作者: Berthold Seitz , Tobias Hager
DOI: 10.1007/978-3-319-43021-8_3
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摘要: The hallmark of Fuchs endothelial corneal dystrophy (FECD) is “guttae”. However, some eyes with cornea guttata will never progress to FECD! Thus, we should talk about FECD not before decompensation = “swelling” “increased central thickness” does occur. Early-onset well-defined genetic cause must be differentiated from late-onset FECD. Differential diagnosis other dystrophies typically an easy task. pseudoexfoliation (PEX) keratopathy respect incidence secondary glaucoma, therapeutic necessities, and prognosis transplantation. Concerning microsurgery, a friend, while PEX challenge. differentiation just academic problem! Progression cannot defined via cell counts, because numbers are notoriously measured wrong. Neither manual nor automated count give valid results in case unevenly distributed guttae. best-corrected visual acuity (worse morning vs afternoon), glare, thickness profile (tomography), morphology. For many decades, symptomatic medical therapy consisted unpreserved hyperosmolar (5 %) sodium chloride solution. Preclinical causative approaches include lithium, N-acetylcysteine, the ROCK inhibitor.