The term allergic fungal rhinosinusitis (AFRS) has been used to describe a clinicopathological entity characterized by: Nasal polyposis Crust formation Atopy Sinus cultures with fungus present Lack of tissue invasion on pathological analysis  Safi rstein  fi rst recognized the similarity between this entity and allergic bronchopulmonary aspergillosis in 1976. Since that time, a great deal of research has been devoted to the understanding, pathophysiology, and treatment of this disease. Despite these eff orts, a large number of questions still remain unanswered and serve as the nidus for future clinical research. The presence of fungus within the paranasal sinuses has a broad range of ramifi cations, ranging from the benign presence of saprophytic fungal growth to invasive fungal rhinosinusitis. The presence of fungus on cultures, the AFRS hallmarks of bony expansion, and radiological evidence of invasion led many clinicians to believe that AFRS was an early stage on the spectrum of invasive fungal rhinosinusitis [12, 25]; hence, an aggressive surgical stance was adopted as the primary mode of management of AFRS. Mc-Guirt and Harrill  stated in 1979, "Without question, the treatment of paranasal sinus aspergillosis is surgical-the key to successful surgical treatment is the removal of diseased mucosa and aeration and drainage of the involved sinus." Such evidence urged surgeons to perform radical surgeries such as lateral rhinotomies, craniofacial resections, and facial degloving procedures to extirpate the diseased mucosa . In 1988, Sarti et al.  reported a case of paranasal sinus aspergillosis that exhibited expansion into the anterior cranial fossa and sella turcica. The patient was treated with a craniofacial resection, and unfortunately died secondary to a pulmonary embolus in the postoperative period. However, on fi nal pathological examination, no evidence of tissue invasion was noted. Numerous studies have subsequently shown AFRS to be a separate clinical entity from invasive fungal rhinosinusitis and have implicated atopy as one of the causative factors. Manning and Holman  showed that in vitro and in vivo allergy to fungal antigens were important to the pathophysiology of AFRS and that the predominance of eosinophil-derived infl ammatory mediators in in vivo tissue specimens diff erentiated AFRS from other forms of chronic rhinosinusitis. These studies gave further credence to the fact that AFRS is an immunological disease rather than an entity on the spectrum of infectious/invasive fungal disease. The change in mindset from invasive disease to immunologically based disease has altered the treatment algorithms for AFRS from that of extensive surgery and antifungal therapy to mucosa-sparing surgery with adjunctive corticosteroids .
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