Abstract
Purpose :
Glucocorticoids (GCs) are frequently used to treat inflammation. Long-term use of topical or systemic GCs may cause GC-induced ocular hypertension/glaucoma. Many studies have shown that GCs cause pathological changes in the proximal outflow tissue [the trabecular meshwork (TM) and inner wall of Schlemm’s canal] which contribute to elevated outflow resistance and intraocular pressure (IOP). Clinical studies showed that in a subpopulation of patients who received microinvasive glaucoma surgeries (to remove/open TM or to bypass the TM), they still develop GC-induced ocular hypertension. Since these patients did not have proximal outflow tissue or their proximal outflow tissue was bypassed, it is likely that GC might have affected their distal outflow tissue which contributed to GC-induced ocular hypertension. In this study, we used our corneal rim perfusion culture model to determine the role of the distal outflow tissue in glucocorticoid-induced ocular hypertension.
Methods :
Paired human corneal rims were used. One rim was used for perfusion cultured directly; while the fellow rim was perfusion cultured after the TM was removed using a Kahook Dual blade. Both rims were treated with 100nM dexamethasone (DEX) after a stable baseline was established, and IOP was recorded using a computerized system.
Results :
We found that most of the corneal rims without the TM showed no DEX-induced IOP elevation compared to their fellow rims containing the TM. However, in a few pairs of corneal rims, the corneal rim without TM showed a higher IOP elevation after DEX treatment compared to the fellow rim with TM.
Conclusions :
The distal outflow tissue may play a role in GC-induced ocular hypertension, especially in eyes receiving microinvasive glaucoma surgeries. Further research is needed to determine morphology and gene expression changes in the distal outflow tissues in those ocular hypertensive eyes.
This abstract was presented at the 2024 ARVO Annual Meeting, held in Seattle, WA, May 5-9, 2024.