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蒂格森浅层点状角膜炎的角膜表面变化:一项在人角膜上进行的临床及非接触式活体显微摄影研究。

Corneal surface changes in Thygeson's superficial punctate keratitis: a clinical and non-contact photomicrographic in vivo study in the human cornea.

作者信息

Tabery H M

机构信息

Department of Ophthalmology, Malmö University Hospital, Malmö, Sweden.

出版信息

Eur J Ophthalmol. 2004 Mar-Apr;14(2):85-93. doi: 10.1177/112067210401400201.

Abstract

PURPOSE

To elucidate mechanisms behind the morphology of Thygeson's superficial punctate keratitis (TSPK).

METHODS

Sixteen patients were examined with the slit lamp and photographed by non-contact photomicrography. The results were compared with morphology of epithelial keratitis in herpes simplex type 1 (HSV1), varicella zoster (VZV), and adenovirus type 8 (Ad8) infections, all previously studied by the same method, and with published histologic findings in TSPK.

RESULTS

In the photographs, the corneal epithelium showed various numbers of abnormal subsurface cells measuring about 10-15 microm in diameter, present individually, in small groups, or aggregated in larger lesions (coarse lesions with the slit lamp). The surface epithelium was well preserved, except in larger lesions, which showed surface debris. The morphology was unlike HSV1 and VZV epithelial keratitis, but strongly resembled epithelial changes occurring in Ad8 infections on day 5, and later, after the onset of symptoms.

CONCLUSIONS

TSPK shows a more widespread epithelial involvement than suspected with the slit lamp. Its morphology seems to reflect an action of a noxious agent targeted at the deeper epithelial layers, with the appearance of abnormal cells as a result. These might represent invading inflammatory cells, damaged intraepithelial ones, or both. The coarse lesions visualize areas of major involvement showing discernible signs of cell destruction. The similarity to Ad8 keratitis suggests that the source of the noxious agent might be located outside the cornea. The morphology, in conjunction with clinical features, is compatible with an immunologically mediated injury. The etiology remains unknown.

摘要

目的

阐明蒂格森表层点状角膜炎(TSPK)形态背后的机制。

方法

对16例患者进行裂隙灯检查并用非接触式显微摄影拍照。将结果与先前用相同方法研究的单纯疱疹病毒1型(HSV1)、水痘带状疱疹病毒(VZV)和8型腺病毒(Ad8)感染的上皮性角膜炎形态以及已发表的TSPK组织学结果进行比较。

结果

在照片中,角膜上皮显示出不同数量的异常基底细胞,直径约为10 - 15微米,单个存在、成小群存在或聚集在较大病变中(裂隙灯下为粗糙病变)。除了较大病变处有表面碎屑外,表面上皮保存良好。其形态与HSV1和VZV上皮性角膜炎不同,但与Ad8感染在症状出现后第5天及以后发生的上皮变化极为相似。

结论

TSPK显示出比裂隙灯检查所怀疑的更广泛的上皮受累。其形态似乎反映了一种针对深层上皮层的有害因子的作用,导致出现异常细胞。这些异常细胞可能代表侵入的炎性细胞、受损的上皮内细胞或两者皆有。粗糙病变显示出主要受累区域,有明显的细胞破坏迹象。与Ad8角膜炎的相似性表明有害因子的来源可能位于角膜外。结合临床特征,其形态与免疫介导的损伤相符。病因仍然不明。

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