Thank you for your inquiry.
Through the years, the literature has been "peppered" with articles attempting to draw a relationship between atopy, elevated levels of IgE, and autoimmune hypoacousia (autoimmune hearing loss). In my opinion, the relationship between elevated levels of IgE and atopy has not been firmly documented, but there are articles which have alluded to such a relationship. For your convenience, I have copied below two examples including the abstracts of the articles in question. They will contain a decent bibliography if you wish to research this issue further.
Thank you again for your inquiry and we hope this response is helpful to you.
Toubi E, Ben-David J, Kessel A, Halas K, Sabo E, Luntz M:The Annals of Otology, Rhinology, and Laryngology [2004, 113(6):445-449]
Different immune disorders are involved in the development of sudden sensorineural hearing loss (SSNHL). This includes a wide spectrum of immune-mediated disorders such as immune complexes, production of autoantibodies to the inner ear proteins, production of anticardiolipin (aCL) antibodies, and cellular immune defects. Some studies have also found an elevation of total IgE levels and a type 1 immune reaction. Our objective was to establish the association of "idiopathic" SSNHL (ISSNHL) with various autoantibodies, and to analyze the persistence over time of existing aCL and anti-beta2 glycoprotein 1 (anti-beta2 GP1) antibodies in such patients. Finally, we sought to establish a possible association between ISSNHL and total IgE elevation and whether this elevation is due to a specific type I immune reaction. In this prospective follow-up study, 51 patients considered as having ISSNHL were compared with 35 age-sex matched healthy volunteers over a 3-year period. All participants were tested for serum antinuclear antibodies, antithyroid antibodies, aCL, and rheumatoid factor. All patients who were positive for aCL antibodies were reanalyzed 3 months later for aCL antibody persistence and for the coexistence and persistence of anti-beta2 GP1 antibodies. Skin prick tests were performed in patients in whom total IgE was elevated. Antinuclear antibodies were positive in 9 of 51 (17%) and antithyroid antibodies in 11 of 51 (21%) ISSNHL patients, as compared to 1 of 35 (3%) and 2 of 35 (6%), respectively, in the control group. Rheumatoid factor was positive in 6 of the 51 patients (12%) and in none of the control group. Positive aCL antibodies were present in 16 of 51 patients (31%), 6 of whom (12%) were also positive for anti-beta2 GP1 antibodies. Three months later, aCL antibodies persisted in 7 patients (14%), and anti-beta2 GP1 in 4 patients. Only 2 of the normal subjects (6%) were positive for aCL antibodies, which persisted in only 1 of them (3%). The level of total IgE was elevated in 14 of 51 patients (27%), in contrast to 3 of 35 controls (8%). Six of them (42%) demonstrated a positive skin test to at least 1 allergen, but only 3 presented allergy symptoms. Our findings support the reported existence of multiple immune-mediated disorders in patients with ISSNHL. The lack of aCL antibody persistence in as many as half of our patients strongly suggests that transient phenomena (eg, viral infection) may trigger aCL antibody activity. However, the presence of aCL antibodies, especially in conjunction with anti-beta2 GP1 antibodies, suggests that in some patients, SSNHL is included among the rare symptoms of the antiphospholipid syndrome
Erol Keles, et al : The role of allergy in the etiopathogenesis of idiopathic sudden sensorineural hearing loss
European Archives of Oto-Rhino-Laryngology May 2013, Volume 270, Issue 6, pp 1795-1801
To evaluate the role of allergy in the etiopathogenesis of sudden hearing loss using cytokine profile, allergic parameters, and lymphocyte subgroups, a total of 31 patients aged between 30 and 62 years (mean age: 42.48 ± 15.86 years) with the diagnosis of sudden hearing loss were enrolled in the study between 2008 and 2011. The control group comprised 30 age-matched adult subjects accepted as clinically healthy individuals living in the same region with comparable socioeconomic parameters. The patient and the control group were questioned for history of allergy. Lymphocyte subgroups in the peripheral blood were evaluated using Becton–Dickinson monoclonal CD4, CD8, CD19, and CD23 antibodies. In the patient and control groups, the levels of IFN- ?, IL4, IL10, and total IgE were measured and compared between the groups. Skin test was used for detection of inhaler allergens in the patient and the control groups, and specific IgE tests were performed using the RAST method for food allergens. The Spearman’s rho correlation, the unpaired t test, the Mann–Whitney U test, and the Shapiro–Wilk test were used to determine the differences between the groups. The limit for statistical significance was p < 0.05. When the patient and the control group were compared, the differences between CD4, CD23, IL4, IL10, and IgE were statistically significant. On analyses of the patients’ serum samples, strongly positive correlations were determined between IgE and CD23, IL10, IL4; IL4 and IL10, CD23, CD4; IL10 and CD23, CD4 (Spearman rho, p = 0.000), while a weakly positive correlation was found between IgE and CD4 (Spearman rho, p = 0.020). A correlation between IFN-? and CD4 was weakly negative (Spearman rho, p = 0.040). The total IgE levels were estimated to be above the normal reference ranges (0–100 IU/ml) in 25.8 % of the cases in the patient group. History of allergy was found in 61.9 % of the patients. The results of this study substantiate the role of allergy in the etiopathogenesis of sudden hearing loss. We think that during the diagnostic work-up of these patients allergy should be interrogated seriously, necessary tests should be performed, and allergy should be considered in the decision-making process of the treatment of sudden hearing loss.
Phil Lieberman, M.D.