The goal of the present study is to elucidate the pathogenic mechanisms that determine the ocular involvement in some systemic diseases.
We have studied 45 patients with ocular diseases and concomitant systemic diseases (systemic lupus erythematosus-SLE, ankylosing spondylitis, Reiter syndrome, juvenile rheumatoid arthritis, Sjögren syndrome). The patients studied have been compared with a control group represented by 20 healthy individuals. In each case we have determined the serum levels of the following humoral markers: the C3 complement fraction, circulating immune complexes, autoantibodies (antinuclear autoantibodies, anti-double stranded DNA autoantibodies, anti-smooth muscle autoantibodies, anti-neutrophilic cytoplasm autoantibodies, anti-cardiolipin autoantibodies, anti-SSA, anti-SSB, rheumatoid factor).
The autoantibodies detected in certain cases of uveitis suggest the existence of an autoimmune etiology; the antibody titers have been high in some severe cases of rheumatic uveitis, especially in patients with ankylosing spondylitis. We have found that there is a correlation between the presence and the titer of certain autoantibodies, and the onset and evolution of the disease. Specifically, the antinuclear autoantibodies may be considered a predictive factor for the development of chorio-retinopathy of SLE. Uveitis mediated by immune complexes has been seen in rheumatoid arthritis, ankylosing spondylitis, and SLE, these being the same systemic diseases where there is an important pathogenic role of immune complexes.
The abnormal immunologic function, that was observed in the ocular inflammatory diseases studied, may be synthesized by the association between two immunopathologic phenomena; both of them are finalized by the non-self transformation of the antigens linked to various eye structures. These are represented by autoimmunity (of humoral, cellular, or mixed type), and the immediate type III hypersensitivity reaction. This study provides important data regarding the involvement of autoimmune diseases in the etiology of ocular diseases.