Abstract
Background: To evaluate the effect of human leukocyte antigen (HLA) on hearing outcome in patients suffering from autoimmune hearing loss (AIHL). Materials and Methods: The diagnosis of AIHL was essentially based on clinical symptoms, such as recurrent, sudden, fluctuating, or quickly progressing (<12 months) sensorineural hearing loss (uni-/bilateral). The molecular typing of HLA alleles was achieved by using polymerase chain reaction procedures. Patients underwent a tapering schema of steroid treatment and audiometric features were recorded. A logistic regression model was used to identify which HLA typing alleles were statistically significant in patients’ response to treatment. Results: Forty patients with AIHL were found to be carriers of HLA B27, B35, B51, C4, C7, and DRB1*04 alleles. No statistically significant influence of HLA B27, B35, B51, C4, C7, DRB1*04 HLA alleles typing was detected for the prognosis of AIHL. In these patients, the onset of AIHL was mainly progressive (53.8%), 29.2% of them had moderate hearing loss, and most of the cases had both bilateral hearing loss (62.5%) and downsloping audiogram (40%). Conclusion: The presence of HLA B27, B35, B51, C4, C7, and DRB1*04 alleles had no significant effect on a favorable outcome of AIHL. However, larger samples of patients are necessary in order to improve the knowledge about the HLA influence on the clinical course of AIHL.
Highlights
Autoimmune hearing loss (AIHL) is a specific clinical entity and may be related to the reaction antigen—autoantibody, the activation of the complement system, a direct action of cytotoxic T cells, or immune complex-mediated damage [1]
The frequency of human leukocyte antigen (HLA) B27, B35, B51, C4, and C7 was lower compared to the control group (Table 1), except for HLA DRB1*04, which was slightly higher than 10% of the healthy control group
The major histocompatibility complex and HLA associations have rarely been investigated for AIHL cases
Summary
Autoimmune hearing loss (AIHL) is a specific clinical entity and may be related to the reaction antigen—autoantibody, the activation of the complement system, a direct action of cytotoxic T cells, or immune complex-mediated damage [1]. After the activation of the immune response and the release of interleukin (IL)-1β, immune-competent lymphocytes, and immunoglobulins can cause an excessive response involving cytokines, tumor necrosis factor, and interferon-gamma into the inner ear [2]. Other forms of HL have been identified to be immune-mediated in origin, such as (i) unilateral cases, in which serological nonspecific inner ear autoantibodies were found to be highly positive [6]; (ii) fluctuating hearing, which makes differential diagnosis between
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