We have located links that may give you full text access.
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Accelerated chronic endothelial cell loss after penetrating keratoplasty in glaucoma eyes.
Journal of Glaucoma 2001 December
PURPOSE: Accelerated 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.
METHODS: Three 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.
RESULTS: During 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).
CONCLUSIONS: Postoperative 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.
METHODS: Three 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.
RESULTS: During 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).
CONCLUSIONS: Postoperative 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.
Full text links
Related Resources
Trending Papers
Challenges in Septic Shock: From New Hemodynamics to Blood Purification Therapies.Journal of Personalized Medicine 2024 Februrary 4
Molecular Targets of Novel Therapeutics for Diabetic Kidney Disease: A New Era of Nephroprotection.International Journal of Molecular Sciences 2024 April 4
The 'Ten Commandments' for the 2023 European Society of Cardiology guidelines for the management of endocarditis.European Heart Journal 2024 April 18
A Guide to the Use of Vasopressors and Inotropes for Patients in Shock.Journal of Intensive Care Medicine 2024 April 14
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app