Uveitis associated with elevation of intraocular pressure – what is the optimal therapy?

Uveitis is the fifth leading cause of blindness in developed countries. The ocular complications of uveitis are not only related to the inflammation itself but also result from glucocorticosteroid therapy, which is the mainstay of treatment. Glucocorticosteroids may be used as eye drops; periocular, intravitreal, suprachoroidal injections; or systemically. One of the most serious side effect of glucocorticosteroid therapy is glucocorticosteroid-induced ocular hypertension (SIOH), which can lead to the glucocorticosteroid-induced secondary glaucoma (SIG). If untreated, SIG may cause irreversible blindness. Therefore, it is important to monitor intraocular pressure (IOP) in the course of glucocorticosteroid therapy. One of the risk factors for SIG is the use of glucocorticosteroids with high anti-inflammatory potency, such as prednisolone or dexamethasone. On the other hand, glucocorticosteroids with lower potency, such as loteprednol or fluorometholone, show a low risk of SIOH. Such response to glucocorticosteroids occurs in approximately 35% of the population; these individuals are referred as “steroid-responders”. If SIG is diagnosed, it is necessary to modify the glucocorticosteroid treatment to maintain a balance between controlling inflammation and normalizing the IOP. β-blockers and carbonic anhydrase inhibitors are the first-line anti-glaucoma drugs in the treatment of SIG in patients with uveitis. α-2 agonists are classified as second-line drugs. Prostaglandins and hyperosmotic agents are of limited use, and miotics are contraindicated in uveitic patients.

The aim of the article is to present the classification and contemporary knowledge about the pathophysiology and pharmacological management of uveitis associated with increased IOP.