| The Diagnosis and Incidence of Allergic Fungal
Sinusitis JENS U. PONIKAU, MD; DAVID A. SHERRIS, MD; EUGENE B. KERN, MD; HENRY A. HOMBURGER, MD; EVANGELOS FRIGAS, MD; THOMAS A. GAFFEY, MD; AND GLENN D. ROBERTS, PHD |
In 1983, Katzenstein1 et al1 described allergic Aspergillus sinusitis as a newly recognized form of sinusitis. The diagnosis was made based on the histologic triad of (1) clumps or sheets of necrotic eosinophils; (2) Charcot-Leyden crystals (from degraded eosinophils); and (3) noninvasive fungal hyphae with morphology consistent with Aspergillus species within the nasal mucus. In 1989, Robson et al2 introduced the term allergic fungal sinusitis (AFS) because they identified a number of fungi thought to cause the same disorder. In 1990, Ence et al3 identified 5 different organisms responsible for AFS. Cody et al4 reported that Aspergillus species were responsible for only about 15% of cases of AFS in a large retrospective study. The incidence of AFS in cases of chronic rhinosinusitis (CRS) treated surgically has been approximately 6% to From the Department of Otorhinolaryngology (J.U.P., D.A.S., E.B.K.), Department of Laboratory Medicine and Pathology (H.A.H., T.A.G., G.D.R.), and Division of Allergy and Outpatient Infectious Disease and Internal Medicine (E.F.), Mayo Clinic Rochester, Rochester, Minn. Presented in part at the annual meeting of the American Rhinologic Society, September 6, 1997, San Francisco, Calif; the American Rhinologic Society at the Combined Otolaryngology Spring Meetings, May 11, 1998, Palm Beach, Fla; and at the 1999 Middle Section Meeting of the Triologic Society, January 24, 1999, Milwaukee, Wis. Address reprint requests and correspondence to Jens U. Ponikau, MD, Department of Otorhinolaryngology, Mayo Clinic Rochester, 200 First St SW, Rochester, MN 55905. |
(93%) of 101 consecutive surgical cases with CRS, based on histopathologic findings and culture results. Immunoglobulin E-mediated hypersensitivity to fungal allergens was not evident in the majority of AFS patients. Conclusion: The data presented indicate that the diagnostic criteria for AFS are present in the majority of patients with CRS with or without polyposis. Since the presence of eosinophils in the allergic mucin, and not a type I hypersensitivity, is likely the common denominator in the pathophysiology of AFS, we propose a change in terminology from AFS to eosinophilic fungal rhinosinusitis. Mayo Clin Proc. 1999;74:877-884
7%.1,4 Nasal polyps were found in 75% and asthma was found in 65% of the AFS cases described.5 Based on the clinical findings in 16 patients, Bent and Kuhn6 proposed 5 criteria for the diagnosis of AFS: (1) nasal polyposis; (2) allergic mucin; (3) computed tomographic (CT) scan findings consistent with CRS; (4) positive fungal histology or culture; and (5) type I hypersensitivity (atopy) diagnosed by history, positive skin test, or serology. Recently, deShazo and Swain7 described 7 patients with AFS in whom they applied similar diagnostic criteria, with the exception of atopy. The reason they excluded atopy as a diagnostic criterion for AFS was their review of the literature in which they found that only two thirds of patients tested had a positive skin test result to the fungi cultured. In addition, 1 of their 7 patients with the histologic diagnosis of AFS had no evidence of atopy. Cody et al4 also stated that the sensitivity and specificity of total and specific immunoglobulin E (IgE) and immunoglobulin G in AFS are unknown, and the usefulness of those tests in determining prognosis or efficiency of treatment is unknown. Both type I and type III hypersensitivity reactions (Gell and Coombs classification) have been postulated to play an instrumental role in the development of AFS. This hypothesis arose from the correlation of AFS with the pulmonary disorder termed allergic bronchopulmonary aspergillosis. Some of the reported cases of AFS demonstrated an elevated level of IgE antibodies specific for fungi. No other evidence, beyond speculation, exists |