息肉状脉络膜血管病变的临床病理表现

Clinicopathologic findings in polypoidal choroidal vasculopathy.

作者信息

Nakashizuka Hiroyuki, Mitsumata Masako, Okisaka Shigekuni, Shimada Hiroyuki, Kawamura Akiyuki, Mori Ryusaburo, Yuzawa Mitsuko

机构信息

Department of Visual Science, Division of Ophthalmology, Nihon University School of Medicine, Tokyo, Japan.

出版信息

Invest Ophthalmol Vis Sci. 2008 Nov;49(11):4729-37. doi: 10.1167/iovs.08-2134. Epub 2008 Jun 27.

DOI:10.1167/iovs.08-2134

PMID:18586873

Abstract

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, alpha-smooth muscle actin (alpha-SMA) and hypoxia-inducible factor (HIF)-1alpha.

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 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-1alpha positive inflammatory cells were located in the stroma of specimens.

CONCLUSIONS

Hyalinization of choroidal vessels, like arteriosclerosis, is characteristic of PCV.

摘要

目的

基于组织病理学发现阐明息肉状脉络膜血管病变（PCV）的发病机制。

方法

对5例患者（平均年龄75.6±3.1岁）的5只眼睛手术切除的PCV标本进行组织病理学研究。还进行了免疫组织化学研究以鉴定CD34、血管内皮生长因子（VEGF）、CD68、α平滑肌肌动蛋白（α-SMA）和缺氧诱导因子（HIF）-1α。

结果

在所有PCV病变标本中均观察到脉络膜血管玻璃样变性以及纤维蛋白和血浆的大量渗出。5只眼中有2只眼的一些血管位于视网膜色素上皮（RPE）上方。免疫组织化学显示，在玻璃样变性血管周围检测到CD68阳性细胞。PCV血管中无α-SMA阳性细胞。CD34染色显示内皮细胞连续性中断。PCV标本中的血管内皮细胞VEGF呈阴性。HIF-1α阳性炎性细胞位于标本的基质中。