To describe histopathologic features of an eye with retinal angiomatous proliferation (RAP) secondary to age-related macular degeneration treated with serial ranibizumab injections and to correlate these findings with spectral domain optical coherence tomography.
Histopathologic features from serial sections through the globe of a 93-year-old man with age-related macular degeneration were studied and compared with spectral domain optical coherence tomography images obtained 7 weeks before his death.
The pathologic correlate of ranibizumab-treated RAP was a circumscribed, branching paucicellular vascular complex extending from the inner plexiform layer to Bruch membrane. The histopathologic findings corresponded to an area of hyperreflectivity on spectral domain optical coherence tomography imaging, substantiating the reported tomographic appearance of RAP lesions. A frank anastomosis with choroidal or retinal vasculature was not seen in this treated RAP lesion. There was a lack of retinal pigment epithelium underlying the lesion in an area of retinal pigment epithelium detachment. The elastic portion of Bruch membrane appeared intact. Treatment with ranibizumab over an extended period of time may have been associated with a loss of cellularity of the RAP lesion.
In a patient with ARMD extensively treated with ranibizumab, color fundus photography, fluorescein angiography and SD-OCT images of RAP correlated histopathologically with a paucicellular intraretinal vascular complex.
The histopathologic features of an eye with retinal angiomatous proliferation treated with serial ranibizumab injections were correlated with the findings on spectral domain optical coherence tomography. The histopathologic findings corresponded to an area of hyperreflectivity on spectral domain optical coherence tomography imaging, substantiating the reported tomographic appearance of retinal angiomatous proliferation lesions.
Department of Ophthalmology, Casey Eye Institute, Oregon Health and Science University, Portland, Oregon.
Reprint requests: Alison H. Skalet, MD, PhD, 3375 S.W. Terwilliger Boulevard, Portland, OR 97239-4197; e-mail: firstname.lastname@example.org
Supported by a Lloyd Research Endowment Faculty Grant (A. H. Skalet); Core Grant P30 EY010572 from the National Institutes of Health (Bethesda, MD) and by an unrestricted departmental grant from Research to Prevent Blindness (New York, NY).
Presented at the American Association of Ophthalmic Oncology and Pathology Annual Meeting, Orlando, FL, October 21, 2011.
None of the authors has any conflicting interests to disclose.
Study Design: A. H. Skalet, M. L. Klein, AJL, and D. J. Wilson; Data Analysis: A. H. Skalet, A. K. Miller, M. L. Klein, A.K. Lauer, and D. J. Wilson; Manuscript: A. H. Skalet, A. K. Miller, M. L. Klein, A.K. Lauer, and D. J. Wilson.