Although a penetrating wound appears to be a predisposing and required condition for the development of SO, not all patients who have an ocular injury develop SO. This suggests a possible genetic predisposition to the development of SO.
Genetic risk factorsThere may be a possible genetic predisposition to the development of SO. Human leukocyte antigen (HLA) types reported in SO include HLA-11,[4] HLA-DR4/DRw53, HLA-DR4/DQw3,[27] HLA-DRB1*O4, -DQA1*03, and -DQB1*04.[14] In addition, the HLA-DRB1*04-DQA1*3 haplotype is a marker of a more severe clinical phenotype in SO, with increased disease susceptibility in British and Irish patients.[28] Recent evidence has shown that cytokine gene polymorphisms are markers for disease severity in SO.[29]Polymorphisms that result in the upregulation of proinflammatory cytokines are predicted to create a proinflammatory environment in the eye and worsen the severity of inflammation. These markers were also associated with disease recurrence. Analyzing …
