Risk of sudden sensorineural hearing loss in patients with dysrhythmia: A nationwide population-based cohort study.

Chih-Wei Luan,Ming-Shao Tsai,Chia-Yen Liu,Ethan I Huang,Geng-He Chang,Cheng-Ming Hsu,Yao-Hsu Yang,Meng-Hung Lin,Ku-Hao Fang,Jung-Jung Chang,Yao-Te Tsai,Bolajoko O Olusanya

doi:10.1371/journal.pone.0218964

Abstract

ObjectiveWhether dysrhythmia is a risk factor of sudden sensorineural hearing loss (SSNHL) remains unclear. In this study, we aimed to investigate the risk of developing SSNHL among patients with dysrhythmia in different age and gender groups by using population-based data in Taiwan.MethodsWe conducted a matched cohort study by analyzing data between January 2000 and December 2013 obtained from the Taiwan National Health Insurance Research Database. 41,842 newly diagnosed dysrhythmia patients and 83,684 comparison subjects without dysrhythmia were selected from claims. The incidence of sudden sensorineural hearing loss at the end of 2013 was determined in both groups. Univariate and multivariate logistic regression analyses were used to investigate the risk of SSNHL among patients with dysrhythmia.ResultsThe incidence of SSNHL was 1.30-fold higher in the dysrhythmia group compared with the control group (53.2 versus 40.9 per 100,000 person-years), and using Cox proportional hazard regressions, the adjusted hazard ratio (HR) was 1.40 (95% confidence interval [CI], 1.15–1.70). Gender-stratified analysis revealed a significantly higher risk of SSNHL in patients with dysrhythmia than in those without dysrhythmia for both men and women (HR = 1.34, 95% CI = 1.02–1.76, P = 0.039, HR = 1.35, 95% CI = 1.02–1.78, P = 0.035, respectively). Age-stratified analysis revealed remarkable associations between dysrhythmia and SSNHL among those aged less than 40 years and more than 65 years (HR = 2.18, 95% CI = 1.03–4.64, P = 0.043 and HR = 1.54, 95% CI = 1.14–2.09, P = 0.006, respectively).ConclusionsOur findings support dysrhythmia as an independent risk factor for SSNHL. Based on the study results, clinicians managing patients with dysrhythmia should be aware of the increased risk of developing SSNHL, especially among patients aged <40 and >65 years, and counsel patients to seek medical advice immediately if they experience any acute change in their hearing ability.

Highlights

Sudden sensorineural hearing loss (SSNHL) is an otologic emergency and defined as an acute loss of 30 dB or more in at least three contiguous audiometric frequencies over a period of less than 3 days [1]
The incidence of SSNHL was 1.30-fold higher in the dysrhythmia group compared with the control group (53.2 versus 40.9 per 100,000 person-years), and using Cox proportional hazard regressions, the adjusted hazard ratio (HR) was 1.40 (95% confidence interval [confidence incidence (CI)], 1.15–1.70)
Gender-stratified analysis revealed a significantly higher risk of SSNHL in patients with dysrhythmia than in those without dysrhythmia for both men and women (HR = 1.34, 95% CI = 1.02–1.76, P = 0.039, HR = 1.35, 95% CI = 1.02–1.78, P = 0.035, respectively)

Summary

Introduction

Sudden sensorineural hearing loss (SSNHL) is an otologic emergency and defined as an acute loss of 30 dB or more in at least three contiguous audiometric frequencies over a period of less than 3 days [1]. The incidence of SSNHL was reported to range from 5 to 20 per 100,000 individuals and increase with age [2]. Previous studies have reported increased risk of developing SSNHL among patients with diabetes mellitus, systemic lupus erythematosus, chronic kidney disease, chronic otitis media, osteoporosis, psoriasis, iron deficiency anemia, and human immunodeficiency virus [5,6,7,8,9,10,11,12]. Chau et al conducted a systematic review of 23 articles and determined that the likely etiologies for SSNHL were 71.0% idiopathic, 12.8% from infection, 4.7% otologic, 4.2% from trauma, 2.8% from vascular or hematologic disorders, 2.3% from neoplasm, and 2.2% from other causes [13]. Four major pathogenetic mechanisms have been proposed to explain SSNHL: vascular compromise, viral infection, rupture of the intracochlear membrane, and autoimmune inner ear disease. Impairment of cochlear perfusion appears to be the most crucial event [14,15]

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Conclusion