allergic mucin

1442 Arch Pathol Lab Med—Vol 125, November 2001 Allergic Mucin With and Without Fungus—Lara & Gomez

Allergic Mucin With and Without FungusA Comparative Clinicopathologic Analysis

Jonathan F. Lara, MD; J. Daniel Gomez, MD

● Context.—Allergic mucin, a lamellated collection of in-spissated inflammatory debris, has been a hallmark of al-lergic fungal sinusitis. While its identification is a clue forpathologists to search for fungi, and directs clinicians to-ward specific therapy and follow-up, recent reports de-scribe cases with allergic mucin but without concomitantfungus. The absence of such organisms in otherwise typicalallergic mucin brings into question the role of fungi in al-lergic fungal sinusitis.

Objectives.—To study clinical and pathologic differencesbetween patients with allergic mucin in surgical nasal re-section specimens and to elucidate the role of fungus inallergic sinusitis.

Design.—Patients with histologic evidence of allergicmucin, with and without fungus, were identified and re-trieved from the surgical pathology files of a tertiary-careinstitution. The patients were separated into 2 groups foranalysis, and their clinical and pathologic findings werereviewed and compared.

Setting.—Tertiary-care institution.Patients.—All patients who underwent sinus mucosal re-

section between 1992 and 1998.Results.—Clinical presentation and radiographic findings

were similar in both groups. Incidence, age, and genderdistribution were similar to data reported previously. How-ever, the amount of allergic mucin was much greater in thegroup with fungus than in the group without fungus, whichto our knowledge is an unreported observation to date.

Conclusion.—The presence of allergic mucin is notunique to allergic fungal sinusitis, but rather is the resultof a process that could have other etiologies. While per-haps not always causative to the disease, the fungus con-tinues to fuel the process and is likely an entrapped by-stander. Allergic fungal sinusitis is more appropriatelytermed allergic mucinous sinusitis or eosinophilic mucin-ous rhinosinusitis.

(Arch Pathol Lab Med. 2001;125:1442–1447)

Sinonasal mycotic disease is classified into 5 distinctforms, each with unique clinical and histopathologic

features.1 The forms include acute fulminant sinusitis,chronic invasive sinusitis, noninvasive colonization (themycetoma or fungus ball), saprophytic infestation, and al-lergic fungal sinusitis.

Acute invasive sinusitis, also referred to by some as ful-minant invasive fungal sinusitis, is often seen in immu-nocompromised patients. Vascular invasion by fungi mayresult in mycotic thrombosis, and usually after presenta-tion with ocular involvement, intracranial extension, orboth, patients follow a downward-spiraling course withrapid deterioration, often resulting in death.

Chronic invasive fungal sinusitis, also known as indolentfungal sinusitis, is often seen in diabetic patients, immu-nocompetent individuals, and in endemic areas such asThe Sudan and Saudi Arabia. The histologic features areusually a collection of organisms with a surroundinggranulomatous, foreign body inflammatory response and

Accepted for publication June 28, 2001.From the Department of Pathology, Saint Barnabas Medical Center,

Livingston, NJ.This work was presented in part at the Annual Meeting of the United

States and Canadian Academy of Pathology, New Orleans, La, March2000.

Reprints: Jonathan F. Lara, MD, Department of Pathology, Saint Bar-nabas Medical Center, 94 Old Short Hills Rd, Livingston, NJ 07039 (e-mail: [email protected]).

demonstrable hyphae invading tissue. The designation ofinvasion rests on both morphologic evidence of tissue in-vasion and radiographic demonstration of bony erosion.This form of sinusitis distinctly lacks evidence of vascularinvasion by fungi, as seen with the acute fulminant typeof infection.

The fungal ball (mycetoma) is an extramucosal collectionof hyphae, usually in the maxillary antrum, which pro-vokes little or no host response. It is seen in immunocom-petent individuals who may have a prior history of sinusdisease, trauma, or a foreign body.

