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      Costen’s syndrome and COPD

      International Journal of Chronic Obstructive Pulmonary Disease

      Dove Medical Press

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          Abstract

          Dear editor I read with great interest the article of systematic review and meta-analysis of Bayat et al,1 which shows a close relationship between loss of hearing and COPD. The article reminds us that the doctor should always make an accurate medical history, because the clinical evaluation is the foundation of what will be the therapy of the patient. The text does not give explanations on the possible causes that induce hearing loss in patients diagnosed with COPD. There is a close embryological and functional relationship between the temporo-mandibular joint (TMJ) and the middle ear.2 The structure of union between these two anatomical areas is the discomalleolar ligament or Pinto’s ligament, which connects the medial retrodiscal portion of TMJ and the malleus of the middle ear.2 Studies show that an altered ligament tension due to an abnormal opening of the mouth leads to dysfunction of the middle ear with risk of hearing loss.3–5 The patient with COPD suffers from many comorbidities, including musculoskeletal disorders, arthritis, arthrosis, with degeneration of the joint functions (as for TMJ), as well as obstructive sleep apnea syndrome (OSAS).6,7 OSAS causes an abnormal opening of the mouth during the night, with a structural and functional alteration of the neck; there is a close relationship between this syndrome and the decrease in hearing.8,9 From a clinical point of view, signs such as hearing loss, functional impairment of the neck and TMJ disorders lead to Costen’s syndrome.10 The latter alters the internal pressure of the middle ear and subsequent decrease in hearing, through muscular (neck), articular (TMJ) and ligament dysfunction (Pinto’s ligament).10 We can strongly hypothesize that one of the most important causes of hearing loss in patients with COPD is the secondary presence of Costen’s syndrome.

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          Most cited references 23

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          Current insights in noise-induced hearing loss: a literature review of the underlying mechanism, pathophysiology, asymmetry, and management options

          Background Noise-induced hearing loss is one of the most common forms of sensorineural hearing loss, is a major health problem, is largely preventable and is probably more widespread than revealed by conventional pure tone threshold testing. Noise-induced damage to the cochlea is traditionally considered to be associated with symmetrical mild to moderate hearing loss with associated tinnitus; however, there is a significant number of patients with asymmetrical thresholds and, depending on the exposure, severe to profound hearing loss as well. Main body Recent epidemiology and animal studies have provided further insight into the pathophysiology, clinical findings, social and economic impacts of noise-induced hearing loss. Furthermore, it is recently shown that acoustic trauma is associated with vestibular dysfunction, with associated dizziness that is not always measurable with current techniques. Deliberation of the prevalence, treatment and prevention of noise-induced hearing loss is important and timely. Currently, prevention and protection are the first lines of defence, although promising protective effects are emerging from multiple different pharmaceutical agents, such as steroids, antioxidants and neurotrophins. Conclusion This review provides a comprehensive update on the pathophysiology, investigations, prevalence of asymmetry, associated symptoms, and current strategies on the prevention and treatment of noise-induced hearing loss.
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            Cigarette smoking and risk for hearing impairment: a longitudinal study in Japanese male office workers.

            The association of cigarette smoking with development of hearing impairment (loss of 30 dB at 1000 Hz and 40 dB at 4000 Hz) over a 5-year follow-up was studied in 1554 non-hearing-impaired Japanese male office workers who ranged in age from 30 to 59 years. After controlling for potential predictors of hearing impairment, the relative risk for low-frequency hearing impairment compared with never smokers was 1.12 (95% confidence interval [CI], 0.57 to 2.17) for ever-smokers, 1.21 (95% CI, 0.65 to 2.25) for current smokers of 1 to 20 cigarettes/day, 1.35 (95% CI, 0.70 to 2.61) for current smokers of 21 to 30 cigarettes/day, and 1.82 (95% CI, 0.98 to 3.38) for current smokers of 31 or more cigarettes/day (P for trend = 0.063). The respective multivariate-adjusted relative risks for high-frequency hearing impairment compared with never smokers were 1.70 (95% CI, 0.85 to 3.40), 1.82 (95% CI, 0.92 to 3.59), 2.00 (95% CI, 0.98 to 4.08), and 2.20 (95% CI, 1.09 to 4.42) (P for trend = 0.025). As the number of pack-years of exposure increased, the risk for high-frequency hearing impairment increased in a dose-dependent manner (P for trend = 0.011), but the risk for low-frequency hearing impairment did not (P for trend = 0.172). Our results indicate that cigarette smoking is highly associated with development of high-frequency hearing impairment in Japanese male office workers.
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              Risk factors related to age-associated hearing loss in the speech frequencies.

              This paper examines the relationship between several risk factors and the development of age-associated hearing loss in the speech frequencies. Hearing loss is defined as an average threshold level of 30 dB HL or greater at the frequencies of 0.5, 1, 2, and 3 kHz. Hearing thresholds from 0.5 to 8 kHz using a pulse-tone tracking procedure were collected on participants of the Baltimore Longitudinal study of Aging since 1965. A proportional hazards regression model was used to study the relationship between several risk factors that have previously been found to be associated with numerous health-related outcomes and the length of follow-up time until the occurrence of unilateral or bilateral hearing loss in a screened group of 531 men. Risk factors considered are age, blood pressure, and alcohol and cigarette consumption. After controlling for age, only systolic blood pressure showed a significant relationship with hearing loss in the speech frequencies (p < .05). Since blood pressure is a modifiable risk factor, these results suggest that preventing hypertension might contribute to an effective program for the prevention of apparent age-associated hearing loss.
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                1176-9106
                1178-2005
                2019
                18 February 2019
                : 14
                : 457-460
                Affiliations
                Foundation Don Carlo Gnocchi IRCCS, Department of Cardiology, Institute of Hospitalization and Care with Scientific Address, Milan 20100, Italy, bordonibruno@ 123456hotmail.com
                [1 ]Department of Audiology, Hearing Research Center, Imam Khomeini Hospital, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
                [2 ]Department of Otorhinolaryngology, Hearing Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
                [3 ]Department of Biostatistics and Epidemiology, School of Health, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
                [4 ]Department of Internal Medicine, Air Pollution and Respiratory Diseases Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
                [5 ]Department of Molecular Medicine, Health Research Institute, Thalassemia and Hemoglobinopathies Research Centre, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran, bioinfo2003@ 123456gmail.com
                Author notes
                Correspondence: Bruno Bordoni, Foundation Don Carlo Gnocchi IRCCS, Department of Cardiology, Institute of Hospitalization and Care with Scientific Address, S Maria Nascente, Via Capecelatro 66, Milan 20100, Italy, Tel +39 02 349 630 0617, Email bordonibruno@ 123456hotmail.com
                Correspondence: Fakher Rahim, Department of Molecular Medicine, Health Research Institute, Thalassemia and Hemoglobinopathies Research Center, Ahvaz Jundishapur University of Medical Sciences, PO Box 61537-15794, Ahvaz, Iran, Tel +98 613 336 7652, Email bioinfo2003@ 123456gmail.com
                Article
                copd-14-457
                10.2147/COPD.S200787
                6388777
                © 2019 Bordoni. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Categories
                Letter

                Respiratory medicine

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