Atopic keratoconjunctivitis: From molecular mechanisms to clinical implications

Atopic keratoconjunctivitis (AKC) is a chronic, bilateral inflammatory disease of the ocular surface that primarily affects young adults with a history of atopic dermatitis, asthma, or allergic rhinitis. AKC is considered the most severe form of ocular surface allergy and can result in serious complications that threaten vision, such as corneal ulceration, neovascularization, and scarring. Genetic predisposition, through regulatory genes that impact skin barrier function, immune system regulation, and allergic responses, plays a crucial role in the development and severity of AKC. Recent research has highlighted the roles of epithelial barrier dysfunction, gastrointestinal and eyelid/conjunctival dysbiosis, Th2-driven cytokines, and eosinophilic inflammation in disease perpetuation. Diagnosing AKC requires a high level of suspicion, careful integration of clinical signs, and a thorough assessment of coexisting atopic conditions. Management is often challenging and involves a stepwise approach, beginning with topical antihistamines and mast cell stabilizers, progressing to corticosteroids, calcineurin inhibitors, and, in severe or refractory cases, systemic immunosuppressive therapy or surgical intervention. Novel therapies, including biologics targeting IL-4 and IL-13, show promise in selected patients. A multidisciplinary approach and long-term follow-up are crucial for minimizing complications and preserving visual function. We provide a comprehensive update on the epidemiology, clinical manifestations, immunopathogenesis, diagnostic approach, and therapeutic strategies for AKC.