Clinicopathological findings of polypoidal choroidal vasculopathy
Hiroyuki Nakashizuka 1*,
Masako Mitsumata 2,
Shigekuni Okisaka 3,
Hiroyuki Shimada 1,
Akiyuki Kawamura 1,
Ryusaburo Mori 4,
and
Mitsuko Yuzawa 4
1 Division of Ophthalmology, Department of Visual Science, Nihon University School of Medicine, Tokyo, Japan
2 Division of Pathology and Microbiology, Nihon University School of Medicine, Tokyo, Tokyo, Japan
3 Laboratory of Ophthalmic Pathology Education, Tokyo, Tokyo, Japan
4 Division of Ophthalmology, Department of Visual Science, Nihon University, Chiyodaku, Japan
* To whom correspondence should be addressed. E-mail: shizuk{at}med.nihon-u.ac.jp.
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Abstract |
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Purpose. To elucidate the pathogenic mechanism of polypoidal choroidal vasculopathy (PCV) based on histopathological findings.
Methods. Specimens obtained by surgical excision of PCV from five eyes of five patients (mean age, 75.6± 3.1 years) were studied histopathologically. Immunohistochemical studies were also performed to identify CD34, vascular endothelial growth factor (VEGF), CD68, alpha smooth muscle actin (alpha-SMA) and hypoxia-inducible factors (HIF-1alpha).
Results. Hyalinization of choroidal vessels, massive exudation of fibrin and blood plasma were observed in all the specimens of PCV lesions. Some blood vessels were located above the RPE in two of the five eyes. Immunohistochemically, CD68 positive cells were detected around the hyalinized vessels. There were no alpha-SMA positive cells in the vessels of PCV. CD34 staining showed endothelial discontinuity. Vascular endothelial cells within the PCV specimens were negative for VEGF. HIF-1 alpha positive inflammatory cells were located in the stroma of specimens.
Conclusion. Hyalinization of choroidal vessels, like arteriosclerosis, is characteristic of PCV.
Key Words:
age-related macular degeneration, neovascularization, pericyte, macrophages
