[Intraocular pressure related to uveitis].

Glaucoma, a common and potentially devastating complication of intraocular inflammation, remains a considerable therapeutic challenge. During uveitis, breakdown of the blood-ocular barrier occurs with subsequent influx of proteins as well as inflammatory and immunocompetent cells. These mediators, including cytokines and chemokines, are considered to have a major impact on secondary elevated intraocular pressure (IOP). Several mechanisms are involved in the pathogenesis of inflammatory glaucoma, including obstruction of the trabecular meshwork by inflammatory cells and proteins, trabeculitis, formation of anterior and/or posterior synechiae, pupillary block, neovascularization, and anterior rotation of the lens-iris diaphragm. In addition, the use of steroids to control intraocular inflammation may cause secondary elevation of IOP.The management of uveitic glaucoma requires a careful balance between adequate anti-inflammatory therapy and appropriate lowering of IOP to prevent long-term visual loss. Despite the availability of many new medical treatments for both conditions, control of IOP in these patients remains challenging.