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Uveitis (intraocular inflammatory diseases) is the cause of approximately 10% of severe visual handicap in the US. It can be of infectious or autoimmune aetiology and can be localised primarily to the anterior chamber (anterior uveitis), the posterior segment of the eye (posterior uveitis) or involve the entire globe (panuveitis). Pathology derives from the presence of inflammatory cells in the optical axis. In the treatment of uveitic conditions, the main therapeutic goals are to downregulate the immune response, preserve the integrity of the ocular architecture and eventually eliminate the inciting uveitogenic stimuli. Current therapy is based on topical or systemic corticosteroid, with or without second line agents, such as cyclosporin A or antimetabolites. The serious adverse effects of these drugs are the impetus for development of less toxic and more specific therapies for uveitis. In this review, we present a brief discussion of ocular immunology, the pathophysiology of uveitis and emerging strategies in the treatment of these blinding diseases.
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Egwuagu et al. (2000) studied this question.
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