In commenting on these findings, the investigators pointed out that use of prostaglandin analogues, such as latanoprost, can result in reductions in the CCT with chronic use of more than 18 months (mean decreases, from 5 µm to 15 µm) during the first six to 12 months of treatment.
These decreases are reversible with cessation of the drug. It is thought that up-regulated matrix metalloproteinases may promote likely negligible degradation of the ocular surface matrix. Rho kinase inhibitors, such as netarsudil, can cause thinning of the CCT; however, the investigators noted that thinning has occurred only in eyes with pathology associated with corneal edema in which the thinning is an approach to normalization of CCT.
The possible mechanisms include promotion of endothelial cell proliferation and migration,, suppressed apoptosis, and faster corneal wound healing.
“The greater reduction in the CCT in our fixed-combination group may indicate that the effects of each drug on the CCT are additive. However, the magnitude of the effect seen for the combination group in this study (1.2%) is likely of negligible clinical significance,” Dr. Wisely concluded.