Abstract
Sympathetic ophthalmia is a rare bilateral granulomatous inflammation that follows accidental or surgical insult to the uvea of one eye. Onset of sympathetic ophthalmia can be insidious or acute, with recurrent periods of exacerbation. Clinical presentation shows mutton-fat keratic precipitates, choroidal infiltrations, and Dalen-Fuchs nodules. Histopathology reveals diffuse or nodular granulomatous inflammation of the uvea. Prevention and treatment strategies for sympathetic ophthalmia are currently limited to two modalities, enucleation of the injured eye and immunosuppressive therapy, aimed at controlling inflammation. The etiology and pathophysiology of the disease is still unclear but is largely thought to be autoimmune in nature. Recent insight on the molecular pathology of the disease as well as developments in imaging technology have furthered both the understanding on the autoimmune process in sympathetic ophthalmia and the targeting of prevention and treatment strategies for the future.
Highlights
Despite the long history of sympathetic ophthalmia, much is still to be elucidated about the pathophysiology of the rare, bilateral, non-necrotizing granulomatous uveitis [1]
Sympathetic ophthalmia presents with posterior inflammation that may include optic nerve swelling, exudative retinal detachment, and anterior granulomatous inflammation with mutton-fat keratic precipitates in severe and/or chronic recurrent cases [1,2]
Furusato et al demonstrated elevated CXCL11, CCL19, IL-18, and IL-23, as well as high IL-17, in granulomatous infiltrates of sympathetic ophthalmia, and increased IFN-γ and CCL17 levels in non-granulomatous inflammatory infiltrates [46]. These cytokine and chemokine expression profiles establish the predominance of M1 macrophages within granulomas and Dalen-Fuchs nodules and the key presence of Th1 cells in nongranulomatous infiltrates, providing a framework to understand the contribution of specific inflammatory cell subsets to the pathogenesis of sympathetic ophthalmia
Summary
Despite the long history of sympathetic ophthalmia, much is still to be elucidated about the pathophysiology of the rare, bilateral, non-necrotizing granulomatous uveitis [1]. Increased knowledge on sympathetic ophthalmia and other ocular inflammatory diseases may have sharpened diagnostic ability and, to some degree, may account for the lower incidence levels reported in more recent literature.
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