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1From the Department of Ophthalmology and Eye Hospital, University Erlangen-Nürnberg, Erlangen, Germany; the 2Department of Ophthalmology, Faculty of Clinical Medicine Mannheim, University of Heidelberg, Mannheim, Germany; the 3Institute of Medical Informatics, Biostatistics, and Epidemiology, Benjamin Franklin School of Medicine, Berlin, Germany; and the 4Berlin Centre Public Health, Department of Medical Informatics, Biometry and Epidemiology, Free University of Berlin, Berlin, Germany.
PURPOSE. To evaluate whether the amount of glaucomatous optic nerve damage at presentation of the patient and the rate of progression of glaucoma during follow-up are related to central corneal thickness.
METHODS. The prospective observational clinical study included 861 eyes of 454 white subjects (239 normal eyes of 121 subjects, 250 ocular hypertensive eyes of 118 patients, 372 eyes of 215 patients with chronic open-angle glaucoma). For 567 eyes (304 patients) with ocular hypertension or chronic open-angle glaucoma, follow-up examinations were performed, with a mean follow-up time of 62.7 ± 33.2 months (median, 60.8; range, 6.2–124.9). All patients underwent qualitative and morphometric evaluation of color stereo optic disc photographs and white-on-white visual field examination. Central corneal thickness was measured by corneal pachymetry.
RESULTS. Central corneal thickness correlated significantly (P < 0.001) and positively with the area of the neuroretinal rim and negatively with the loss of visual field. Development or progression of glaucomatous visual field defects detected in 119 (21.0%) eyes was statistically independent of central corneal thickness, in univariate (P = 0.99) and multivariate Cox regression analyses (P = 0.19).
CONCLUSIONS. At the time of patient referral, the amount of glaucomatous optic nerve damage correlated significantly with a thin central cornea. Progression of glaucomatous optic nerve neuropathy was independent of central corneal thickness, suggesting that central corneal thickness may not play a major role in the pathogenesis of progressive glaucomatous optic nerve damage.
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