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波士顿1型人工角膜中角膜后假体膜的特征描述

Characterization of retrokeratoprosthetic membranes in the Boston type 1 keratoprosthesis.

作者信息

Stacy Rebecca C, Jakobiec Frederick A, Michaud Norman A, Dohlman Claes H, Colby Kathryn A

机构信息

David G. Cogan Laboratory of Ophthalmic Pathology, Massachusetts Eye and Ear Infirmary, and Harvard Medical School, Boston, MA 02114, USA.

出版信息

Arch Ophthalmol. 2011 Mar;129(3):310-6. doi: 10.1001/archophthalmol.2011.26.

DOI:10.1001/archophthalmol.2011.26
PMID:21402987
Abstract

OBJECTIVE

To evaluate retroprosthetic membranes that can occur in 25% to 65% of patients with the Boston type 1 keratoprosthesis (KPro).

METHODS

Two patients with Peter anomaly and 2 with neurotrophic scarred corneas underwent revisions of their type 1 KPros because of visually compromising retroprosthetic membranes. The excised membranes were studied by light microscopy with hematoxylin-eosin, periodic acid-Schiff, and toluidine blue stains. Immunohistochemical and transmission electron microscopic examination were also used.

RESULTS

Light microscopic examination revealed that the retro-KPro fibrous membranes originated from the host's corneal stroma. These mildly to moderately vascularized membranes grew through gaps in the Descemet membrane to reach behind the KPro back plate and adhere to the anterior iris surface, which had undergone partial lysis. In 2 cases, the fibrous membranes merged at the pupil with matrical portions of metaplastic lens epithelium, forming a bilayered structure that crossed the optical axis. Retro-KPro membranes stained positively for α-smooth muscle actin but negatively for pancytokeratin. Electron microscopy confirmed the presence of actin filaments within myofibroblasts and small surviving clusters of metaplastic lens epithelial cells.

CONCLUSIONS

Stromal downgrowth, rather than epithelial downgrowth, was the major element of the retro-KPro membranes in this series. Metaplastic lens epithelium also contributed to opacification of the visual axis. Florid membranous inflammation was not a prominent finding and thus probably not a requisite stimulus for membrane development. Further advances in prosthetic design and newer antifibroproliferative agents may reduce membrane formation.

摘要

目的

评估波士顿1型人工角膜(KPro)患者中25%至65%可能出现的人工角膜后膜。

方法

两名彼得异常患者和两名神经营养性瘢痕角膜患者因人工角膜后膜影响视力而对其1型KPro进行翻修。对切除的膜进行苏木精-伊红、过碘酸-希夫和甲苯胺蓝染色的光镜研究。还采用了免疫组织化学和透射电子显微镜检查。

结果

光镜检查显示,人工角膜后纤维膜起源于宿主角膜基质。这些轻度至中度血管化的膜通过后弹力层的间隙生长,到达KPro背板后方并附着于部分溶解的虹膜前表面。在2例中,纤维膜在瞳孔处与化生晶状体上皮的基质部分融合,形成跨越光轴的双层结构。人工角膜后膜α-平滑肌肌动蛋白染色阳性,全细胞角蛋白染色阴性。电子显微镜证实肌成纤维细胞内存在肌动蛋白丝以及化生晶状体上皮细胞的小存活簇。

结论

在本系列中,基质内生而非上皮内生是人工角膜后膜的主要成分。化生晶状体上皮也导致视轴混浊。明显的膜性炎症不是一个突出的发现,因此可能不是膜形成的必要刺激因素。假体设计的进一步改进和更新的抗纤维增殖剂可能会减少膜的形成。

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