December 2002
Volume 43, Issue 13
ARVO Annual Meeting Abstract  |   December 2002
Clinicopathologic Correlation of Progressive Atypical Fibrovascular Proliferation in Age-related Macular Degeneration (AMD)
Author Affiliations & Notes
  • GA Byrnes
    Ophthalmology US Navy Bethesda MD
  • J Baffi
    National Eye Institute Bethesda MD
  • C-C Chan
    National Eye Institute Bethesda MD
  • KG Csaky
    National Eye Institute Bethesda MD
  • Footnotes
    Commercial Relationships   G.A. Byrnes, None; J. Baffi, None; C. Chan, None; K.G. Csaky, None.
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 2788. doi:
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      GA Byrnes, J Baffi, C-C Chan, KG Csaky; Clinicopathologic Correlation of Progressive Atypical Fibrovascular Proliferation in Age-related Macular Degeneration (AMD) . Invest. Ophthalmol. Vis. Sci. 2002;43(13):2788.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: To compare the clinical / angiographic findings with histopathologic, immunohistochemical and cytokine profiling in a surgically excised lesion from a patient with atypical fibrovascular changes and AMD. Methods: Subretinal surgery was performed to excise an atypical subretinal fibrovascular complex. The lesion was comprehensively analyzed using routine histopathology, immunohistochemistry for inflammatory cells (CD3 T-lymphocyte and CD68 macrophages), hematopoetic vascular stem cells and endothelial cells (CD34, AC133, CD31 and von-Willebrand factor- vWF), apoptotic molecules (CD95-Fas and CD178- FasL), and growth factors (platelet-derive growth factor B – PDGF - B and vascular endothelial growth factor - VEGF). The subretinal fluid was additionally assayed for VEGF and monocyte chemotactic protein – 1 (MCP-1) by ELISA. Results: A male patient with age-related macular degenration developed an atypical subretinal fibrovascular lesion characterized by increasing fibrous tissue clinically with areas of pinpoint leakage angiographically. There was a rapid expansion of the process with vision deterioration over a 6 month period and the lesion was excised through a standard pars plana approach. Microscopic analysis of the neovascular complex demonstrated a well-demarcated lesion with extensive minimally cellular fibrous tissue internal to Bruch's membrane. Many small vascular channels were evident adjacent to the retinal pigmented epithelium (RPE) both within the fibrous tissue and the choroid. Bruch's membrane was relatively intact. The RPE layer was attenuated with focal disruption. The choroid was markedly hypercellular and infiltrated by both T lymphocytes and macrophages with cells strongly positive for CD 3, CD 31, CD 34, CD 68, CD 95, and CD 178. Many of the inflammatory cells stained for both Fas and FasL. Staining for AC133 cells was equivocal. Within the subretinal lesion, multiple isolated cells were CD34 positive but vWF negative. VEGF and MCP-1 in the subretinal fluid were below the detectable levels by ELISA. Staining for VEGF was negative but positive for PDGF – B. Conclusion: The surgically excised choroidal neovascular complex demonstrated distinctive features that included prominent hypercellularity of the choroid which was comprised of both inflammatory and endothelial cells and a predominance of PDGF-B. These findings support the inflammatory paradigm of CNVM in AMD and suggest that PDGF – B may be involved in the fibrotic response.

Keywords: 308 age-related macular degeneration • 346 choroid: neovascularization • 434 immunohistochemistry 

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