Corticosteroids and glaucoma risk

Corticosteroids (glucocorticoids), used frequently as potent anti-inflammat ory agents, increase the risk of glaucoma by raising the intraocular pressu re (IOP) when administered exogenously (topically, periocularly or systemic ally) and in certain conditions of increased endogenous production (e.g. Gu shing's syndrome). Approximately 18 to 36% of the general population are co rticosteroid responders. This response is increased to 46 to 92% in patient s with primary open-angle glaucoma (POAG). Patients over 40 years of age an d with certain systemic diseases (e.g. diabetes mellitus, high myopia) as w ell as relatives of patients with POAG are more vulnerable to corticosteroi d-induced glaucoma. The association of corticosteroid-induced ocular hypert ension in other conditions which are considered as risk factors for glaucom a (racial origins, hypertension, migraine, vasospasm) is likely but not ful ly established. The proposed mechanism of corticosteroid-induced glaucoma includes morpholo gical and functional changes in the trabecular meshwork system and is simil ar to the pathogenesis of POAG. Trabecular cells exposed to corticosteroids in vitro show endoreplication of nuclei, an increase in cell size and exce ssive production of an approximately 56kD glycoprotein, identified as myoci lin and transcribed by the GLC1A gene. Induction of ocular hypertension aft er corticosteroid administration depends on the specific drug, the dose, th e frequency of administration and the corticosteroid responsiveness of the patient. The risk of corticosteroid-induced glaucoma can be minimised with judicious use of corticosteroids, as well as education of patients and medi cal practitioners. New treatment modalities include modified steroids and n onsteroidal anti-inflammatory agents that will have less effect on the elev ation of IOP.