The Diagnosis and Incidence of Allergic Fungal Sinusitis

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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

Objective: To reevaluate the current criteria for diagnosing allergic fungal

sinusitis (AFS) and determine the incidence of AFS in patients with chronic

rhinosinusitis (CRS).

Methods: This prospective study evaluated the incidence of AFS in 210

consecutive patients with CRS with or without polyposis, of whom 101 were

treated surgically. Collecting and culturing fungi from nasal mucus require

special handling, and novel methods are described. Surgical specimen

handling emphasizes histologic examination to visualize fungi and

eosinophils in the mucin. The value of allergy testing in the diagnosis of

AFS is examined.

Results: Fungal cultures of nasal secretions were positive in 202 (96%) of

210 consecutive CRS patients. Allergic mucin was found in 97 (96%) of 101

consecutive surgical cases of CRS. Allergic fungal sinusitis was diagnosed

in 94

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 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

AFS = allergic fungal sinusitis; CRS = chronic rhinosinusitis; CT = computed

tomographic; IgE = immunoglobulin E; RAST = radioallergosorbent test

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

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