title: Keratectasia after laser in situ keratomileusis: a histopathologic and immunohistochemical study.
abstract: OBJECTIVE
  To examine histopathologic and immunohistochemical features of human corneal buttons from patients who developed keratectasia after laser in situ keratomileusis (LASIK).
  
  
  METHODS
  Five corneal buttons were obtained during penetrating keratoplasty from patients who developed keratectasia after LASIK. Histologic features were examined by hematoxylin-eosin staining using paraffin-embedded sections and by transmission electron microscopy. Immunostaining for alpha(1)-proteinase inhibitor, Sp1, and matrix metalloproteinases 1, 2, and 3 was performed with 2 healthy corneas and 2 corneas with keratoconus as controls.
  
  
  RESULTS
  Central stromal thinning was observed after hematoxylin-eosin staining in all corneas with keratectasia. No histologic features specific to keratoconus, including Bowman layer disruption, were identified in the corneas with keratectasia. By transmission electron microscopy, collagen fibril thinning and decreased interfibril distance were observed in the stromal bed. Immunostaining intensity and/or pattern for alpha(1)-proteinase inhibitor and Sp1 in the corneas with keratectasia was comparable to that of healthy corneas and differed from that in the corneas with keratoconus. No significant staining with anti-matrix metalloproteinases 1, 2, and 3 antibodies was observed in either the corneas with keratectasia or the healthy corneas.
  
  
  CONCLUSIONS
  Histologic findings suggest that post-LASIK keratectasia results in collagen fibril thinning and decreased interfibril distance within the residual stromal bed. Discrepant results between keratectasia and keratoconus suggest that the pathogenesis of the 2 conditions differ.
authors.affiliation: Department of Ophthalmology, University of Illinois at Chicago, Chicago, IL, USA.
authors.forename: Beeran
authors.initials: B
authors.lastname: Meghpara
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nakamura
authors.forename: Marian
authors.initials: M
authors.lastname: Macsai
authors.forename: Joel
authors.initials: J
authors.lastname: Sugar
authors.forename: Ahmed
authors.initials: A
authors.lastname: Hidayat
authors.forename: Beatrice Y J T
authors.initials: BY
authors.lastname: Yue
authors.forename: Deepak P
authors.initials: DP
authors.lastname: Edward
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000378:metabolism; D003315:Cornea / Q000378:metabolism / Q000648:ultrastructure; D003316:Corneal Diseases / Q000209:etiology / Q000378:metabolism / Q000473:pathology* / Q000601:surgery; D019781:Corneal Topography; D004108:Dilatation, Pathologic / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D024022:Fibrillar Collagens / Q000648:ultrastructure; D006801:Humans; D007124:Immunoenzyme Techniques; D007640:Keratoconus / Q000378:metabolism; D020731:Keratomileusis, Laser In Situ / Q000009:adverse effects*; D015948:Keratoplasty, Penetrating; D020781:Matrix Metalloproteinase 1 / Q000378:metabolism; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism; D019278:Matrix Metalloproteinase 3 / Q000378:metabolism; D008875:Middle Aged; D011183:Postoperative Complications; D016329:Sp1 Transcription Factor / Q000378:metabolism; D000515:alpha 1-Antitrypsin / Q000378:metabolism
chemical_list: D015415:Biomarkers; D024022:Fibrillar Collagens; D016329:Sp1 Transcription Factor; D000515:alpha 1-Antitrypsin; D019278:Matrix Metalloproteinase 3; D020778:Matrix Metalloproteinase 2; D020781:Matrix Metalloproteinase 1