May 2003
Volume 44, Issue 13
ARVO Annual Meeting Abstract  |   May 2003
Predicting Endothelial Cell Loss and Long-Term Corneal Graft Survival
Author Affiliations & Notes
  • W.J. Armitage
    Ophthalmology, University Bristol, Bristol, United Kingdom
  • A.D. Dick
    Ophthalmology, University Bristol, Bristol, United Kingdom
  • W.M. Bourne
    Ophthalmology, Mayo Clinic, Rochester, MN, United States
  • Footnotes
    Commercial Relationships  W.J. Armitage, None; A.D. Dick, None; W.M. Bourne, None.
  • Footnotes
    Support  Support (WMB): NIH Grant EY02037
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 4329. doi:
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      W.J. Armitage, A.D. Dick, W.M. Bourne; Predicting Endothelial Cell Loss and Long-Term Corneal Graft Survival . Invest. Ophthalmol. Vis. Sci. 2003;44(13):4329.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: A simple exponential decay equation is inadequate to describe long-term corneal endothelial cell (EC) loss after penetrating keratoplasty. A more complex model that fitted the sum of two exponentials was therefore evaluated for describing the post-operative loss of EC both after penetrating keratoplasty and after cataract surgery. Methods: Data from studies of EC loss reported in the literature were identified. These included EC loss with age as well as after penetrating keratoplasty (up to 20 years post-op) or cataract surgery (up to 10 years post-op). A bi-exponential decay model was fitted to the data to determine the half-times of the rapid and slow components of the EC loss. Results: The half-time for the slow component of the loss with age was 224 years, underlining the excess endothelial capacity in normal eyes. The rapid component of the loss had a half time of 3 years, suggesting that this component should be negligible after approximately 15 years of age. After surgery, the rapid component of the EC loss had a half time of just a few months, and was likely due to surgical trauma and, following penetrating keratoplasty, cell-mediated rejection and other complications. The half times of the slow component were only 26 years after cataract surgery and 21 years after penetrating keratoplasty. Conclusions: The half times for the slow component after surgery were considerably less than for the loss with age, underlining the persistence of the accelerated EC loss even many years after surgery. Given the similarity of the half times following cataract surgery and penetrating keratoplasty, a common mechanism for this continued EC loss is suggested that involves a non-specific, innate response initiated by the breakdown of the blood-ocular barrier. The model can also be used to calculate EC loss in the long term after penetrating keratoplasty and thus predict when EC density may reach levels that are incompatible with the maintenance of transparency and graft function. Thus, a rationale is presented for the setting of minimum donor EC densities by eye banks.

Keywords: cornea: endothelium • transplantation 

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