Journal
RETINA-THE JOURNAL OF RETINAL AND VITREOUS DISEASES
Volume 32, Issue 4, Pages 647-651Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/IAE.0b013e31823fb847
Keywords
acquired vitelliform lesion; age-related macular degeneration; cuticular drusen; fundus autofluorescence; large drusen; spectral domain optical coherence tomography
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Funding
- LuEsther T. Mertz Retinal Research Center, Manhattan Eye, Ear, and Throat Hospital
- Macula Foundation, Inc.
- Topcon Inc.
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Purpose: The purpose of this study was to describe the association of acquired vitelliform lesion (AVL) and large drusen in patients with non-neovascular age-related macular degeneration. Methods: A retrospective review of clinical examination and multimodal imaging data of patients with AVL and large drusen seen over a 12-month period was performed. Acquired vitelliform lesion was defined as subretinal accretion of hyperautofluorescent yellowish material within the macular region not due to vitelliform macular dystrophy. Large drusen were diagnosed by the presence of mounded deposits in the subretinal pigment epithelial space between the retinal pigment epithelium and the Bruch membrane using multimodal imaging analysis (color photography, autofluorescence, and spectral domain optical coherence tomography). Results: Thirteen eyes of 9 white patients with a mean age of 74 years were observed to have AVL associated with large drusen. The median visual acuity was 20/60. All AVLs were hyperautofluorescent and were located in the subretinal space between the retinal pigment epithelium and the photoreceptor inner segment/outer segment junction. The AVL in this series had similar color, autofluorescence, and optical coherence tomographic findings as the AVL seen in association with cuticular drusen and subretinal drusenoid deposits. Conclusion: Acquired vitelliform lesions, which have previously been related to cuticular drusen and subretinal drusenoid deposits, can occur in association with large drusen. Abnormalities leading to drusen formation or processes that function in parallel to these may be causative in AVL formation. RETINA 32:647-651, 2012
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