Allergic fungal sinusitis affects immunocompetent indi-viduals from the third to fifth decades of life. Allergic fun-gal sinusitis is usually noninvasive and follows a benignalbeit uncomfortable course. Patients present with a his-tory of chronic allergy, asthma, nasal polyps, and sinusitis,which is often refractory to medical therapy. Chest radio-graphs are often normal, but computed tomographic ex-aminations of nasal sinuses reveal areas of high attenua-tion and increased density. Bony erosion is rare, but re-modeling can occur. The disorder has a tendency to recurafter surgical evacuation. Characteristic allergic mucin isseen in histologic specimens and serves as an indicationto the surgeon and pathologist to be aware of and lookfor fungal organisms. Following surgical removal and di-agnosis, low-dose corticosteroid therapy and, in some cas-es, immunotherapy have been used as long-term adjunc-tive treatments with varying success.

Arch Pathol Lab Med—Vol 125, November 2001 Allergic Mucin With and Without Fungus—Lara & Gomez 1443

Saprophytic fungal infestation is the finding of fungalspores on mucous crusts of respiratory passages. The in-cidence is unknown, but investigators generally agree thatit is best separated from asymptomatic individuals withpositive fungal cultures, the incidence of which may beclose to 100%.2

In 1983, Katzenstein et al3 reported the histopathologicfindings from nasal resections of 7 patients found to havetenacious eosinophilic/basophilic material within whichthere were scattered fungal hyphae. They thought this wasa previously undescribed form of sinusitis that was his-tologically similar to mucoid impaction of the bronchus.Katzenstein et al proposed the term allergic aspergillus si-nusitis because of the similarity to mucoid impaction ofthe bronchus, which in turn is commonly associated withacute bronchopulmonary aspergillosis. Acute bronchopul-monary aspergillos is now referred to as acute broncho-pulmonary fungal disease. Prior to their report, Saferstein4

described the case of a woman with acute bronchopul-monary aspergillosis and nasal obstruction, and Millar etal5 reported 5 cases of sinusitis with histologic features ofacute bronchopulmonary aspergillosis. In 1989, Robson etal6 proposed the term allergic fungal sinusitis, because theyidentified dematiaceous fungi instead of Aspergillus spe-cies in their patient. Since then, there have been other re-ports describing various saprophytic fungal organisms incultures from allergic mucin. However, there have alsobeen reports describing allergic mucin without the pres-ence of fungi.7–12 These reports propose terms such as eo-sinophilic mucin rhinosinusitis, allergic mucin sinusitis withoutfungus, and allergic fungal sinusitis–like syndrome. The sig-nificance of allergic mucin devoid of fungus is currentlyunknown and there is a need for comparative clinicopath-ologic study of patients with allergic fungal sinusitis andan allergic fungal sinusitis–like syndrome.

MATERIALS AND METHODSCases with evidence of allergic mucin were accrued from sur-

gical pathology specimens of patients who underwent nasal re-section for chronic sinusitis at Saint Barnabas Medical Center,Livingston, NJ, between 1992 and 1998. Allergic mucin was con-firmed by hematoxylin-eosin examination. Its microscopic char-acteristics are of a thick, green to gray, lamellated aggregate ofdense inflammatory cells, mostly eosinophils and some neutro-phils, in a background of tenacious-appearing gray mucus, se-rum, and Charcot crystals. Macroscopically, it is chalky gray orsometimes black and gumlike in consistency. These criteria wereapplied to diagnose allergic mucin.

A total of 25 cases were identified out of 400 nasal surgicalresections reviewed. All tissue specimens were totally embedded,and the paraffin sections were reviewed with hematoxylin-eosinstain and further evaluated with Gomori methenamine-silver andperiodic acid–Schiff to try and identify fungal organisms. Sincethis study was retrospective, there was no deliberate intraoper-ative effort to ensure that all tissue was obtained without suctionor not put on absorbent gauze. The material submitted to thepathology department was processed similarly for all tissue spec-imens used in this study. All specimens were embedded totallyfor microscopic evaluation.

