TY - JOUR
T1 - Correlations of inflammatory biomarkers with the onset and prognosis of idiopathic sudden sensorineural hearing loss
AU - Masuda, Masatsugu
AU - Kanzaki, Sho
AU - Minami, Shujiro
AU - Kikuchi, Jun
AU - Kanzaki, Jin
AU - Sato, Hiroaki
AU - Ogawa, Kaoru
PY - 2012/9
Y1 - 2012/9
N2 - HYPOTHESIS: We investigated whether inflammatory biomarkers and stress are involved in the pathophysiology of idiopathic sensorineural hearing loss (ISHL). STUDY DESIGN: Individual cohort study. SETTING: Two tertiary centers. PATIENTS: 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. INTERVENTION: 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. MAIN OUTCOME MEASURES: Correlations between biomarkers and ISHL severity and prognosis were evaluated by statistical analysis. RESULTS: 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. CONCLUSION: 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.
AB - HYPOTHESIS: We investigated whether inflammatory biomarkers and stress are involved in the pathophysiology of idiopathic sensorineural hearing loss (ISHL). STUDY DESIGN: Individual cohort study. SETTING: Two tertiary centers. PATIENTS: 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. INTERVENTION: 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. MAIN OUTCOME MEASURES: Correlations between biomarkers and ISHL severity and prognosis were evaluated by statistical analysis. RESULTS: 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. CONCLUSION: 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.
KW - Idiopathic sensorineural hearing loss
KW - Natural killer cell
KW - Neutrophil
KW - Stress response theory
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U2 - 10.1097/MAO.0b013e3182635417
DO - 10.1097/MAO.0b013e3182635417
M3 - Article
C2 - 22872174
AN - SCOPUS:84865610566
SN - 1531-7129
VL - 33
SP - 1142
EP - 1150
JO - Otology and Neurotology
JF - Otology and Neurotology
IS - 7
ER -