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Granular corneal dystrophy recurrence at the posterior graft-host interface after type 1 big bubble deep anterior lamellar keratoplasty

PURPOSE: To describe our observations of granular corneal dystrophy (GCD) recurrence isolated to the posterior graft-host interface after type 1 big bubble (BB) deep anterior lamellar keratoplasty (DALK). OBSERVATIONS: We performed a retrospective chart review of 3 eyes in 2 patients, and literature...

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Detalles Bibliográficos
Autores principales: Oke, Isdin, Haddad, Narmien, Lee, Hyunjoo Jean
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7582045/
https://www.ncbi.nlm.nih.gov/pubmed/33117914
http://dx.doi.org/10.1016/j.ajoc.2020.100960
Descripción
Sumario:PURPOSE: To describe our observations of granular corneal dystrophy (GCD) recurrence isolated to the posterior graft-host interface after type 1 big bubble (BB) deep anterior lamellar keratoplasty (DALK). OBSERVATIONS: We performed a retrospective chart review of 3 eyes in 2 patients, and literature review to summarize GCD recurrence patterns after DALK. A 29-year-old man with GCD underwent DALK by type 1 BB technique. Three years following surgery, he was found to have recurrence of GCD deposits isolated to the posterior graft-host interface. Similarly, a 53-year-old woman with GCD underwent DALK by BB type 1 technique, and was noted to have trace residual deposits at the posterior graft-host interface that increased in number and size over the course of 6 years. Her fellow eye underwent DALK with type 2 BB formation, without evidence of graft-host interface recurrence over a four year period. Our literature review describes the recurrence patterns of 18 cases of GCD following DALK. CONCLUSIONS AND IMPORTANCE: DALK can be prone to GCD recurrence in the central posterior graft-host interface. Recurrent deposits isolated to the posterior graft-host interface following type 1 BB DALK supports the hypothesis that GCD recurrence may be due to residual pathologic keratocytes in the pre-Descemet layer (PDL).