The Effect of Allograft Rejection After Penetrating Keratoplasty on Central Endothelial Cell Density

Musch, David C.; Schwartz, A.; Fitzgerald-Shelton, Karen; Sugar, Alan; Meyer, Roger F.

doi:10.1016/s0002-9394(14)76782-0

Cited by 55 publications

(49 citation statements)

References 12 publications

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“…54 Episodes of endothelial allograft rejection, although successfully aborted, cause a decrease in endothelial cell density. 55 In our study of 500 consecutive penetrating keratoplasties performed between 1976 and 1986, transplants that had no known rejection episodes or reoperations lost central endothelial cells at average rates of 7.8%/year between 3 and 5 years postkeratoplasty, and 4.2%/year between 5 and 10 years. 56 Our most recent data on this long-term prospective study indicate that the rate of cell loss gradually decreases, but remains more than three times the normal loss of 0.6%/year 8 for 20 years postkeratoplasty.…”

Section: Secondary Corneal Endotheliopathiesmentioning

confidence: 73%

Biology of the corneal endothelium in health and disease

Bourne

2003

Eye

260

198

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Section: Secondary Corneal Endotheliopathiesmentioning

confidence: 73%

Biology of the corneal endothelium in health and disease

Bourne

2003

Eye

260

198

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“…Several studies indicate that alloimmune-mediated destruction of graft tissue is primarily a CD4 T-cell-mediated reaction that targets the corneal endothelium (4)(5)(6)(7)(8). In humans, the corneal endothelium has little to no regenerative capability and responds to loss of neighboring cells by spreading and enlargement (5).…”

Section: Introductionmentioning

confidence: 99%

Corneal Graft Rejection Is Accompanied by Apoptosis of the Endothelium and Is Prevented by Gene Therapy With Bcl‐xL

Bárcia

Dana

Kazlauskas

2007

American Journal of Transplantation

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Corneal transplants normally enjoy a high percentage of survival, mainly because the eye is an immuneprivileged site. When allograft failure occurs, it is most commonly due to rejection, an immune-mediated reaction that targets the corneal endothelium. While the exact mechanism by which the endothelium is targeted is still unknown, we postulate that corneal endothelial cell loss during allograft failure is mediated by apoptosis. Furthermore, because corneal endothelial cells do not normally regenerate, we hypothesize that suppressing apoptosis in the graft endothelium will promote transplant survival. In a murine model of transplantation, TUNEL staining and confocal microscopy showed apoptosis of the graft endothelium occurring in rejecting corneas as early as 2 weeks posttransplantation. We found that bcl-xL protected cultured corneal endothelial cells from apoptosis and that lentiviral delivery of bcl-xL to the corneal endothelium of donor corneas significantly improved the survival of allografts. These studies suggest a novel approach to improve corneal allograft survival by preventing apoptosis of the endothelium.

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“…Several studies have reported low endothelial cell density (ECD) values after allograft rejection [28][29][30][31][32], however control for the expected loss of endothelial cells in PKP patients without rejection is sometimes lacking as well as information on the different pre-and postoperative variables influencing the extent of the endothelial cell loss. We performed a study to examine the decline in ECD in PKP patients experiencing allograft rejection, by comparing this decline to the normal evolution in PKP patients with an uneventful follow-up [33].…”

Section: Effect On Endothelial Cell Attritionmentioning

confidence: 99%

Graft failure: I. Endothelial cell loss

2007

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Graft failure through endothelial cell loss is a constant threat throughout the lifetime of a corneal graft. It can occur at various time points after transplantation. Primary graft failure has nowadays become increasingly rare owing to meticulous eye banking methods and improved surgical techniques. Corneal graft rejection is always held responsible for endothelial cell loss. However a rejection episode that is promptly and adequately treated does not necessarily lead to a higher than expected cell loss. A more smouldering danger to ultimate graft survival is late endothelial failure. This gradual graft decompensation is secondary to a decrease in cell density below that necessary to maintain corneal deturgesence. The process of transplantation itself seems to set off a series of events (possibly immunological) that greatly exacerbates the endothelial cell loss compared to virgin corneas. This accelerated cell loss persists for at least 10-15 years after transplantation, after which a more-stable situation is reached and cell attrition returns to normal rates. This provides a strong rationale for setting high donor standards of minimal cell density. Newer transplantation techniques such as deep anterior lamellar keratoplasty and deep lamellar endothelial keratoplasty could provide possible solutions to prevent this late endothelial failure. However they still have to prove themselves in the long run.

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The Effect of Allograft Rejection After Penetrating Keratoplasty on Central Endothelial Cell Density

Cited by 55 publications

References 12 publications

Biology of the corneal endothelium in health and disease

Biology of the corneal endothelium in health and disease

Corneal Graft Rejection Is Accompanied by Apoptosis of the Endothelium and Is Prevented by Gene Therapy With Bcl‐xL

Graft failure: I. Endothelial cell loss

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