Prognostic factors for corneal graft recovery after severe corneal graft rejection following penetrating keratoplasty

BACKGROUND: To investigate the outcome and prognostic factors for corneal graft recovery after severe corneal graft rejection following penetrating keratoplasty (PKP) treated with topical and systemic steroids. METHODS: Fifty-eight eyes in 58 patients with severe corneal graft rejection following PKP were treated with topical and systemic steroids. Factors affecting the reversibility and maintenance of graft transparency were analyzed. RESULTS: Graft transparency was restored in 37 of 58 eyes (63.8%). Clarity of the graft was maintained in 25 of 37 eyes after transparency was restored, while corneal decompensation developed at a mean of 6.0 ± 4.3 months in the remainder. The interval between rejection and treatment with systemic steroids was shorter in cases that recovered graft transparency (OR, 0.88, 95% CI. 0.80–0.97, P = 0.0093). Corneal decompensation after the recovery of corneal transparency tend to occur in cases of regraft (OR, 0.09, 95% CI. 0.01–0.54, P = 0.0091). CONCLUSIONS: Severe corneal graft rejection after PKP was reversible in approximately two-thirds of the cases, with graft transparency being maintained in two-thirds of them when treated with both topical and systemic steroids. Early treatment confers a benefit in terms of the recovery of graft transparency

Development of a Transgenic Mouse with R124H Human TGFBI Mutation Associated with Granular Corneal Dystrophy Type 2.

To investigate the phenotype and predisposing factors of a granular corneal dystrophy type 2 transgenic mouse model.Human TGFBI cDNA with R124H mutation was used to make a transgenic mouse expressing human protein (TGFBIR124H mouse). Reverse transcription PCR (RT-PCR) was performed to analyze TGFBIR124H expression. A total of 226 mice including 23 homozygotes, 106 heterozygotes and 97 wild-type mice were examined for phenotype. Affected mice were also examined by histology, immunohistochemistry and electron microcopy.RT-PCR confirmed the expression of TGFBIR124H in transgenic mice. Corneal opacity defined as granular and lattice deposits was observed in 45.0% of homozygotes, 19.4% of heterozygotes. The incidence of corneal opacity was significantly higher in homozygotes than in heterozygotes (p = 0.02). Histology of affected mice was similar to histology of human disease. Lesions were Congo red and Masson Trichrome positive, and were observed as a deposit of amorphous material by electron microscopy. Subepithelial stroma was also stained with thioflavin T and LC3, a marker of autophagy activation. The incidence of corneal opacity was higher in aged mice in each group. Homozygotes were not necessarily more severe than heterozygotes, which deffers from human cases.We established a granular corneal dystrophy type 2 mouse model caused by R124H mutation of human TGFBI. Although the phenotype of this mouse model is not equivalent to that in humans, further studies using this model may help elucidate the pathophysiology of this disease

Demographic features.

<p>Demographic features.</p

Demographic features.

<p>Demographic features.</p

Incidence of corneal opacity.

<p>Incidence of corneal opacity.</p