Systemaattinen katsaus «Sena DF, Lindsley K. Neuroprotection for treatment...»1, «Neuroprotection for treatment of glaucoma in adults»1
Neuroprotection for glaucoma refers to any intervention intended to prevent optic nerve damage or cell death. The objective of the review was to systematically examine the evidence regarding the effectiveness of neuroprotective agents for slowing the progression of OAG in adults.
Systematic literature review was conducted through October 16, 2012 including registries of trials. No date or language restrictions were used. RCT’s in which topical or oral treatments were used for neuroprotection in adults with OAG were selected. Minimum follow up time was 4 years.
One trial was identified for this review. Two studies comparing memantine to placebo are currently awaiting classification until additional study details are provided.
One multi-center RCT of adults with low-pressure glaucoma (Low-pressure Glaucoma Treatment Study, LoGTS) conducted in the USA was included. The primary outcome was visual field progression after 4 years of treatment with either brimonidine or timolol. Of the 190 adults enrolled in the study, 12 (6 %) were excluded after randomization and 77 (41 %) did not complete 4-year follow up. The rate of attrition was unbalanced between groups with more participants dropping out of the brimonidine group (55 %) than the timolol group (29 %). Of those remaining in the study at 4 years, participants assigned to brimonidine showed less visual field progression than participants assigned to timolol (5/45 participants in the brimonidine group compared with 18/56 participants in the timolol group). Since no information was available for the 12 participants excluded from the study, or the 77 participants who dropped out of the study, the authors were unable to draw any conclusions from these results as the participants for whom data are missing may or may not have progressed. The mean IOP was similar in both groups at the 4-year follow up among those for whom data were available: 14.2 mmHg (standard deviation (SD) = 1.9) among the 43 participants in the brimonidine group and 14.0 mmHg (SD = 2.6) among the 48 participants in the timolol group. Among the participants who developed progressive visual field loss, IOP reduction ≥ 20 % was not significantly different between groups: 4/9 participants in the brimonidine group and 12/31 participants in the timolol group. The study authors did not report data for visual acuity or vertical cup-disc ratio. The most frequent adverse event was ocular allergy to study drug, which occurred more frequently in the brimonidine group (20/99 participants) than the timolol group (3/79 participants).
Although neuroprotective agents are intended to act as pharmacological antagonists to prevent cell death, this trial did not provide evidence that they are effective in preventing retinal ganglion cell death, and thus preserving vision in people with OAG. Further clinical research is needed to determine whether neuroprotective agents may be beneficial for individuals with OAG. Such research should focus outcomes important to patients, such as preservation of vision, and how these outcomes relate to cell death and optic nerve damage. Since OAG is a chronic, progressive disease with variability in symptoms, RCTs designed to measure the effectiveness of neuroprotective agents would require long-term follow up (more than four years) in order to detect clinically meaningful effects.