After histopathologic examination, which included completemicroscopic examination with step sections and histochemicalstains for fungus on all appropriate tissue submitted, patientswere separated into 2 groups, one with identifiable fungi and theother without fungi. Each group was analyzed for amount ofmaterial available for examination, including number of slides percase, number of slides with allergic mucin, extent of allergic mu-cin per slide (measured by ocular micrometry using a grid pat-tern of 1 mm2 and examined at 32.5 magnification for quanti-

tation), percent of involvement per slide (assessed by quantifyingmm2 of tissue on each slide relative to the mm2 involved by al-lergic mucin, averaged for each case), and a visual estimation ofabundance of fungal hyphae.

All patients’ histories, including hospital charts and doctors’office records, were obtained for review. The patients’ medicalhistories, preoperative impressions, intraoperative findings, ra-diographic studies, and follow-up reports were collated withineach group, and the groups were compared. Criteria for exclusionwere radiographic evidence of bone erosion and/or demonstra-tion of hyphae invading tissue. Culture results were also docu-mented when performed.

RESULTSOf the 400 cases reviewed during the 6-year time frame,

a total of 25 cases with allergic mucin were identified. Thisnumber represents an incidence of 6.25%. Of the 25 caseswith allergic mucin, fungal organisms were identified in10. Fifteen patients did not have fungal organisms in allsections reviewed. This finding was the basis for separa-tion into the 2 groups.

Clinical FindingsBoth groups were compared with respect to past med-

ical history, including history of atopy, asthma, physicalfindings, prior therapy, and intraoperative findings. Therewas no difference between the 2 groups, with an equaldistribution of a history of atopy in both. Both groupswere composed of young to middle-aged, immunocom-petent individuals. None of the patients had received priorantifungal or antibiotic therapy for their sinusitis. The av-erage age for the group with fungus was 41 years (agerange, 29–54 years) and for the group without fungus, 43years (age range, 23–66 years). Gender distribution wasequal for the group with fungus and showed a slight fe-male predilection for the group without fungus. The clin-ical presentation in both groups included nasal obstruc-tion and rhinorrhea, with durations ranging from severalmonths to years. There were no clinical signs of invasivedisease. Bilaterality was not a dominant finding in onegroup over the other. White blood cell differentials in bothgroups of patients were within normal limits. One patientfrom each group manifested peripheral eosinophilia (16%in a patient without fungus and 8% in a patient with fun-gus). Physical examinations in both groups of patients out-side the head and neck were normal. The preoperativeimpression was chronic sinusitis or allergic fungal sinus-itis equally in both groups.

Radiographic FindingsComputed tomographic scans of the paranasal sinuses

revealed identical findings in both groups (Tables 1 and2). These findings included total opacification, pansinus-itis, and polyp formation. All chest studies were normal.There was no clinical evidence of allergic bronchopulmo-nary fungal disease.

Intraoperative Findings

Both groups had similar intraoperative findings, includ-ing the identification of gray to black inspissated debris.This finding occasionally prompted the surgeon to sendtissue for fungal culture and, in one instance, for frozensection. However, there was no greater frequency for cul-ture request in one group over the other. Patients withfungi had more material submitted to pathology com-pared to the group without fungus; however, the proce-


Table 1. Allergic Mucin With Fungus: Clinical and Radiographic Findings

Case No. Age, y/Sex Clinical Impression Computed Tomographic Scan Results

12345

47/M40/M41/M29/M49/F

Nasal obstruction, polyps, deviated septumNasal obstruction, polypsNasal obstruction, polyps, rhinorrheaAnosmia, pain, polypsNasal obstruction, polyps, mucocele

UnavailableOpacification, expansion of sinus wallsSinus changes ‘‘consistent with fungal sinusitis’’Pansinusitis with opacificationOpacification of sinuses and fullness

6789

10

36/F29/F32/M53/F54/F

Nasal obstruction, polyps, rhinorrheaNasal obstruction, polyps, rhinorrheaNasal obstruction, polypsNasal obstruction, polypsPolyps, mucocele

Opacification of sinusesNear total opacification of sinusPansinusitis, deviated septumPolyps with obstruction and mucoceleOpacification with choanal polyp

