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Philippe G Kestelyn, Dirk De Bacquer, Anna Stevens; Switch from BAK-preserved to preservative-free latanoprost decreases anterior chamber flare in POAG patients. Invest. Ophthalmol. Vis. Sci. 2014;55(13):547.
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We previously showed that BAK-preserved and preservative-free timolol both increase flare measurements, but that the increase in BAK treated eyes is significantly higher than in preservative-free treated eyes (Stevens et al. Acta Ophthalmologica, 2012). To corroborate the hypothesis that BAK induces low grade inflammation in the anterior chamber, we designed another study to investigate whether switching from BAK-preserved to preservative-free latanoprost in patients with POAG would reduce the flare levels
Clinical trial. We measured baseline flare values in 22 patients with primary open angle glaucoma who took BAK-preserved latanoprost for at least 6 months. We then switched all patients to preservative-free latanoprost and took flare measurements at month 1 after the switch
Baseline flare value : 6.59 photons/millisecond Flare values 1 month after the switch : 5.71 photons/millisecond Decrease in flare : -0.882 ( -1.441 to -0.323) F-statistic mixed models p = 0.0038
The switch from BAK-preserved to preservative-free latanoprost indeed reduced the flare values. This finding confirms our hypothesis that BAK induces low grade inflammation in the anterior segment since both preservative -free betablockers and latanoprost generate lower flare values than the BAK-preserved drugs. The potential implications of long term low grade inflammation due to chronic use of BAK preserved drugs are not yet clear but raise important questions: - is BAK potentially harmful to the trabecular meshwork cells? - Is BAK implicated in the slow loss of efficacy of glaucoma medications over time? - could the low grade inflammation account for the higher failure rate of filtering surgery in patients on BAK-preserved glaucoma medication? Our findings obtained over a short periode of time certainly justify further research on the potential toxicity of BAK at the level of the anterior chamber and the trabecular meshwork in glaucoma patients since they are exposed to this substance for years or decades
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