We investigated whether inflammatory biomarkers and stress are involved in the pathophysiology of idiopathic sensorineural hearing loss (ISHL).
Individual cohort study.
Two tertiary centers.
Forty-three ISHL and 10 non-ISHL patients seen in our ENT departments from 2004 to 2010 within a week from the onset of new symptoms and without steroid administration before visiting our departments.
Multiple audiologic evaluations, blood tests including leukocyte counts, natural killer cell activity (NKCA), interleukin 6 (IL-6), tumor necrosis factor, high-sensitivity CRP (hCRP), and the General Health Questionnaire were used to evaluate the systemic stress and inflammatory response.
Correlations between biomarkers and ISHL severity and prognosis were evaluated by statistical analysis.
In the ISHL patients, a neutrophil count above the reference range was associated with severe hearing loss and poor prognosis, and was accompanied by low NKCA and high IL-6. In the non-ISHL patients, these associations were not present. The abnormal neutrophil count was independent of preexisting vascular diseases. The abnormal counts responded to treatment and decreased into the reference range.
Neutrophil counts above the reference range of a facility will be a useful indicator of poor prognosis of ISHL. Synchronism of different types of NF-κB activation pathways could be required to cause severe ISHL. An NKCA decrease, an acute neutrophil count increase, and an IL-6 increase can induce NF-κB activation in the cochlea and cause severe ISHL. Further epidemiologic surveys should be conducted to evaluate whether stressful life events increase the risk of severe ISHL onset.
*Department of Otolaryngology, School of Medicine, Keio University, Tokyo; †Department of Otolaryngology, School of Medicine, Iwate Medical University, Iwate; and ‡Department of Otolaryngology, School of Medicine, Kyorin University, Tokyo, Japan
Address correspondence and reprint requests to Masatsugu Masuda, M.D., Ph.D., Department of Otolaryngology, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-0085, Japan; E-mail: firstname.lastname@example.org
Financial Disclosure: This research was supported by a Grant from the Ministry of Health, Labor and Welfare and a Grant-in-Aid for Young Scientists (B).
The authors disclose no conflicts of interest.