title: A clinical and histopathologic examination of accelerated TGFBIp deposition after LASIK in combined granular-lattice corneal dystrophy.
abstract: OBJECTIVE
  To report the clinical and histopathologic features of accelerated TGFBI protein (TGFBIp) deposition after lamellar keratorefractive surgery in a patient with combined granular-lattice corneal dystrophy (CGLCD) who underwent bilateral corneal transplantation.
  
  
  METHODS
  Interventional case report.
  
  
  METHODS
  A 28-year-old woman with a presumed TGFBI corneal dystrophy, but who retained best corrected visual acuity of 20/20 in each eye, underwent myopic laser-assisted in-situ keratomileusis (LASIK) both eyes (OU). For definitive diagnosis of the corneal dystrophy, buccal epithelial cells were collected as a source of genomic DNA and screening of TGFBI exons 4 and 12 was performed.
  
  
  RESULTS
  Four months after the performance of an uncomplicated LASIK procedure, the patient's uncorrected visual acuity was 20/15 OU. Over the following two years, the appearance of confluent white stromal deposits at the LASIK flap interface resulted in disabling glare and a reduced best-corrected visual acuity of 20/40 OU. Corneal transplantation was performed in each eye, and histopathologic examination of the excised corneal buttons was performed. Eosinophilic material that stained positively with the Masson trichrome stain was present in the LASIK flap interface, as well as in the stroma of the flap and the anterior portion of the stromal bed. No amyloid deposits were identified with the Congo red stain. Screening of TGFBI exons 4 and 12 revealed the Arg124His mutation associated with CGLCD.
  
  
  CONCLUSIONS
  Accelerated deposition of TGFBIp may occur after lamellar corneal surgery in patients with CGLCD. Therefore, LASIK surgery should be avoided in patients with any of the TGFBI dystrophies, and surgeons should be aware of the potential for rapid interface TGFBIp deposition after lamellar corneal surgery.
authors.affiliation: Jules Stein Eye Institute, The University of California Los Angeles Medical Center, Los Angeles, California 90095, USA. aldave@jsei.ucla.edu
authors.forename: Anthony J
authors.initials: AJ
authors.lastname: Aldave
authors.forename: Baris
authors.initials: B
authors.lastname: Sonmez
authors.forename: S Lance
authors.initials: SL
authors.lastname: Forstot
authors.forename: Sylvia A
authors.initials: SA
authors.lastname: Rayner
authors.forename: Vivek S
authors.initials: VS
authors.lastname: Yellore
authors.forename: Ben J
authors.initials: BJ
authors.lastname: Glasgow
mesh_terms: D000328:Adult; D003317:Corneal Dystrophies, Hereditary / Q000378:metabolism* / Q000473:pathology* / Q000601:surgery; D003319:Corneal Stroma / Q000378:metabolism* / Q000473:pathology / Q000601:surgery; D005091:Exons / Q000235:genetics; D016326:Extracellular Matrix Proteins / Q000235:genetics / Q000378:metabolism*; D005260:Female; D006801:Humans; D020731:Keratomileusis, Laser In Situ; D015948:Keratoplasty, Penetrating; D009154:Mutation; D020641:Polymorphism, Single Nucleotide; D011183:Postoperative Complications; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism*; D014792:Visual Acuity; D000099222:betaIG-H3 Protein
chemical_list: D016326:Extracellular Matrix Proteins; D016212:Transforming Growth Factor beta; D000099222:betaIG-H3 Protein