Abstract
The effect of dextromethorphan (DXM) use in sensorineural hearing loss (SNHL) has not been fully examined. We conducted an animal model and nationwide retrospective matched-cohort study to explore the association between DXM use and SNHL. Eight-week-old CBA/CaJ hearing loss was induced by a white noise 118 dB sound pressure level for 3 h. DXM (30 mg/kg) was administered intraperitoneally for 5 days and boost once round window DXM socking. In population-based study, we examined the medical records over 40 years old in Taiwan’s National Health Insurance Research Database between 2000 and 2015 to establish retrospective matched-cohort to explore the correlation between DXM use and SNHL. Using click auditory brainstem response (ABR), hearing threshold was measured as 48.6 ± 2.9 dB in control mice compared with 42.6 ± 7.0 dB in DXM mice, which differed significantly (p = 0.002) on day 60 after noise exposure with a larger ABR wave I amplitude in DXM mice. In human study, we used a Cox regression hazard model to indicate that a significantly lower percentage individuals developed SNHL compared with and without DXM use (0.44%, 175/39,895 vs. 1.05%, 1675/159,580, p < 0.001). After adjustment for age and other variables [adjusted hazard ratio: 0.725 (95% confidence interval: 0.624–0.803, p < 0.001)], this study also demonstrated that DXM use appeared to reduce the risk of developing SNHL. This animal study demonstrated that DXM significantly attenuated noise-induced hearing loss. In human study, DXM use may have a protective effect against SNHL.
Highlights
Hearing loss is a growing and alarmingly high burden in the world reporting from the GlobalBurden of Disease Studies and the third leading cause of years lived with disability [1,2]
Multivariate Cox proportional hazards regression was used to determine the risk of sensorineural hearing loss (SNHL), and the results are presented as a hazard ratio (HR) with 95% confidence interval (CI)
We investigated the sensitivity test for duration use and thea test demonstrated diseases, ischemia heart disease (IHD), pneumonia, head injury, and chronicofliver disease had significantly highera lower risk of risk of developing SNHL was associated with longer duration of DXM use (Table 2)
Summary
Hearing loss is a growing and alarmingly high burden in the world reporting from the Global. The common causes of genetic, age-related, noise-induced, and drug-induced hearing loss display intriguing similarities in terms of particular cellular responses of the cochlear sensory cells comprising potential involvement of impaired mitochondrial function, ischemia, oxidative stress with reactive oxygen species, inflammation, apoptosis, autophagy, and/or necrosis [3]. Cochlear synpatopathy is involved in genetic, noise, ototoxicity and age-related hearing loss [7,8,9,10] This mechanism may contribute to glutamate excitotoxicity involving N-methyl-d-aspartate (NMDA) receptor activation and related auditory nerve excitation [9,11,12]. DXM has been reported to reduce neuronal damage or degeneration, cortical infarct volume and improve neurological functions in numerous animal models of stroke and traumatic brain injury (TBI) [18,20]. We explore whether DXM, an NMDA antagonist, exhibits any potential effect against SNHL in both animal models and population-based study
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