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Glaucoma in Patients With Corneal Endothelial Dystrophy

Ali, Zahra K M.D.; Whitson, Jess T M.D.; Mootha, V Vinod M.D.; Witherspoon, S Robert M.D.; Joseph, J Arun B.A.; Joseph, Ashley M B.A.; Hynan, Linda S Ph.D.; Cavanagh, H Dwight M.D., Ph.D.

doi: 10.1097/ICL.0b013e31822d0fa6

Objectives: The prevalence of primary open-angle glaucoma (POAG) in patients with corneal endothelial dystrophy has not been previously studied. Prevalence of POAG in patients with endothelial dystrophy was compared with that in the general population to determine the presence of a relationship between the diseases.

Design: Retrospective case-control study.

Methods: A study of the prevalence of POAG in 430 eyes of 215 patients with endothelial dystrophy was conducted. Patients followed for less than 6 months were excluded. Relative risk of POAG was calculated using age- and race-matched control data from the Baltimore Eye Survey and the Los Angeles Latino Eye Survey for comparison. Ocular hypertension (OHT) and secondary glaucoma (SG) rates after penetrating keratoplasty (PK) and Descemet stripping endothelial keratoplasty (DSEK) were separately analyzed.

Results: Relative risk of POAG in white, African American, and Hispanic patients with endothelial dystrophy was 0.94, 2.59, and 3.7, respectively (P = 0.89, 95% confidence interval [CI], −0.028 to 0.0289; P = 0.13; 95% CI, 0.011–0.274; P = 0.055; 95% CI, 0.0423–0.356). Relative risk of SG and combined OHT/SG in PK versus DSEK was 4.15 and 1.95 (P < 0.001; 95% CI, 0.0654–0.322; P = 0.005; 95% CI, 0.116–0.332), respectively. No differences in OHT/SG rates were found comparing PK-triple with PK, DSEK-triple with DSEK, and repeat with primary PK or DSEK (P = 0.98; P = 0.62; P = 0.95; P = 0.87), respectively.

Conclusions: No increased risk of POAG was found in patients with endothelial dystrophy. Increased prevalence of OHT/SG was shown with PK versus DSEK; possible mechanisms include mechanical closure of Schlemm's canal by running suture and prolonged steroid use.

UT Southwestern Medical Center (Z.K.A., J.T.W., V.V.M., J.A.J., A.M.J., L.S.H., H.D.C.), Dallas, TX; and Retina Institute of Texas (S.R.W.), Dallas, TX.

Supported by the chair funds derived from the Dr. W. Maxwell Thomas Chair Professorship at the University of Texas Medical Center at Dallas; National Institutes of Health infrastructure grant EY-016664; and an unrestricted grant from the Research to Prevent Blindness, Inc; New York, NY.

J.T. Whitson is funded by the Speaker's Bureau, Allergan, and Alcon.

Author Contributions. Design of the study: Z.K. Ali, J.T. Whitson, V.V. Mootha, S.R. Witherspoon, and H.D. Cavanagh; Conduct of the study: Z.K. Ali and H.D. Cavanagh; Collection of data: Z.K. Ali, J.A. Joseph, and A.M. Joseph; Management of data: Z.K. Ali, J.A. Joseph, and A.M. Joseph; Analysis: Z.K. Ali, J.T. Whitson, V.V. Mootha, S.R. Witherspoon, J.A. Joseph, H.D. Cavanagh, and L.S. Hynan; Interpretation of data: Z.K. Ali, J.T. Whitson, V.V. Mootha, S.R. Witherspoon, and H.D. Cavanagh; Preparation and review of the manuscript: Z.K. Ali, J.T. Whitson, V.V. Mootha, S.R. Witherspoon, and H.D. Cavanagh.

The research was approved by the University of Texas Southwestern Institutional Review Board.

The authors have no conflicts of interest to disclose.

Address correspondence and reprint requests to H. Dwight Cavanagh, M.D., Ph.D., UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390; e-mail:

Accepted July 10, 2011.

© 2011 Lippincott Williams & Wilkins, Inc.