Table 2. Allergic Mucin Without Fungus: Clinical and Radiographic Findings

Case No. Age, y/Sex Clinical Impression Computed Tomographic Scan Results

12345

46/F63/F47/F32/F35/M

Nasal obstructionNasal obstructionAnosmia, pain, rhinorrheaNasal obstructionRhinorrhea, pain

Opacification of all sinusesPansinusitis with opacificationOcclusion of osteomeatal complexPolyps and opacificationOpacification and air fluid levels in sinuses

6789

10

23/F47/M44/F41/F56/M

Asthma exacerbationNasal obstructionNasal obstructionNasal obstruction, rhinorrheaNasal obstruction, polyps

Pansinusitis and polypsPansinusitis with obstruction and polypsOpacification of all sinusesUnavailableOpacification and possible bone loss or erosion

1112131415

66/F29/F40/M30/F48/F

Nasal obstruction, rhinorrheaNasal obstructionNasal obstruction, headacheNasal obstruction, polypsNasal obstruction, polyps

Pansinusitis and opacificationPolypsNear complete opacificationPansinusitis, opacificationUnavailable

dure for obtaining specimens generally was the same inall cases.

Histopathologic Findings

Review of the macroscopic specimen descriptions fromboth groups revealed no distinguishing differences. Oc-casionally there was mention in the operative report ofblack or chalky gray material macroscopically, but this ob-servation was not unique to one group or the other. Theaverage number of slides prepared per case was roughlyequal for both groups. However, there were more slidesthat contained allergic mucin in the group with fungus(Figure 1) than in the group without fungus (Figure 2).The difference was 4.3 versus 3.1 slides on average percase. It was also apparent from the hematoxylin-eosin–stained sections that the group with fungi had much moreallergic mucin on each slide. The surface area of allergicmucin per slide was measured with an ocular micrometer,quantitated, and averaged for each case, then comparedbetween the 2 groups. There was a significant differencebetween the amount of allergic mucin in both groups. Thegroup with fungus had almost 10 times more allergic mu-cin in terms of surface area (measured in mm2) than thegroup without. Furthermore, allergic mucin covered 42.5%of the slide surface area on average in the group withfungus, compared to 25% for the group without (Tables 3and 4).

Fungi, when present, were seen singly or in small ag-gregates (Figure 3). Often they were not intact, but frag-mented. Usually they were present well within the tena-cious allergic mucin. Charcot crystals were seen in bothgroups.

COMMENT

Allergic mucin in nasal tissue specimens from patientswith chronic sinusitis serves as a clue for the otolaryngol-ogist to suspect and the surgical pathologist to look forfungal organisms. Since its description by Saferstein4 andthe histopathologic association of allergic mucin with mu-coid impaction of the bronchus and acute bronchopul-monary fungal disease, otolaryngologists and pathologistshave come to accept allergic fungal sinusitis as an entityand acknowledge that different species of fungus are as-sociated with this finding.13–15 These organisms includedifferent Aspergillus species, as well as many common de-matiaceous fungi. The most accepted form of therapy iscomplete surgical exenteration of diseased tissues, fol-lowed by low-dose steroids either locally or systemically.4

While this procedure may be curative in some cases, re-currence requiring repeat surgery is not uncommon. Im-munotherapy has been used with some success in limitedstudies, and while immunotherapy may be the treatmentof choice in the future, it is not currently standard prac-tice.16

The subsequent identification of allergic mucin withoutfungus has elicited interest with respect to histogenesisand pathogenesis. Is the absence of fungus indicative of aseparate entity, distinct from allergic fungal sinusitis?There is evidence, according to Ferguson,7 that this is in-deed the case. In that report, the author found significantclinical differences between the groups, most notably age,bilaterality, and allergy to aspirin, but no histopathologicdifference. We found no such clinical differences, althoughour study group was smaller and limited to our own cas-


Figure 1. Low-power view of tissue from a patient with allergic mucinwith fungus. Note the abundant allergic mucin (arrows) (hematoxylin-eosin, original magnification 340).

