Steroids in susceptible individuals can cause a clinical condition similar to primary open-angle glaucoma. Five percent of the population are high steroid responders and develop an intraocular pressure (IOP) elevation of more than 15 mm Hg above baseline. IOP elevation may occur as early as 1 day to as late as 12 weeks after intravitreal triamcinolone in 20–65% of patients. On average, 75% of eyes with steroid implants require IOP-lowering therapy at some point within 3 years of follow-up. The exact mechanism of steroid-induced glaucoma is not totally understood, but decreased trabecular meshwork outflow is regarded as the main cause of IOP elevation. High-risk patients who receive steroids should be monitored closely and if they develop elevated IOP, steroids with lower potency or steroid-sparing agents should be used. The IOP usually returns to normal within 2–4 weeks after stopping the steroid. About 1–5% of patients do not respond to medical therapy and need surgery. Trabeculectomy, trabeculotomy, shunt surgery, and cyclodestructive procedures are among the methods employed. Removal of residual sub-Tenon or intravitreal steroids may help hasten the resolution of the steroid response. Early results with anecortave acetate, an analog of cortisol acetate with antiangiogenic activity, in controlling IOP have been promising.

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