A Clinical and Histopathologic Examination of Accelerated TGFBIp Deposition After LASIK in Combined Granular-Lattice Corneal Dystrophy

Aldave, Anthony J.; Sönmez, Barış; Forstot, S. Lance; Rayner, Sylvia A.; Yellore, Vivek S.; Glasgow, Ben J.

doi:10.1016/j.ajo.2006.11.056

Cited by 37 publications

(29 citation statements)

References 12 publications

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“…111,112 The TGFBIp deposits were located in the LASIK interface, the stroma of the flap, and the anterior portion of the stromal bed. 113,114 In fact, LASIK has been recently shown to enhance the progression of GCD2 dystrophy. 115 …”

Section: Corneal Surface Ablationmentioning

confidence: 99%

Clinical and Genetic Aspects of the TGFBI-associated Corneal Dystrophies

et al. 2014

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Section: Corneal Surface Ablationmentioning

confidence: 99%

Clinical and Genetic Aspects of the TGFBI-associated Corneal Dystrophies

et al. 2014

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“…One of those reports, published by Aldave and associates, describes the findings of the right eye corneal graft of our patient. 16 The findings consisted of eosinophilic materials staining positive with the Masson trichrome stain with no uptake with Congo red stain. Most of the deposits were described to be located in the LASIK interface, the stroma of the flap, and the anterior portion of the stromal bed.…”

Section: Discussionmentioning

confidence: 99%

“…13-19 A previous article published in the American Journal of Ophthalmology by Aldave and associates reported on a 28-year-old woman with an accelerated granular-lattice corneal dystrophy course after LASIK, with a bilateral penetrating keratoplasty (PK) performed thereafter. 16 Histopathologic findings of the corneal graft of the right eye were presented, which included negative Congo red staining, with the conclusion that there is an accelerated TGFB-induced protein response in patients with ACD after excimer laser ablation. We had the chance to examine the patient subsequently at the University of Texas Southwestern Medical Center.…”

Section: Methodsmentioning

confidence: 99%

“…The clinical and histopathologic findings were described in details in the report of Aldave and associates, who later performed a BIGH3 gene screening using polymerase chain reaction on a blood sample from the patient confirming heterozygousity for the Arg124His mutation. 16 At one year post-PK, the patient was referred to the University of Texas Southwestern Medical Center at Dallas for evaluation. BCVA was 20/20 in the right eye, and 20/30 in the left eye with the patient complaining of significant glare.…”

Section: Methodsmentioning

confidence: 99%

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

Awwad

Pascuale

Hogan

et al. 2008

American Journal of Ophthalmology

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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

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“…The only available treatments of TGFBI corneal dystrophies are lamellar keratoplasty or phototherapeutic keratectomy for disorders that only affect the superficial cornea; full-thickness corneal transplant can be used in severe cases with TGFBIp deposits throughout the corneal stroma 6–9 . However, the impact of these treatments is normally transient because there is a risk of new protein accumulation in the donor cornea 10–12 . Moreover, donor corneas may be scarce.…”

mentioning

confidence: 99%

Fibril Core of Transforming Growth Factor Beta-Induced Protein (TGFBIp) Facilitates Aggregation of Corneal TGFBIp

Sørensen¹,

Runager²,

Scavenius³

et al. 2015

Biochemistry

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Mutations in the transforming growth factor beta-induced (TGFBI) gene result in a group of hereditary diseases of the cornea that are collectively known as TGFBI corneal dystrophies. These mutations translate into amino acid substitutions mainly within the fourth fasciclin 1 domain (FAS1-4) of the transforming growth factor beta-induced protein (TGFBIp) and cause either amyloid or non-amyloid protein aggregates in the anterior and central parts of the cornea, depending on the mutation. The A546T substitution in TGFBIp causes lattice corneal dystrophy (LCD), which manifests as amyloid-type aggregates in the corneal stroma. We previously showed that the A546T substitution renders TGFBIp and the FAS1-4 domain thermodynamically less stable compared with the wild-type (WT) protein, and the mutant FAS1-4 is prone to amyloid formation in vitro. In the present study, we identified the core of A546T FAS1-4 amyloid fibrils. Significantly, we identified the Y571-R588 region of TGFBIp, which we previously found to be enriched in amyloid deposits in LCD patients. We further found that the Y571-R588 peptide seeded fibrillation of A546T FAS1-4 and, more importantly, we demonstrated that native TGFBIp aggregates in the presence of fibrils formed by the core peptide. Collectively, these data suggest an involvement of the Y571-R588 peptide in LCD pathophysiology.

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A Clinical and Histopathologic Examination of Accelerated TGFBIp Deposition After LASIK in Combined Granular-Lattice Corneal Dystrophy

Cited by 37 publications

References 12 publications

Clinical and Genetic Aspects of the TGFBI-associated Corneal Dystrophies

Clinical and Genetic Aspects of the TGFBI-associated Corneal Dystrophies

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

Fibril Core of Transforming Growth Factor Beta-Induced Protein (TGFBIp) Facilitates Aggregation of Corneal TGFBIp

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