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Endogenous uveitis encompasses a diverse group of non-infectious ocular inflammatory disorders, the aetiopathogenesis of which is both complex and incompletely understood.1–3 While the precise immune mechanisms undoubtedly differ for each condition, nearly four decades of evidence derived from both animal and human studies strongly supports the current belief that antigen-activated T lymphocytes are central to the initiation and maintenance of uveitis in most patients. B lymphocytes and antibodies, circulating proinflammatory cytokines such as tumour necrosis factor α, and components of the innate immune system, most notably complement4 5 and pattern recognition receptors,6 also appear to play a greater or lesser role in some settings. Initiation factors in patients with uveitis are only now beginning to be elucidated, but emerging evidence suggests at least some role for external or environmental triggers, including psychological stress,7–9 infection,3 10 11 trauma12 and immune-mediated food intolerance.13–15 A genetic predisposition also appears to be important in some patients given the well-documented link between disease development and expression of specific human leucocyte antigens (HLAs) in a number of disorders.16 17
The ‘exogenous factor’ perhaps most important in controlling endogenous uveitis is patient compliance. Although not studied systematically in patients with ocular inflammation, poor compliance is well known to limit the therapeutic efficacy of both systemic18 and topical ocular medications.19 In addition, patients often, with or without their doctors' knowledge, add or substitute medications or treatments, some of which may interfere with conventional medicines when taken concurrently. Smith and colleagues, for example, found that 42% …
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