Allergic fungal rhinosinusitis (AFRS or AFS in the literature) is a hypersensitivity disease of the paranasal sinuses afflicting patients who are immunocompetent albeit with a history of atopy and allergic rhinitis to fungi. The disease process begins as the fungi become entrapped within the nasal cavity, presumably because of ostium obstruction or mucociliary disorder, and initiate a hypersensitive immune response. Just as with the other forms of fungal sinusitis, A. fumigatus is the most common etiological agent associated with AFRS (Table 1.1).
Traditionally it has been believed the mechanistic process underlying this disorder was IgE and IgG (Type I and Type III) mediated (Bent and Kuhn, 1997; Stewart and Hunsaker, 2002). However, as mentioned earlier, recent observations concerning patients who exhibit AFRS without increased IgE levels have questioned this mechanism, and has led to the suggestion of renaming AFRS to "eosinophilic fungal rhinosinusitis" to account for this disparity (Ponikau et al., 1999; Braun et al., 2003; Corradini et al., 2003). It is important to note that AFRS is most likely a multifac-toral process, though the decisive factor is almost certainly the patients' hyperimmune response to the fungus (Stewart and Hunsaker, 2002). The production of an allergic mucin develops, which contains high levels of eosinophils, Charcot-Leyden crystals (by-products of eosinophilia) and non-invasive hyphal bodies (Washburn, 1994; Houser and Corey, 2000). The mucin is a thick, greenish-brown, viscous material that traps the fungi, not allowing it to be cleared from the sinuses. This leads to a cyclical immune response as more eosinophilia occurs in response to the fungus, thereby overwhelming the nasal cavity and adding to the chronicity of this disease. Additionally, as AFRS is a form of CRS, nasal polyposis is almost always associated with patients suffering from this disease.
Strong parallels have been made between AFRS and allergic bronchopulmonary aspergillosis (ABPA), a hypersensitivity disorder limited to the lungs and specific to A. fumigatus. ABPA is a late-phase allergic inflammatory response occurring in patients diagnosed with asthma or Cystic Fibrosis (Knutsen, 2003). In patients with ABPA, hyphal Aspergillus can be found in the airspaces and parenchyma of the lungs. Increased IgE levels, as well as systemic and pulmonary eosinophilia, characterize the disease. The disease can have a number of clinical presentations including hemoptysis (in which patients cough up large amounts of blood) as well as bronchietasis (a condition where large amounts of fibrous tissue are formed within the lungs). In humans the CD4+ T-cell population in ABPA
produces increased levels of IL-4, -5, -10, and -13 (Grünig, 1997; Houser and Corey, 2000; Knutsen, 2003). This response increases class switching of B cells to stimulate IgE production as well as maturation and activation of eosinophils, resulting in skewing the immune response towards a Th2 reaction. Additionally there is increased adhesion molecule (VCAM) production, an increase in mast cell degranulation, and eventually anergy to A. fumigatus is reached via delayed type hypersensitivity (DTH).
Recent findings by Shah and others examined the incidence of AFRS in ABPA patients. Ninety-five patients with diagnosed ABPA were assessed radiologically for AFRS. Of those 95, 22 patients scored positive for having fungal rhinosinusitis (23%). All patients demonstrated positive skin tests and had increased total and specific IgE levels. In addition, allergic mucin was seen in all patients, with five patients having hyphal development within the paranasal region (Shah et al., 2001).
Therapy for AFRS includes reduction of fungal burden and restoration of normal sinus drainage. To achieve the latter goal, abnormal soft tissue masses are extirpated with endoscopic surgery, however, reports suggest surgery alone results in recurrence of the diseased state (Washburn, 1994; Kupferberg et al., 1997; Marple et al., 2002). In a study put forward by Kupferberg, 19 of 24 patients who had undergone surgery for AFRS suffered a recurrence of symptoms postsurgery (Kupferberg et al., 1997). Similar studies noted patients who were given fungal immunotherapy postopera-tively were more likely to experience remittance than those patients who received no immunotherapy (Marple et al., 2002). In addition to surgery and antifungal treatments, long-term topical nasal corticos-teroids are also utilized, though steroid therapy is thought to increase the likelihood of a secondary fungal invasion (Washburn, 1994).
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