The role of IgE-mediated hypersensitivity in the development of otitis media with effusion

The potential mechanisms of IgE-mediated hypersensitivity in OME have been reviewed. Two important questions were addressed at the beginning of this manuscript: (1) is OME an allergic disease, or (2) is OME a complication of an allergic disease in another part of the respiratory system? In regard to the first question, recurrent OME is associated with allergic rhinitis in about one-third of the studied population. However, of the patients who do have allergic rhinitis, in the great majority of children the middle ear mucosa is not the target organ. Rather, there appears to be increasing evidence that with both nasal provocation and natural antigen provocation in children during a normal allergen season, eustachian tube function is altered by nasal allergy. Whether this is truly physiologic or an artificial phenomenon cannot be determined at this time, as it is not absolutely clear whether the nine-step eustachian tube function test currently performed is really a measure of eustachian tube dysfunction, despite its forming the basis of all studies published so far, although one must conclude from current data that allergic rhinitis can produce eustachian tube dysfunction; there have been no cases in these studies in which allergic rhinitis produced otitis media. However, eustachian tube dysfunction is one of the major precursors in the development of OME. We believe that the anatomic part of the upper respiratory tract involved in the IgE-mediated hypersensitivity is most likely the mucosa of the nasopharyngeal portion of the eustachian tube. Inasmuch as total nasal obstruction, at least in adults, does not produce eustachian tube dysfunction in the great majority of cases, it is proposed that eustachian tube dysfunction that follows nasal provocation and occurs during the normal allergy season does so as a result of the transport of mediators of inflammation from inflammatory cells in the nasal mucosa via the nasal mucociliary system to the nasopharyngeal orifice of the eustachian tube. The role of food allergy is still problematic, but this author suggests that there is some supportive evidence that food immune complexes, particularly with dairy products, may play a role, especially in the otitis- prone child under the age of 2 years. Although this article has not addressed the medical and surgical treatment of otitis media, it is necessary to conclude with the important caveat that once the eustachian tube is functionally obstructed and fluid forms in the middle ear cavity, inflammatory mediators in the fluid can produce not only permanent damage to the middle ear but can possibly traverse the round window membrane to cause permanent sensorineural hearing loss and speech and language delay. Therefore, it is incumbent on the treating physician, whether pediatrician, general physician, or otolaryngologist, to advise removal of this fluid by surgical means if medical therapy is ineffective.