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Progression of retinal nerve fibre layer damage in betaxolol‐ and timolol‐treated glaucoma patients

Purpose:  It has been suggested that there are differences between selective and non‐selective beta‐blocking agents in their ability to protect glaucomatous eyes. The purpose of this study was to follow glaucoma patients treated with either betaxolol 0.5% or timolol 0.25% ophthalmic solutions and to...

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Bibliographic Details
Published in:Acta ophthalmologica Scandinavica 2002-10, Vol.80 (5), p.495-500
Main Authors: Vainio‐Jylhä, Elina, Vuori, Marja‐Liisa, Nummelin, Kari
Format: Article
Language:English
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Summary:Purpose:  It has been suggested that there are differences between selective and non‐selective beta‐blocking agents in their ability to protect glaucomatous eyes. The purpose of this study was to follow glaucoma patients treated with either betaxolol 0.5% or timolol 0.25% ophthalmic solutions and to compare the rate and degree of progression in retinal nerve fibre layer (RNFL) defects between the groups. Methods:  A total of 64 patients were prospectively recruited in a double‐masked study and randomly divided into two treatment groups. Retinal nerve fibre layer photographs were analysed. The incidence and total amount of progression in each group were recorded. The rate of impairment was demonstrated using Kaplan Meier survival curves. Results:  The analysis included 27 patients treated with betaxolol and 28 patients treated with timolol. Of these, 30% of betaxolol‐treated patients and 46% of timolol‐treated patients had RNFL damage progression (p = 0.20). The total amount or rate of progression did not differ significantly between the two groups. There was no significant difference in intraocular pressure (IOP) levels between the groups (p = 0.68) during follow‐up. The degree of RNFL deterioration did not correlate to the amount of IOP reduction. Conclusion:  The group treated with betaxolol 0.5% and the group treated with timolol 0.25% did not differ significantly in RNFL damage progression.
ISSN:1395-3907
1600-0420
DOI:10.1034/j.1600-0420.2002.800507.x