ASSOCIATION BETWEEN MATERNAL CHRONIC INFLAMMATORY BOWEL DISEASE DURING PREGNANCY AND CONGENITAL CATARACTS IN OFFSPRING: AN IN-DEPTH RETROSPECTIVE MULTICENTER COHORT STUDY

Congenital cataract is a major cause of pediatric visual impairment and blindness, characterized by lens opacification present at birth or during early infancy. Its incidence ranges from 1 to 15 per 10,000 live births depending on geographic and diagnostic factors. If not detected and treated early, congenital cataracts can severely disrupt visual development, leading to amblyopia, nystagmus, and strabismus. This retrospective cohort study investigated the association between maternal inflammatory bowel disease (IBD), including Crohn’s disease and ulcerative colitis, during pregnancy and the risk of congenital cataracts in offspring. A total of 150,000 mother–child dyads from international healthcare databases in the United Kingdom, United States, Canada, Scandinavia, and Europe were analyzed over the period 2000–2025. Among them, 2,500 pregnancies (1.67%) were complicated by maternal IBD. After extensive adjustment for sociodemographic, behavioral, obstetric, environmental, pharmacological, and genetic confounders, maternal IBD was associated with a significantly increased risk of congenital cataracts in offspring (adjusted OR 1.88; 95% CI: 1.48–2.39; p<0.001). Stratified analyses demonstrated that disease activity during early gestation conferred the greatest risk, with IBD flares in the first trimester showing the strongest association (OR 2.45), followed by the second trimester (OR 2.10), while third-trimester activity exhibited a weaker but still significant effect. Importantly, when IBD remained well controlled throughout pregnancy without active flares, the risk of congenital cataracts was largely attenuated (OR 1.10). Standard maintenance therapies, including 5-aminosalicylic acid agents and anti-TNF biologics, were not associated with a meaningful increase in risk, whereas prolonged or high-dose systemic corticosteroid exposure during disease exacerbations showed a moderate risk elevation (OR 1.68). These findings suggest that maternal systemic inflammation, rather than IBD diagnosis or baseline therapy alone, plays a central role in disrupting fetal lens development. The results highlight the importance of preconception disease optimization, close inflammatory monitoring during pregnancy, multidisciplinary care, and targeted neonatal ophthalmologic screening in high-risk infants. Future prospective studies integrating molecular and placental biomarkers are warranted to clarify causal mechanisms linking maternal inflammation to fetal ocular development.

Ҳали таржима қилинмаган