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.