Figure 2. Low-power view of tissue from a patient with allergic mucinwithout fungus. Compare the amount of allergic mucin present (arrows)with that shown in Figure 1 (hematoxylin-eosin, original magnification340).

Figure 3. High-power view of fungal organisms (arrows) on Gomorimethenamine-silver stain. Note the sparse and fractured hyphae (orig-inal magnification 3400).

Table 3. Allergic Mucin With Fungus: PathologicFindings

Case No.No. ofSlides

WithMucin Area, mm (mm2) % on Slide

12345

1012542

97342

23 3 22 (506)15 3 10 (150)10 3 0.4 (4)4 3 3 (12)

17 3 5 (85)

7550252550

6789

10Average

336545.4

235444.3

19 3 18 (342)10 3 10 (100)20 3 15 (300)12 3 5 (60)2 3 2 (4)

159.90

502550255042.5

Table 4. Allergic Mucin Without Fungus: PathologicFindings

Case No.No. ofSlides

WithMucin Area, mm (mm2) % on Slide

12345

22322

22112

8 3 4 (32)0.2 3 0.1 (0.2)7 3 5 (35)1 3 0.9 (0.9)7 3 3 (21)

2525252525

6789

10

18244

12131

0.95 3 0.92 (0.82)6 3 4 (24)10 3 4 (40)3.4 3 3.1 (10.5)15.4 3 0.9 (15)

2525252525

1112131415

Average

8143

1985.5

723

1183.1

9 3 5 (45)1.98 3 1.44 (3)4 3 3 (12)0.95 3 0.63 (0.65)0.36 3 0.15 (0.5)16.03

252525252525.0

es. We did not evaluate aspirin sensitivity. Furthermore,Ferguson7 did not describe any histopathologic differencebetween the 2 groups. Ferguson proposed use of the termeosinophilic mucin rhinosinusitis when the mucin is devoidof identifiable fungus. It is descriptive of the morphology,but the term is noncommittal to the pathophysiology ofthe disorder, although Ferguson alluded to a form of sys-

temic immunologic dysregulation. The study by Ponikauet al2 is significant in that the investigators consistentlydemonstrated fungus in all of their patients with chronicrhinosinusitis, as well as in their control subjects. Theyproved that fungi can be identified in virtually all patientswith chronic rhinosinusitis if meticulous, painstaking ef-forts are taken to procure samples. This finding then rais-es the question of what role the fungus plays in the dis-order, since one could make the claim that fungal organ-isms are most likely present in the respiratory passages ofall people. They also propose replacement of the term al-lergic with eosinophilic, although they do not address indetail eosinophilic mucin without fungus as a true entity.

It is plausible that some individuals react more intenselyto the same allergens compared to others, eliciting a great-er and more volatile response. Therefore, could we be see-ing a 2-part response? The first part, common to bothgroups, an allergic response, elicits an eosinophilic reac-tion producing the eosinophilic mucin. The second, a re-sponse to the antigens of entrapped fungal organisms,promotes a self-amplifying inflammatory response.17 Thisscenario could explain the abundance of eosinophilic mu-cin in one set of patients and scantiness of it in the other.The likelihood of sampling is a legitimate thought; how-ever, our study was a retrospective investigation and de-void of bias. No special attention was given to procuringas much sample as possible, and the procedure for obtain-ing specimens was the same for patients from both


groups, since in most cases allergic fungal sinusitis wasnot a preoperative diagnosis in either group. The tenacityof the mucin may be an issue, allowing more watery mu-cin to escape into suction and necessitating manual re-moval of the more tenacious debris-containing fungus.Surgical resection was usually complete and the speci-mens were always completely embedded, so sampling er-ror in the laboratory is unlikely. In essence, the findingsof our study truly reflect the experience in a communitypractice setting, one without any particular skew.

The incidence of allergic mucin in our study is similarto that reported by others.3,11,14 The fact that, for the mostpart, studies from different institutions describe similartypes of patients in both groups with similar clinical pre-sentations, radiographic findings, and responses to ther-apy, favors a single pathogenesis in different stages of de-velopment and/or with different degrees of response.While some authors have noted a significant difference inage between the 2 groups,7 the age difference in our serieswas much less significant. This difference could be due toidentification and treatment at a later stage of the disorder.

