Pediatric cataracts are a significant cause of childhood blindness globally.
1 A better understanding of the etiologies for pediatric cataracts is crucial for ensuring optimal clinical outcomes for these vulnerable patients. Uveitis is one of the most common ophthalmologic conditions affecting pediatric eyes and is known to be associated with an increased risk for cataract formation.
2,3 Other factors that could contribute to this risk for cataract formation include the use of steroid eye drops and other immunosuppressive medications commonly prescribed for uveitis management. While the exact mechanisms remain unknown, certain animal models have demonstrated that immunosuppressive agents can adversely affect the growth of lens epithelial cells, potentially leading to cataract formation.
4 Additionally, intraocular surgeries could lead to a postoperative increase in inflammation within the vitreous.
5 Such a postoperative increase in inflammation could then potentially cause damage to lens proteins through oxidative stress. Although inflammation may be one of the important links between uveitis and cataract formation, the actual pathophysiological mechanism behind cataract development among patients younger than 18 years with uveitis remains unknown. However, as pediatric patients are known to have immature blood-ocular barriers,
6 it is possible that this immaturity may play a crucial role in initiating or perpetuating intraocular inflammatory reactions, subsequently leading to cataracts. This is because the eye is normally an immune-privileged site due to the blood-ocular barrier. However, when this barrier is disrupted, it can allow infiltration of inflammatory cells, leading to intraocular inflammatory reactions or uveitis. This has potential implications for future cataract development, supported by previous laboratory studies suggesting that oxidative stress may be integral to cataract formation.
7 For example, Lesiewska et al
8 demonstrated higher concentrations of oxidative products like superoxide dismutase among cataract eyes compared with noncataract eyes. It is also possible that the combination of other factors, such as inherited pro-cataract mutations in the
SOX2 gene, could further increase the susceptibility of patients younger than 18 years in developing cataracts, especially after uveitis (eFigure 5 in Supplement 1). However, these hypotheses remain speculative, and as of now, no study, to our knowledge, has definitively established a conclusive association between all of these mediating factors in the context of uveitis and cataract development.