Emerging Insights Into Revision Surgery for Allergic Fungal Rhinosinusitis: Contemporary Perspectives on Risk Factors and Management

Allergic fungal rhinosinusitis (AFRS), a subtype of chronic rhinosinusitis with nasal polyps (CRSwNP), is characterised by potent fungal antigen‐induced inflammation, eosinophilic mucin, elevated postoperative recurrence rates and a poorer prognosis compared to other subtypes, emphasising the critical need for research into recurrence mechanisms. AFRS recurrence involves complex interactions. Pathophysiologically, fungal‐induced Th2 cytokine production leads to eosinophil aggregation, mucus hypersecretion and fungal‐specific IgE production. Eosinophilic mucin fosters Staphylococcus aureus overgrowth, releasing enterotoxins as superantigens to amplify inflammation. Type 3 sinonasal immune response defects in AFRS lead to decreased expression of antimicrobial peptides (AMPs) regulated by IL‐17 and IL‐22, thereby impeding AMP‐mediated fungal clearance. Epithelial barrier disruption by IL‐4/IL‐13 further increases fungal colonisation. AFRS combined with asthma perpetuates Th2 inflammation and amplifies eosinophil inflammation to promote fungal colonisation. Concomitant aspirin‐exacerbated respiratory disease (AERD) amplifies eosinophilic inflammation to facilitate fungal colonisation through dysregulated cyclooxygenase/lipoxygenase pathway. Meanwhile, anatomical abnormalities (e.g., concha bullosa, nasal septum deviation) and surgical factors (e.g., prior sinus surgery, middle turbinate mismanagement, insufficient corticosteroid use) further contribute to recurrence. Biomarkers such as eosinophils, IgE, eosinophilic mucin and IL‐17A predict recurrence by reflecting inflammatory activity. For refractory AFRS, long‐term control often requires antifungal therapy, biologics and immunotherapy. Comprehensive management targeting underlying mechanisms and optimising surgical and medical strategies can improve AFRS outcomes and reduce revision surgery rates.