Tip of the Month
Publishing date: September 2012
Tip Editors: Ann Hoste, John Salmon and John Thygesen
Tip reviewer: Roger Hitchings
The Science behind the Tip
The enzyme carbonic anhydrase is present in the corneal endothelium where it is involved in fluid transport (1). It thus determines corneal hydration. Studies have been done to verify whether inhibition of corneal carbonic anhydrase by dorzolamide (1) (Trusopt® and Cosopt®) might have any clinical impact.
It appears that the drug can safely be used in eyes with normal corneas, where it had no significant effects on either corneal thickness or endothelial cell count after 1 year of therapy (2).
However, application of dorzolamide can increase corneal thickness in patients with cornea guttata (3), where the functional reserve of the endothelium is lower. What's more, the drug can cause irreversible corneal decompensation in patients with severe endothelial compromise (4).
Caution is thus required in patients with corneal endothelial dysfunction due to primary endothelial disease, intraocular inflammation, full thickness graft or any other cause. The same probably holds true for the other topical carbonic anhydrase inhibitor brinzolamide (Azopt® and Azarga®).
Contributor: Ann Hoste, Antwerp
1. Srinivas SP, Ong A, Zhai CB, et al. Inhibition of carbonic anhydrase activity in cultured bovine corneal endothelial cells by dorzolamide. Invest Ophthalmol Vis Sci. 2002;43:3273-8.
2. Lass JH, Khosrof SA, Laurence JK, et al. A double-masked, randomized, 1-year study comparing the corneal effects of dorzolamide, timolol, and betaxolol. Dorzolamide Corneal Effects Study Group. Arch Ophthalmol. 1998;116:1003-10.
3. Wirtitsch MG, Findl O, Kiss B, et al. Short-term effect of dorzolamide hydrochloride on central corneal thickness in humans with cornea guttata. Arch Ophthalmol. 2003;121:621-5.
4. Konowal A, Morrison JC, Brown SV, et al. Irreversible corneal decompensation in patients treated with topical dorzolamide. Am J Ophthalmol. 1999;127:403-6.