Ear, Nose & Throat Journal2023, Vol. 102(2) 83–84© The Author(s) 2022Article reuse guidelines:sagepub.com/journals-permissionsDOI: 10.1177/01455613221104502journals.sagepub.com/home/ear
We commend Varghese et al. for “mandating a different outlook” in their recent article on eosinophilic otitis media (EOM). Their statements are supported by medical literature dating back to 1931, reported by Proetz, Shambaugh, Zhang, Draper, Doyle, Pelikan, Ojala, McMahan, Tomonaga, Nsouli, Lasisi, Nguyen, Tian, Sobol, Smirnova, Shim, Smirnova, Luong, and ourselves. Allergy causes EOM and it responds to immunotherapy.
Keywords
otitis media, eosinophil, allergy, middle ear, immunotherapy
Eosinophils have been associated with allergic disease for over a century. In addition to the presence of eosinophils in chronic middle ear effusions, Varghese’s minor criteria for the diagnosis of eosinophilic otitis media (EOM)—resistance to conventional treatment for otitis media, bronchial asthma, and nasal polyposis—are all consequences of allergy.1 Corso’s systematic review of 3,010 papers provides an in-depth explanation of pathophysiologic factors linking allergy to increased risk of middle ear inflammation.2 Varghese et al.’s account (PMID: 32744905) that middle ear effusion (MEE) is rich in ECP, confirming the findings that we (Hurst and Venge) reported in 1993.3
The presence of eosinophilic cationic protein (ECP) proves local eosinophilic degranulation. In 23 patients with chronic MEE, mean effusion ECP levels of 329μg were elevated to 5–12 times greater than normal serum values. Effusion ECP correlated with positive allergy tests but not with serum IgE or serum ECP levels—indicating a localized process.3 These works should help dispel the question as to the causal relationship of atopy/allergic hypersensitivity to chronic OME.
We later reported that among 46 patients (62 ears), of whom 95% had confirmation of allergy by positive intradermal skin testing (IDT) or RAST, levels of ECP in the middle ear could reach 5 to 20 times those found in an asthmatic lung.4 While concurrently elevated MEE myeloperoxidase (MPO) indicates the presence of neutrophils, eosinophil cationic protein was elevated only in allergic patients. Middle ear ECP was also a more sensitive indicator of allergy than total serum IgE.
In 2000, we (Hurst and Venge) studied OME effusions of 97 children, 81% with atopy, for presence of eosinophils (ECP), neutrophils (MPO), and mast cells (tryptase).5 Allergic children had significantly higher ECP and tryptase in middle ear fluids than non-atopic children (P < .001). Elevated ECP again strongly indicated allergy: MEE ECP had a positive predictive value of 97.1% and a diagnostic sensitivity of 86%. Total serum IgE did not differ between atopics and nonatopics. (P = .28 = NS)5 As stated: “the concept of the “unified airway” closely links IgE-mediated hypersensitivity with allergic rhinitis/chronic sinusitis, asthma, and otitis media with effusion.” In only 29% of the 118 with OME was ear disease the sole manifestation of their allergy.6 Table 4
Histologic, epidemiologic, and clinical studies based on objective allergy testing6 have, firstly, established that the majority of OME patients are atopic and, secondly, demonstrated that all the mediators necessary for a Th2 allergic response are present in the middle ear.5
Varghese et al. used systemic or topical glucocorticoids—classic short-term treatments for allergic asthma and nasal polyps. Optimal therapy for an allergic condition is successful hypo-sensitization immunotherapy.7 Eosinophilic otitis media simply represents the most viscous end of the spectrum of OME. Hurst and Denne reported that immunotherapy cured OME and prevented recurrence in 85% of 89 patients.1
Allergen immunotherapy based on allergen testing6 is the only immune-modulating treatment available for safe, simplistic, and long lasting relief for patients suffering from atopic diseases such as allergic rhinoconjuctivitis, allergic asthma,8 and OME.1 Eosinophilic otitis media is an allergic disease.
Sincerely,
David Hurst, MD, PhD,
Bruce Gordon, MD,
Alan McDaniel, MD,
Diego Saporta, MD
The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
The author(s) received no financial support for the research, authorship, and/or publication of this article.
David S. Hurst https://orcid.org/0000-0002-1216-9861
1 Department of Otolaryngology, Tufts University, Boston, MA, USA
2 American Academy of Otolaryngologic Allergy, Harvard U. Dept of Otolaryngology
3 American Academy of Environmental Medicine, University of Louisville, KY, USA
4 Pan American Society of Otolaryngology, Private Practice, Associates in ENT & Allergy, Springfield, NJ, USA
Corresponding Author:
David S. Hurst, MD, PhD, Otolaryngology, Tufts University, 800 Washington, Boston, ME 04038, USA.
Email: oto72hurst@gmail.com
