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Hiroyuki Nakashizuka, Masako Mitsumata, Shigekuni Okisaka, Hiroyuki Shimada, Akiyuki Kawamura, Ryusaburo Mori, Mitsuko Yuzawa; Clinicopathologic Findings in Polypoidal Choroidal Vasculopathy. Invest. Ophthalmol. Vis. Sci. 2008;49(11):4729-4737. doi: 10.1167/iovs.08-2134.
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© ARVO (1962-2015); The Authors (2016-present)
purpose. To elucidate the pathogenic mechanism of polypoidal choroidal vasculopathy (PCV) based on histopathologic 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, α-smooth muscle actin (α-SMA) and hypoxia-inducible factor (HIF)-1α.
results. Hyalinization of choroidal vessels and 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 α-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-1α positive inflammatory cells were located in the stroma of specimens.
conclusions. Hyalinization of choroidal vessels, like arteriosclerosis, is characteristic of PCV.
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