Original article
Avellino Corneal Dystrophy Worsening after Laser In Situ Keratomileusis: Further Clinicopathologic Observations and Proposed Pathogenesis

https://doi.org/10.1016/j.ajo.2007.12.008Get rights and content

Purpose

To study the nature of the deposits in Avellino corneal dystrophy (ACD) worsening after laser in situ keratomileusis (LASIK), and suggest a mechanism for histopathogenesis.

Design

Interventional case report.

Methods

A 28-year-old woman previously diagnosed with bilateral ACD underwent bilateral LASIK. The corneal dystrophy progressively worsened bilaterally, one year later. A penetrating keratoplasty was subsequently performed on the right eye at 31 years of age, and in the left eye a year later. The clinical and histopathologic findings of the corneal graft of the right eye were reported in the literature, with positivity to the Masson trichrome stain, negative staining with Congo red, and heterozygosity for the Arg124His mutation by serum DNA studies. Histopathologic studies of the corneal graft of the left eye were conducted at the University of Texas Southwestern Medical Center.

Results

Histopathologic examination of the excised cornea showed the Masson trichrome positive deposits present from underneath the Bowman layer to the LASIK interface, with absence of deposits posterior to the latter. In contrast to the prior report describing findings in the corneal graft of the left eye, the deposits stained lightly with Congo red, but failed to show birefringence under polarized light, or fluorescence with thioflavin T.

Conclusion

Accelerated deposits developing after LASIK in ACD eyes seem to harbor pre-amyloid features. The epithelium is likely to be the culprit, in a pathway independent of with human transforming growth hormone beta (TGF-beta), with deposits developing in the anterior stroma and the stromal interface.

Section snippets

Methods

The condition, along with other types of granular corneal dystrophies, lattice corneal dystrophies, and Reis-Buckler dystrophy, results from a specific mutation in the BIGH3 gene on chromosome 5q31, dictating a TGF-beta (TGFB)-induced cell adhesion protein, keratoepithelin (68 Kda), which is mainly expressed by the corneal epithelium and normally present in the corneal stroma, with highest density in the Bowman layer.9, 10, 18, 19, 20 In the case of Avellino corneal dystrophy, a mutation in

Discussion

Recurrence of ACD as well as granular and lattice dystrophies has been documented after treatment by PTK and PRK.11, 12 Worsening ACD has also been reported after LASIK.13, 14, 15, 16, 17, 18, 19 The deposits were described clinically and histologically to be located in the LASIK flap interface and the stroma anterior to it. Three reports have so far described histopathologic findings in eyes with ACD after LASIK. One of those reports, published by Aldave and associates, describes the findings

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