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增生性玻璃体视网膜病变病理生理学的新见解:玻璃体劈裂诱导的玻璃体皮质残片的作用。

Novel insights into the pathophysiology of proliferative vitreoretinopathy: The role of vitreoschisis-induced vitreous cortex remnants.

机构信息

Department of Vitreoretinal Surgery, the Rotterdam Eye Hospital, Rotterdam, The Netherlands.

Department of Pathology, Section Ophthalmic Pathology, Erasmus University Medical Center Rotterdam, Rotterdam, The Netherlands.

出版信息

Acta Ophthalmol. 2022 Dec;100(8):e1749-e1759. doi: 10.1111/aos.15197. Epub 2022 Jun 8.

Abstract

PURPOSE

We previously hypothesized a causal relationship between vitreoschisis-induced vitreous cortex remnants (VCR) and the development of proliferative vitreoretinopathy (PVR). This study aims to substantiate this association through histopathological analysis of surgical specimens in support of strategies to improve therapeutic outcomes.

METHODS

A descriptive, prospective, non-consecutive case series. Histopathological and immunohistochemical analyses were performed on membranes removed from the peripheral retinal surface during initial vitrectomy for primary rhegmatogenous retinal detachment (RRD) (n = 11) or recurrent retinal detachment (n = 12). The clinical aspect of the membranes ranged from loose-meshed membranes visualized with triamcinolone to more fibrotic membranes stained with trypan blue.

RESULTS

Consistent with the clinical presentation, histopathological analysis revealed membranes with different area characteristics. Paucicellular lamellar collagen-rich areas, suggestive of VCR, appeared to transition to areas of increased cellularity and eventually more fibrotic areas of low cellularity. Five different area characteristics could be identified that seemed to correspond to five histopathological stages in PVR formation, with lamellar VCR collagen acting as an essential precondition: 1. Lamellar collagen, low cellularity (hyalocytes). 2. Lamellar collagen, increased cellularity (hyalocytes, glial cells). 3. Lamellar collagen, high cellularity (macrophages, glial cells, RPE-cells). 4. Early fibrosis, decreased cellularity (myofibroblasts). 5. Fibrosis, low cellularity (myofibroblasts).

CONCLUSION

These findings confirm the role of VCR in preretinal PVR formation posterior to the vitreous base. We propose that the presence of VCR over the retinal surface should be qualified as a risk factor for PVR formation. Detection and adequate removal of VCR may improve the success rate of vitreoretinal surgeries.

摘要

目的

我们之前假设玻璃体后脱离引起的玻璃体皮质残余物(VCR)与增生性玻璃体视网膜病变(PVR)的发展之间存在因果关系。本研究旨在通过对手术标本进行组织病理学分析来证实这种关联,以支持改善治疗效果的策略。

方法

描述性、前瞻性、非连续病例系列。对初次玻璃体切除术中从周边视网膜表面取出的膜进行组织病理学和免疫组织化学分析,这些膜是用于原发性孔源性视网膜脱离(RRD)(n=11)或复发性视网膜脱离(n=12)的。膜的临床外观从用曲安奈德观察到的稀疏网眼状膜到用台盼蓝染色的更纤维化的膜不等。

结果

与临床表现一致,组织病理学分析显示膜具有不同的区域特征。富含少细胞层状胶原的区域,提示 VCR,似乎向细胞增多的区域过渡,最终向细胞密度较低的更纤维化区域过渡。可以识别出 5 种不同的区域特征,它们似乎对应于 PVR 形成的 5 个组织病理学阶段,层状 VCR 胶原作为一个基本的前提:1. 层状胶原,低细胞密度(玻璃体细胞)。2. 层状胶原,细胞增多(玻璃体细胞、神经胶质细胞)。3. 层状胶原,细胞高度增生(巨噬细胞、神经胶质细胞、RPE 细胞)。4. 早期纤维化,细胞密度降低(肌成纤维细胞)。5. 纤维化,细胞密度低(肌成纤维细胞)。

结论

这些发现证实了 VCR 在玻璃体基底部后视网膜前 PVR 形成中的作用。我们提出,视网膜表面存在 VCR 应被视为 PVR 形成的危险因素。检测和适当去除 VCR 可能会提高玻璃体视网膜手术的成功率。

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