In a retrospective cohort study published in the journal eClinicalMedicine, researchers from South Korea investigated the potential association between coronavirus disease 2019 (COVID-19), hearing loss (HL), and sudden sensorineural hearing loss (SSNHL) in adults aged 20–39 years. They found that young adults with COVID-19 had a significantly higher risk of developing HL and SSNHL compared to those without COVID-19.
Study: Incidence of hearing loss following COVID-19 among young adults in South Korea: a nationwide cohort study. Image Credit: ozrimoz / Shutterstock
Background
COVID-19, with over 770 million cases and nearly 7 million deaths globally, affects multiple body systems, including the auditory system. Initial reports from Thailand and Turkey showed potential links between COVID-19 and HL or SSNHL. Evidence suggests brainstem involvement or viral meningitis in COVID-19 may contribute to neuroauditory issues. An increase in SSNHL cases during the pandemic and findings from Danish research also support this association. Recent case reports show sudden HL in young adults post-COVID-19, raising new public health concerns due to the impact of HL on their academic and occupational performance, quality of life, as well as social functioning. However, a systematic review highlighted the need for more extensive studies to confirm this link.
Given these conflicting results from various studies, it is essential to investigate the link between COVID-19 and in a large-scale cohort while considering confounding factors. Therefore, researchers in the present study examined the risk of HL and SSNHL following COVID-19 in a large cohort of young adults in South Korea.
About the study
In the present population-based cohort study, data were obtained from the Korea Disease Control and Prevention Agency (KDCA)-COVID-19 and the National Health Insurance Service (NHIS) and were combined. The study was conducted between 2020 and 2022 and included 6,716,879 young adults aged 20–39 years without a history of HL. The mean age of the participants was 29.6 years, and 51% were female. While 2.7% of the participants had hypertension, 2.5% of them had dyslipidemia, and 0.9% of them had diabetes. The exposure was infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), diagnosed via real-time reverse transcription polymerase chain reaction (RT-PCR) assays from nasopharyngeal or oropharyngeal swabs. At baseline, 72% of the included individuals had contracted COVID-19, and 93.1% had completed the primary series of vaccinations against the disease.
The primary outcomes were composite HL and SSNHL, which were diagnosed based on criteria from the International Classification of Diseases-10th revision (ICD-10). Covariates included age, sex, household income, Charlson comorbidity index (CCI), and COVID-19 vaccination status. Additional variables for the health screening cohort included body mass index, systolic blood pressure, fasting serum glucose, smoking status, alcohol consumption, and physical activity levels. Statistical analysis involved the use of the Fine–Gray sub-distribution hazard regression model, inverse probability of treatment weighting, and stratified and sensitivity analyses.
Results and discussion
Throughout the follow-up period, a total of 38,269 cases of HL were recorded. The incidence of HL was found to be 11.9 per 10,000 person-months in the COVID-19 group, over three times higher than in the non-COVID-19 group. Similarly, the incidence of SSNHL was found to be more than three times higher in the COVID-19 group.
In the sensitivity analyses, the risks of HL and SSNHL in the COVID-19 group remained consistently high compared to the non-COVID-19 group. Stratified analyses revealed the highest risk of HL in young adults with diabetes and the highest risk of SSNHL in those with diabetes and dyslipidemia. No significant interaction was found for COVID-19 vaccination status.
Theories speculate the mechanisms potentially underlying the link observed between COVID-19 and HL and SSNHL. One of these mechanisms may be direct damage to inner ear tissues by the virus. Additionally, SARS-CoV-2 could persist in the middle ear, contributing to HL. The virus binds to angiotensin-converting enzyme 2 (ACE2) receptors present in ear tissues, potentially affecting hearing. Further, microvascular damage and inflammation caused by the virus may impact cochlear function, while an abnormal immune response and oxidative stress in the inner ear could further contribute to hearing issues. However, more research is needed to confirm these potential mechanisms.
The study is strengthened by its large sample size, use of comprehensive national data, and robust statistical analyses. However, the study is limited by its potential selection bias, lack of objective audiometric data, limited generalizability, retrospective design issues, and insufficient evaluation of COVID-19 vaccination effects on hearing loss.
Conclusion
In conclusion, the study suggests that COVID-19 may independently increase the risk of HL and SSNHL in young adults with otherwise healthy ears. It is essential for even healthy individuals to be aware of this risk to improve the prevention and management of COVID-19-related hearing issues. The study highlights a previously underrecognized complication of COVID-19 and informs public health policies, warranting further research into COVID-related auditory damage and treatments.
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