Evaluation – Questions & answers
[expand title=”What is the diagnosis?” tag=”strong”]Sympathetic ophthalmia (SO) is a rare, bilateral, non-necrotizing, granulomatous uveitis that occurs after ocular trauma or surgical procedures to one eye threatening sight in the fellow eye. The integrity of the inciting eye leads to an autoimmune reaction against the exposed ocular antigens in the injured eye as well as in the sympathizing eye.[/expand] [expand title=”What is/are the main predisposing factors for this condition?” tag=”strong”]Penetrating eye injury or eye surgery.[/expand] [expand title=”What are the most common presenting signs and symptoms?” tag=”strong”] Bilateral eye pain, panuveitis and decreased vision in the non affected eye.[/expand] [expand title=”What is the pathophysiology of sympathetic ophthalmia?” tag=”strong”]Ocular antigens are normally sequestered within the eye behind the blood-retinal barrier, thus preventing their exposure and detection from the systemic immune system. However, in the event of a penetrating injury or surgical procedure this barrier is breached and ocular antigens leak into the systemic environment. The tissue damage alerts and recruits antigen presenting cells, such as macrophages and dendritic cells to the site, which phagocytose these released ocular antigens. They are then processed for HLA class II presentation to CD4+ helper T cells. Usually these CD4+ helper T cells won’t recognize ocular protein peptides because autoreactive T cells have been deleted in the thymus. However, in rare instances, autoreactive T cells can be generated due to the ocular peptide resembling similar peptides encountered previously during infections. This process is known as molecular mimicry. When this occurs T cells that respond to the ocular antigen undergo clonal expansion and migrate to the site of inflammation.
Inflammatory cytokines such as IL-1 and TNF-a cause the blood retinal layer to become more permeable allowing CD4+ helper T cells to penetrate the usually impervious blood-retinal barrier in the damaged eye. The inflammatory response continues to recruit more immune cells overwhelming the mechanisms that maintain the immune privilege status of the eye and further damage continues. Due to the inflammatory status impacting on the unaffected eye, these ocular antigen-specific T cells enter the fellow eye causing retinal damage and the condition of sympathetic opthalmia. [/expand] [expand title=”What can be done to prevent this from occurring?” tag=”strong”]Treatment with immunosuppressive therapy.[/expand]
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