The immunologic mechanism behind allergic fungal si-nusitis has been thought to be a combined type I and typeIII immune hypersensitivity response, mainly because ofthe similarity to mucoid impaction of the bronchus andacute bronchopulmonary fungal disease.11,15 Recent stud-ies question this thinking, although the original mecha-nism is still assumed to be of an allergic nature.2,18 Typeof response notwithstanding, the result elicits an inflam-matory reaction with mucosal edema, a copious release ofeosinophils, subsequent impaction, and stasis of the re-active material, leading to what pathologists have identi-fied as allergic mucin. It would follow that if untreated,the process would continue to expand, attracting and en-trapping more of the allergic mucin. In the process, thisexpansion could, and most likely does, entrap whatevermay find its way through the nasal passages, promotinga self-amplifying inflammatory response.17 Entrapped ma-terial could include saprophytic fungal organisms, such asthe dematiaceous fungi, which are normally found in soiland plants. It is easy to surmise that such normally non-pathogenic, low-virulence organisms may accidentallygain access to respiratory passages and become entrappedin the tenacious and proliferating allergic mucin. There-fore, one must consider the possibility that the organismis merely a bystander and not the instigator of the process,which could explain why these organisms are often seenas broken and fragmented hyphae that are scattered spo-radically in a vast and copious expanse of allergic mucinand why there does not seem to be a stark difference inresponse to therapy from patients in either group.

The findings of our study call attention to a strikingsimilarity between both groups and support the findingsof other studies. The fact that both groups have similarclinical and radiographic findings and that the groupwithout fungus had significantly less allergic or eosino-philic mucin are otherwise undescribed observations thatsupport the theory that this malady may represent thesame disorder either at a different stage or with a differentdegree of response. The paucity and sporadic distributionof fungal organisms in our cases raise the question ofwhether the organism is truly of etiologic significancefrom the start, later as the process escalates, or merely abystander incorporated into an expansive trap of tena-cious and laminated allergic debris. The course of therapy

is, as of now, similar for both groups mainly because ofthe noninvasive nature of the disorder. While the presenceor absence of fungal hyphae in allergic mucin does notseem to affect therapy, immunotherapy notwithstanding,it is important for us to realize that we are most likelydealing with an immunologic rather than infectious dis-order.11 The identification of this histologically intriguingmucin is important information for the clinician to helpmonitor these patients and properly advise them with re-spect to adjuvant medical therapy, including low-dose ste-roid treatment, and to make them aware of the possibilityof recurrence and need for follow-up. Understanding thenature of the disorder will lead physicians in the correctdirection with respect to future therapeutic options.

In summary, we present a comparative clinicopatholog-ic study of 25 patients with allergic/eosinophilic mucinseparated into 2 groups, one with and the other withoutfungus. We found no significant clinical or radiographicdifferences between the 2 groups and no differences in theappearance of the allergic mucin. There was, however, asignificant difference in the amount of allergic mucin be-tween the 2 groups, a finding that to our knowledge hasnot been described in the literature to date. Because of theretrospective nature of the study, there was no specificeffort to try and obtain all resected tissues from patients,which therefore led to similar methods of procurement inboth groups. The amount of material obtained in bothgroups would reflect the type of specimen obtained inroutine practice. In spite of not going through painstakingefforts to obtain as much tissue as possible, there was stillan overwhelming amount of eosinophilic mucin in thegroup of patients with identifiable fungal organisms com-pared to the group without fungi. The fact that all clinicaland radiographic findings were essentially the same inboth groups leads us to believe that the presence of fungimay not be as important to the initiation of the disorderas once suspected. However, the identification of classicallergic or eosinophilic mucin may be the pathognomonicfinding that dictates therapy. Furthermore, the amount ofsuch mucin may be a hint as to whether fungi will beidentified histologically and may provide perspective asto the stage and extent of the disorder. A controlled, pro-spective comparative study is necessary to validate the ob-servations presented in this article. If our observations arecorrect, the amount of mucin identified at surgery mayindicate patient susceptibility and possibly even predis-position to recurrence. Also, the mere presence of allergic/eosinophilic mucin alone may be the sole feature neededto initiate a specific treatment protocol for what is nowcalled fungal sinusitis. In essence, the fungus may not nec-essarily be the initial cause of the disorder, but merely alater catalyst or an entrapped passenger/victim of an ex-pansive process of proliferating tenacious and lamellateddebris eliciting more production of allergic mucin. Follow-ing such thought, we agree that consideration should begiven to changing the name of the entity from allergicfungal sinusitis to eosinophilic or allergic mucin sinusitis.The relation to mucoid impaction of the bronchus andacute bronchopulmonary fungal disease should also be re-evaluated.

