A morphologic study of Fuchs dystrophy and bullous keratopathy.

نویسندگان

  • Hunter K L Yuen
  • Charles E Rassier
  • Maria Stephanie R Jardeleza
  • W Richard Green
  • Zenaida de la Cruz
  • Walter J Stark
  • John D Gottsch
چکیده

PURPOSE To describe the morphologic features of Fuchs corneal dystrophy and compare them with those of bullous keratopathy. METHODS This was an observational case series. The study group consisted of 32 corneal buttons with a diagnosis of Fuchs dystrophy and the comparison group consisted of 22 corneal buttons with bullous keratopathy. Morphologic analysis was performed of corneal buttons from patients with the clinical diagnosis of Fuchs dystrophy or bullous keratopathy by light and electron microscopy. RESULTS The main outcome measure was identification of degenerated keratocytes, granular material in and around keratocytes, and lipid keratopathy. The overall morphologic features of Fuchs dystrophy and bullous keratopathy are similar to those described in previous literature. A high proportion of keratocytes exhibited degenerative changes (78.9% in Fuchs dystrophy versus 50.5% in bullous keratopathy). Granular material was identified in and around variably degenerated keratocytes in all cases of Fuchs dystrophy and in 14 of 22 (64%) of the corneas with bullous keratopathy. The percentage of keratocytes with granular deposits was higher in Fuchs dystrophy corneas as compared with corneas with bullous keratopathy (51.7% versus 14.1%, P < 0.0005). Lipid keratopathy was a common occurrence in both Fuchs dystrophy and bullous keratopathy (23/32 [72%] versus 12/22 [55%]). CONCLUSIONS Histopathologic changes in the corneal stroma and keratocytes occur in Fuchs dystrophy. Secondary lipid keratopathy ensues and may contribute to corneal haze. A higher proportion of keratocytes in Fuchs dystrophy have granular deposit than in bullous keratopathy. That a high proportion of keratocytes had degenerative changes in both Fuchs dystrophy and bullous keratopathy suggests that keratocytes may degenerate secondary to altered stromal microenvironment because of endothelial cell loss.

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عنوان ژورنال:
  • Cornea

دوره 24 3  شماره 

صفحات  -

تاریخ انتشار 2005