Topical timolol administration reduces the incidence of glaucomatous damage in ocular hypertensive individuals. A randomized, double-masked, long-term clinical trial(1)

Michael A. Kass, Mae O. Gordon, Mark R. Hoff, John M. Parkinson, Allan E. Kolker, William M. Hart, Bernard Becker

Research output: Contribution to journalArticlepeer-review


Objectives A randomized, double-masked, 5-year clinical trial was conducted to determine whether topical timolol therapy was more effective than placebo in delaying or preventing the onset of glaucomatous damage in moderate-risk ocular hypertensive subjects. Methods One eye was chosen randomly to receive timolol therapy twice daily; the fellow eye received placebo (timolol vehicle). The primary end point of the study was reproducible visual field loss detected on three consecutive tests. Automated static threshold visual fields were added to the protocol as the study proceeded, and criteria for reproducible defects for the automated fields were developed. The secondary end point was progressive optic disc cupping confirmed by examination of stereoscopic disc photographs. Intraocular pressure was not used as an end point (i.e., eyes were not withdrawn from the study because they reached a predetermined level of intraocular pressure). Inclusion criteria were: 1. baseline intraocular pressure in both eyes greater than 24 mm Hg but less than 35 mm Hg 2. a difference in baseline intraocular pressure of less than 3 mm Hg between right and left eyes 3. age greater than or equal to 40 years 4. open angles on gonioscopy in both eyes 5. normal and reliable kinetic visual fields on the Goldmann perimeter in both eyes 6. adequate pupillary dilation for optic disc exam-ination and stereoscopic disc photography 7. normal optic discs in both eyes 8. patient willingness to participate in a randomized study involving thrice-yearly examinations for 5 years 9. best corrected visual acuity greater than or equal to 20/50 in either eye Exclusion criteria were: 1. medical contraindications to topical (3-blockers 2. systemic illness that could interfere with follow-up examinations 3. recent ocular infection, inflammation, trauma, or previous intraocular surgery (including laser) 4. use of systemic medications that might alter in-traocular pressure (e.g., corticosteroids, (3-ad- renergic antagonists, clonidine) 5. presence of disease that could produce visual field loss 6. previous unilateral treatment of increased intra-ocular pressure 7. women who were pregnant or breast-feeding Results Of 65 patients recruited for the study, 43 completed the 5-year follow-up and 11 developed visual field loss (Table 1). In almost every case, visual field end points were confirmed by both kinetic and automated threshold perimetry. During the course of the study the mean ± SD difference in intraocular pressure between the timolol-treated and the placebo-treated eyes was 2.3 ± 2.6 mm Hg (Fig. 1). Timolol reduced intraocular pressure by approximately 5 mm Hg (±3.3 mm Hg) in the treated eye and by 3 mm Hg (±3.0 mm Hg) in the fellow eye. Reproducible visual field loss developed in four timolol-treated eyes and ten placebo-treated eyes (p = 0.039, one-tailed McNemar test). Progressive optic disc cupping was noted in four timolol-treated and eight placebo-treated eyes (p = 0.11; one-tailed McNemar test). A computerized image analysis system was used to measure optic disc pallor: the mean (±SD) increase in optic disc pallor during the course of this study was 0.86% ± 2.4% in the timolol-treated eyes as opposed to 1.80% ± 3.6% in the placebo-treated eyes (p = 0.02, one-tailed paired Student’s t test). Conclusion This study provides evidence that lowering intra-ocular pressure with timolol reduces the incidence of glaucomatous damage in ocular hypertensive in-dividuals.

Original languageEnglish
Pages (from-to)S1-S2
JournalJournal of Glaucoma
StatePublished - Jan 1 1993


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