Currently, the pathophysiology of allergic fungal sinusitis (AFS) is postulated to be similar to that of allergic bronchopulmonary fungal disease (a term replacing bronchopulmonary aspergillosis). Manning and colleagues have suggested that several interrelated factors and events lead to the development and perpetuation of allergic fungal sinusitis (AFS). First, an atopic host is exposed to fungi, theoretically via normal nasal respiration, which provides the initial antigenic stimulus. An initial inflammatory response ensues as the result of both a Gell and Coombs type I (IgE-mediated) and type III (immune complex–mediated) reaction, causing subsequent tissue edema. The resulting obstruction of sinus ostia, which may be accentuated by anatomic factors such as septal deviation or turbinate hypertrophy, results in stasis within the sinuses. This creates an ideal environment for further proliferation of the fungus, thus increasing the antigenic exposure to which the host is allergic.
At some point, the cycle becomes self-perpetuating, resulting in the eventual product of this process, allergic mucin, the material that fills the involved sinuses of patients with allergic fungal sinusitis (AFS). Accumulation of this debris obstructs the involved sinuses and propagates the process.
The production of this allergic mucin and its eventual clinical, histologic, and radiographic characteristics are unique to allergic fungal sinusitis (AFS) and serve as a hallmark of the disease. Grossly, allergic fungal mucin is thick, tenacious, and highly viscous. Its color may vary from light tan to brown or dark green, as depicted in the images below. Its characteristic gross appearance has resulted in the use of such descriptive terms as peanut butter and axle grease when referring to allergic fungal mucin.


In a study of 74 patients, White et al indicated that in cases of allergic fungal sinusitis, younger patients and African Americans are more likely to suffer bony erosion, suggesting that these individuals have a more severe inflammatory response in the disease. [15]
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Left middle meatus with suctioning of thick allergic mucin from the ethmoid bulla in the center of the picture; the end of the suction is in the inferior portion of the picture.
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The viscosity of a thick allergic mucin being suctioned from the nasal cavity and vestibule in a patient with allergic fungal sinusitis.
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View just inside the nasal vestibule showing diffused polyposis extending into the anterior nasal cavity and vestibule; the septum is on the right, and the right lateral vestibular wall (nasal ala) is on the left. The polyps all are in the center. The polyps almost hang out of the nasal vestibule.
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A 15-year-old boy with allergic fungal sinusitis causing right proptosis, telecanthus, and malar flattening; the position of his eyes is asymmetrical, and his nasal ala on the right is pushed inferiorly compared to the left.
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A 9-year-old girl with allergic fungal sinusitis displaying telecanthus and asymmetrical positioning of her eyes and globes.
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Coronal CT scan showing extensive allergic fungal sinusitis involving the right side with mucocele above the right orbit and expansion of the sinuses on the right.
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Typical view of a middle meatus in a patient with allergic fungal sinusitis with expansion of the ethmoid complex and extension of the middle turbinate more inferiorly. This is a postoperative view.
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Coronal CT scan showing typical unilateral appearance of allergic fungal sinusitis with hyperintense areas and inhomogeneity of the sinus opacification; the hyperintense areas appear whitish in the center of the allergic mucin.
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Coronal MRI showing expansion of the sinuses with allergic mucin and polypoid disease; the hypointense black areas in the nasal cavities are the actual fungal elements and debris. The density above the right eye is the mucocele. The fungal elements and allergic mucin in allergic fungal sinusitis always look hypointense on MRI scanning and can be mistaken for absence of disease.
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Immediate postoperative 30° angled view showing the complete removal of polyps with a widened frontal sinus recess superiorly and widened ethmoid cavity in the mid portion. The middle turbinate is on the right, pushed against the septum. The lateral nasal wall is on the left.
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Fungal ball in the right maxillary sinus.
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Fungal debris being removed from the ethmoid complex. A suction device is seen in the right lower corner of the picture.
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Allergic mucin, fungal debris, and polyps are shown after removal from the patient. The scale is in inches.
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Coronal CT scan showing the postoperative view following removal of disease after significant disease recurred on both the right and left sides of the nasal cavity and sinuses; mild mucosal thickening of all involved sinuses is present, with some moderate thickening of the left maxillary sinus. All disease, even the lateral mucocele, was removed or drained endoscopically.
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Two-week postoperative endoscopic picture showing polypoid thickening already in the ethmoid cavities while the patient was still on tapering steroids; on the left is the lateral nasal wall. The right shows the middle turbinate next to the septum.
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A polypoid recurrence in the center of the ethmoid cavity. The septum is on the left.