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Friedrich E Kruse, Johannes Menzel-Severing, Theofilos Tourtas, Martha Patricia Koeferl, Ursula Schlotzer-Schrehardt; Splitting of the host Descemet’s membrane in patients with Fuchs endothelial corneal dystrophy during DMEK. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):1559.
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© ARVO (1962-2015); The Authors (2016-present)
Specific alterations in structure and composition of the extracellular matrix in Descemet’s membrane (DM) of patients with Fuchs endothelial corneal dystrophy (FECD) have previously been described. Here, we report on ultrastructural abnormalities of DM in a subgroup of FECD patients which may be surgically relevant for Descemet’s membrane endothelial keratoplasty (DMEK).
In a prospective single-center nonrandomized consecutive case series of 120 patients with FECD scheduled for DMEK, the stripping feasibility of DM in the recipients’ eyes was recorded. Stripped DM explants were examined by transmission electron microscopy
17/120 (14%) of patients with FECD showed lamellar splitting of DM resulting in the dissociation of two separate layers, i.e. a posterior thicker lamella (10-20 µm in thickness) and an anterior delicate brittle lamella (4-8 µm in thickness) adhering to the corneal stroma. Transmission electron microscopy revealed the thicker layer to comprise an abnormal posterior banded layer of DM containing accumulations of wide-spaced collagen, and the thin layer to comprise a well-formed anterior banded layer of DM directly adjoining linear or patchy accumulations of wide-spaced collagen, which occasionally formed wart-like structures resembling guttae. A distinct posterior nonbanded layer of DM was absent in these cases.<br />
A subgroup of FECD patients showed abnormal collagenous material deposits in DM that appeared to have been laid down early in life, possibly indicating early-onset forms of FECD, which may form a breaking point during stripping and cause splitting of DM. These observations may be relevant for DMEK, requiring careful removal of all DM layers, and potentially also for future corneal endothelial cell replacement strategies in FECD patients.
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