Purchase this article with an account.
M. Awai, R. Futa, T. Hamanaka, T. Miyagawa, H. Tanihara; Ultrastructural Studies on Trabecular Meshwork and Iris Specimen of Chandler Syndrome . Invest. Ophthalmol. Vis. Sci. 2003;44(13):4342.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Purpose: To investigate ultrastructural evaluation of abnormalities in the aqueous outflow route and to speculate mechanisms associated with intraocular pressure (IOP) elevation in patients with Chandler syndrome. Methods: Included in this study were three patients who underwent trabeculectomy because of uncontrolled IOP elevation caused by Chandler syndrome. In all three patients, corneal edema and high IOP were observed although no iris atrophy was found at the first visit to our department. Clinical data such as IOP levels, gonioscopic and slit lamp findings, visual field defects and optic nerve structure were collected from patients’ medical records. In one of the three cases, surgically-obtained specimen of trabecular meshwork and iris root tissues were subjected to morphological analysis with the use of electron microscopy. In this case, corneal endothelial abnormalities such as endothelial cell loss and corneal edema were observed while gonioscopic findings showed open angle structure and no peripheral anterior synechiae. Glaucomatous optic nerve changes and associated visual field defect was detected. Results: Light microscopic findings demonstrated open Schlemm’s canal structure and normal appearance of the trabecular meshwork. On the other hand, they showed increase in cellular components including inflammatory cells within trabecular spaces in the specimen and formation of the membrane on the meshwork. Electron microscopic findings revealed the presence of a monolayer composed of corneal endothelium-like cells and thick basement membrane–like material. Also, neovasularization was observed in the corneoscleral trabeculum. Conclusions: Our results showed that several mechanisms; (1) formation of basement membrane-like tissue, (2) infiltration of inflammatory cells and (3) neovascularization, may contribute to the elevations in IOP in patients with Chandler syndrome even when no history of conspicuous inflammatory reaction in the anterior ocular segments was clinically confirmed.
This PDF is available to Subscribers Only