This study determined the rate of response to latanoprost compared with timolol in patients with glaucoma or ocular hypertension, whether some patients convert from non-responders to responders after more prolonged therapy, and whether this conversion represents a delayed response or random fluctuation.
In a previously described, multicenter, randomized, double-masked, parallel group study, patients received either 0.005% latanoprost once daily (n = 128) or 0.5% timolol twice daily (n = 140) for 6 months. Intraocular pressure (IOP) was assessed at baseline and at 0.5, 1.5, 3, 4.5, and 6 months of treatment at 8 am on all visits, and also at noon and 4 pm at baseline and 6 months. Rate of response based on diurnal measurement at 6 months compared with baseline was assessed using several criteria for response. Eyes with an IOP reduction of less than 15% compared with baseline at 8 am arbitrarily were classified as non-responders at each of the 5 visits during treatment. Consistency of non-responder classifications for individual eyes was assessed.
Mean IOP reduction was greater (P < 0.001) in latanoprost-versus timolol-treated patients throughout the course of therapy. A greater rate of response occurred in patients treated with latanoprost, and differences in response rates between the 2 drugs increased as the definitions of response became more stringent. A greater percentage of non-responders at any single visit were classified as responders at all other visits with latanoprost in comparison with timolol.
Latanoprost produces a greater rate of response compared with timolol. A higher percentage of non-responders to latanoprost compared with timolol on any individual visit are responders on all other visits. Likewise, a higher proportion of patients who do not initially respond will become responders with continued treatment with latanoprost compared with timolol.
From the Department of Ophthalmology, University of Nebraska Medical Center, Omaha, Nebraska (Dr Camras); Department of Neuroscience Ophthalmology, University Hospital, Uppsala, Sweden (Dr Hedman); Members of the US Latanoprost Study Group are listed in the appendix at the end of this article.
Received for publication February 25, 2003; accepted June 20, 2003.
Reprints: Carl B. Camras, MD, Department of Ophthalmology, University of Nebraska Medical Center, 985540 Nebraska Medical Center, Omaha, NE, 68198-5540 (e-mail: firstname.lastname@example.org).
Presented in part at the American Glaucoma Society in San Antonio, TX in March 2000.
Supported in part by an unrestricted grant from Research to Prevent Blindness, Inc., New York, NY. The multicenter trial was sponsored by the Pharmacia Corporation, Peapack, NJ.
Dr. Camras is a consultant to the Pharmacia Corporation, Peapack, NJ, and is a Research to Prevent Blindness Senior Scientific Investigator. Dr Hedman was a consultant to the Pharmacia Corporation at the time the research was conducted.