The authors gratefully acknowledge Tracy Murray for photo-graphic assistance and Samantha M. Lara for assistance in thepreparation of this study and manuscript.


References1. Ferguson BJ. Definitions of fungal rhinosinusitis. Otolaryngol Clin NorthAm.

2000;33:227–235.2. Ponikau JU, Sherris DA, Kern EB, et al. The diagnosis and incidence of

allergic fungal sinusitis. Mayo Clin Proc. 1999;74:877–884.3. Katzenstein AL, Sale SR, Greenberger PA. Pathologic findings in allergic

aspergillus sinusitis: a newly recognized form of sinusitis. Am J Surg Pathol. 1983;7:439–443.

4. Saferstein BH. Allergic bronchopulmonary aspergillosis with obstruction ofthe upper respiratory tract. Chest. 1976;70:788–796.

5. Millar JW, Johnston A, Lamb D. Allergic aspergillosis of the maxillary sinuses[abstract]. Thorax. 1981;36:710.

6. Robson JMB, Benn RAV, Hogan PG, et al. Allergic fungal sinusitis presentingas a paranasal sinus tumor. Aust N Z J Med. 1989;19:351–353.

7. Ferguson BJ. Eosinophilic mucin rhinosinusitis: a distinct clinico-pathologicentity. Laryngoscope. 2000;110:799–813.

8. Allphin AL, Strauss M, Abdul-Karim FW. Allergic fungal sinusitis: problemsin diagnosis and treatment. Laryngoscope. 1991;101:816–820.

9. Bent JP, Kuhn FA. Allergic fungal sinusitis/polyposis. Allergy Asthma Proc.1996;17:259–268.

10. Cody DT, Neel HB, Ferreiro JA, Roberts DG. Allergic fungal sinusitis: theMayo Clinic experience. Laryngoscope. 1994;104:1074–1079.

11. Corey JP, Delsupehe KG, Ferguson BJ. Allergic fungal sinusitis: allergic,infectious or both? Otolaryngol Head Neck Surg. 1995;113:110–119.

12. Ramadan HH, Quraishi HA. Allergic mucin sinusitis without fungus. AmJ Rhinol. 1997;11:145–147.

13. Kupferberg SB, Bent JP, Kuhn FA. Prognosis for allergic fungal sinusitis.Otolaryngol Head Neck Surg. 1997;117:35–41.

14. Torres C, Ro JY, El-Nagger AK, et al. Allergic fungal sinusitis: a clinico-pathologic study of 16 cases. Hum Pathol. 1996;27:793–799.

15. DeShazo RD, Swain RE. Diagnostic criteria for allergic fungal sinusitis. JAllergy Clin Immunol. 1995;96:24–35.

16. Mabry RL, Mabry CS. Allergic fungal sinusitis: the role of immunotherapy.Otolaryngol Clin North Am. 2000;33:227–235.

17. Folker RJ, Marple BF, Mabry RL, et al. Treatment of allergic fungal sinusitis:a comparison trial of postoperative immunotherapy with specific fungal antigens.Laryngoscope. 1998;108:1623–1627.

18. Manning SC, Holman M. Further evidence for allergic pathophysiology inallergic fungal sinusitis. Laryngoscope. 1998;108:1485–1496.

allergic mucin

Documents