Cataract Induced by Glucocorticoids

Glucocorticoids (GCs) remain a cornerstone therapy for noninfectious uveitis and autoimmune disorders; however, chronic administration is strongly associated with sight-threatening complications, particularly glucocorticoid-induced cataracts (GIC). This comprehensive review synthesizes current evidence on the molecular pathogenesis, epidemiological patterns, and clinical management of GIC. Epidemiological analyses indicate that over 50% of patients receiving systemic corticosteroids for >60 days develop ocular complications, with cataract formation (36%) and glaucoma (16%) representing the predominant sequelae. Histopathologically, GIC manifests as posterior subcapsular opacities, mechanistically linked to oxidative stress, epithelial-mesenchymal transition (EMT), vimentin dysregulation, Na⁺/K⁺-ATPase inhibition, apoptosis, and endoplasmic reticulum (ER) stress. Risk stratification models identify cumulative GC dose (>20,000 mg/m² prednisolone equivalents), treatment duration (>6 months), and administration route (oral > topical > intravitreal) as critical determinants of cataractogenesis. Although early-stage GIC is clinically silent, progressive opacification leads to debilitating visual acuity loss, photophobia, and impaired quality of life. Current interventions encompass antioxidants, molecular targeting strategies, advanced drug delivery systems, and glucocorticoid-sparing agents. Through systematic integration of epidemiology, pathogenesis, and therapeutic advances, we aim to resolve the GC therapeutic paradox and provide robust frameworks for future clinical management.