Allergic fungal rhinosinusitis: current theories and management strategies

The combination of nasal polyposis, crust formation, and sinus cultures yielding Aspergillus was first noted in 1976 by Safirstein,1 who observed the clinical similarity that this constellation of findings shared with allergic bronchopulmonary Aspergillosis (ABPA). Eventually this disease came to be known as allergic fungal rhinosinusitis (AFS). As clinical evidence of AFS accumulated, controversy regarding its etiology, pathogenesis, natural history, and appropriate treatment naturally emerged. Despite past and current efforts, many of these controversies remain incompletely resolved, but continuing clinical study has illuminated some aspects of the disease and has led to an improved understanding of AFS and its treatment. Fungi associated with the development of AFS are ubiquitous and predominantly of the dematiaceous family. The eosinophilic host response to the presence of these fungi within the nose and paranasal sinuses gives rise to those clinical manifestations of the disease (nasal polyps, expansile mucocele formation, allergic fungal mucin, etc.). Exposure alone to these fungi, however, appears to be insufficient to initiate the disease. At the present time it is likely that initiation of the inflammatory cascade leading to AFS is a multifactorial event, requiring the simultaneous occurrence of such things as IgE-mediated sensitivity (atopy), specific T-cell HLA receptor expression, exposure to specific fungi, and aberration of local mucosal defense mechanisms. A variety of treatment plans for AFS have emerged, but the potential for recidivism remains well recognized, ranging from 10% to nearly 100%, suggesting the need for continued study of this disease and fueling present controversy. This article is intended to review current data and theories regarding the pathophysiology of AFS, as well as the role of various surgical and nonsurgical forms of therapy.