Accelerated Chronic Endothelial Cell Loss After Penetrating Keratoplasty in Glaucoma Eyes

PurposeAccelerated chronic endothelial cell loss may be the main reason for limited prognosis of penetrating corneal grafts in glaucoma eyes. This hypothesis, however, has not yet been proven and is examined in this article. MethodsThree groups of normal-risk keratoplasty patients were followed up prospectively. Group I consisted of 172 patients (without glaucoma history and without postoperative increase in intraocular pressure), group II comprised 15 patients (with glaucoma history, but without postoperative increase in intraocular pressure), and group III consisted of seven patients (with glaucoma history and with postoperative increase in intraocular pressure). Immune reactions in the postoperative course were an exclusion criterion. Follow-up periods averaged 2.7 ± 1.7 years (group I), 2.8 ± 1.7 years (group II), and 2.6 ± 2.0 years (group III). Only patients with at least three postoperative endothelial cell density values were included in the study. Loss of endothelial cells · mm−2 · d−1 was derived from the postoperative endothelial values of each patient by calculating the slope of the regression line for each scatterplot of endothelial cell density values plotted against time. ResultsDuring the follow-up period 0.82 ± 0.97 cells · mm−2 · d−1 were lost in group I, 1.01 ± 1.04 cells · mm−2 · d−1 were lost in group II, 2.67 ± 2.16 cells · mm−2 · d−1 were lost in group III (ANOVA and Gabriel post-hoc test: I/II P = 0.82, I/III P < 0.001, II/III P = 0.004). ConclusionsPostoperative increase in intraocular pressure may be a possible cause for accelerated endothelial cell loss in glaucoma eyes, but this result is tentative because of the small number of patients included in the two glaucoma groups. Confirmation by long-term observation of larger patients groups is desirable. The result implies good control of intraocular pressure after penetrating keratoplasty. Whether this method is the correct means by which to prevent accelerated endothelial cell loss in such eyes must be shown in future studies.

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