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Impressum
Ocular hypotensive effects of latanoprost and brimonidine and associated oral NSAID therapy
Weber A., Paris G., Trigo Y., Pena M., Sponsel W. E.
Augenklinik der RWTH Aachen, Pauwelsstrasse,52074 Aachen South Texas Ocular Imaging Center,Ophthalmology,Univ of Texas Hlth Sci Center, San Antonio,Tx,USA
Purpose: Latanoprost is an analogue of an end-product of the arachidonic
acid pathway. Brimonidine has been proposed to facilitate uveoscleral
outflow by inducing endogenous PG production, and if so, might be subject
to NSAID monooxygenase inhibition. The purpose of this study was to assess
any modulating effects oral indomethacin therapy might exert upon the
ocular hypotensive actions of the prostaglandin latanoprost or the alpha
agonist brimonidine.
Methods: Forty eyes of 20 OHT or early POAG patients underwent
a 3- week washout of any topical ophthalmic agents before initiating monotherapy
in one eye with either brimonidine or latanoprost. Oral indomethacin (25mg,4
times daily) was started on day 14, and continued through day 28, during
which time ocular treatment was maintained with each of the 2 topical
agent in their randomly assigned eyes.
Results: IOP had decreased significantly after 1 week of topical
therapy relative to baseline (~19.5 ± 1.2 mmHg for both treatments),
to 16.5 ± 1.2 with brimonidine (p = 0.004), and 13.8 mmHg ±
1.1 with latanoprost (p<0.001). After 2 weeks of oral indomethacin,
IOP was 17.1 ± 1.7 mmHg in the brimonidine-treated eyes (ns) and
12.8 ± 1.4 (p < 0.0001) in the fellow eyes treated simultaneously
with latanoprost (-8% and 31%, respectively; interdrug difference (p <
0.0001)).
Conclusions: Both topical drugs were associated with significant
reduction in intraocular pressure after 1 week, consistent with previously
published data. After 2 weeks of coadministration of the NSAID indomethacin,
the IOP reduction with brimonidine failed to attain statistically significance,
while the fellow eye receiving latanoprost in the masked randomized protocol
demonstrated further pressure reduction. These findings support the contention
that brimonidine may indeed act via stimulation of endogenous prostaglandin
production, which may in turn be inhibited by commonly used NSAIDs.