Abstract
Glucocorticoid (GC)-induced ocular hypertension and secondary iatrogenic open-angle glaucoma are serious side effects of GC therapy. Its clinical presentation is similar in many ways to primary open-angle glaucoma, including increased aqueous outflow resistance and morphological and biochemical changes to the trabecular meshwork (TM). Therefore, a large number of studies have examined the effects of GCs on TM cells and tissues. GCs have diverse effects on the TM, altering TM cell functions, gene expression, extracellular matrix metabolism, and cytoskeletal structure. Some or all of these effects may be responsible for the increased outflow resistance associated with GC therapy. In contrast to GCs, several different classes of steroids appear to lower IOP. Additional research will help better define the molecular mechanisms responsible for GC-induced ocular hypertension and steroid-induced IOP lowering activity.
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