Allergic fungal sinusitis (AFS) is a chronic non?invasive disease.
Hypersensitive immune response is usually initiated by allergens of
filamentous fungi Aspergillus, Penicillium, Cladosporium, Fusarium,
Bipolaris, Curvularia and Alternaria. AFS is a clinical and immune analogue
of the allergic bronchopulmonary aspergillosis (ABPA) as the sinus exudate
resembles that of the bronchoalveolar lavage (BAL) in ABPA. Patients with AFS
are usually immunocompetent, atopic and males. The most common symptoms are
headache, fullness in the paranasal sinuses, and difficult breathing through
the nose. Clinically, there is a chronic mucosal inflammation and
histopathologic finding shows allergic mucin and eosinophils. Specific
staining methods, Gomori?s Methenamine Silver (GMS) or periodic acid?Schiff
(PAS), are used for microscopic visualisation of hyphae, which are, in
addition to the isolated fungi, most reliable evidence of AFS. Computerized
tomography (CT) of paranasal sinuses shows the areas of hyperdensity. In
cases where AFS is complicated by the erosion of bone tissue, discontinuation
of the sinus bone wall can be seen. Significant laboratory finding, which
correlate highly with the AFS, are high immunoglobulin E (IgE) antibodies
specific for fungi, detected by the skin prick test or in serum. Treatment is
often surgical, and after removal of the allergic mucin, therapy involves
oral and nasal corticosteroids, immunotherapy and locally applied
antimycotics (with verified fungal etiology). During treatment, the
total/specific IgE is monitored - concentration increases with the
development of AFS, and decreases during the improvement process. Knowledge
of the pathophysiological mechanisms of AFS is scarce, and represents the
focus of further research in order to define an optimal diagnostic and
therapeutic approach.
Visual loss in the setting of allergic fungal sinusitis: pathophysiology and outcome
