmentioning

confidence: 99%