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      A possible pathological link among swallowing dysfunction, gastro-esophageal reflex, and sleep apnea in acute exacerbation in COPD patients

      International Journal of Chronic Obstructive Pulmonary Disease

      Dove Medical Press

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          Abstract

          Dear editor With interest, we read the review article by Lee and Goldstein1 published in the recent issue of the International Journal of Chronic Obstructive Pulmonary Disease. The authors have comprehensively summarized the possible roles of gastroesophageal reflux disease (GERD) in a variety of aspects of pathogenesis of COPD. However, the considerable associations among GERD, swallowing dysfunction, sleep apnea, and acute exacerbation (AE) of COPD have not been fully discussed. GERD-related chronic cough (CC) may have multifactorial causes. GER is known to induce esophagopharyngeal reflux (EPR), resulting in CC. Importantly, symptoms of CC fully responded to full-dose proton pump inhibitor therapy in CC patients with GERD.2 There are evidences of increase of weakly acidic gas EPR and swallowing-induced acidic EPR in patients with COPD.3 The GERD and its related swallowing impairment may be closely associated with unwitnessed pulmonary aspiration, such as mis-swallowing or silent aspiration in older patients with COPD. Further, sleep apnea, which is relatively common in COPD patients, also causes GER and non-acidic reflux. The sleep apnea-related GER events also cause pulmonary aspiration that is accompanied with bronchial constriction and hypoxic responses in their lungs. Pulmonary aspiration is a risk factor for upper and lower respiratory tract infections in COPD patients. We have previously reported that more than eight of 48 (16.7%) COPD patients showed an abnormal swallowing function.4 In our experience, the higher prevalence of GER, abnormal swallowing reflex or sleep apnea has been investigated in COPD patients who experienced AE but not in those without AE. These three disorders are mainly related with the pathogenesis of each disease and contribute to inducing pulmonary infection and/or AE.5 From these points of view, GER may have a significant impact on the increased frequency of AE in patients with COPD. Thus GERD, swallowing dysfunction, and sleep apnea may be important risk factors for AE through the pulmonary aspiration-related events in COPD patients.

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          Most cited references 12

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          Gastroesophageal reflux disease in COPD: links and risks

          COPD is a long-term condition associated with considerable disability with a clinical course characterized by episodes of worsening respiratory signs and symptoms associated with exacerbations. Gastroesophageal reflux disease (GERD) is one of the most common gastrointestinal conditions in the general population and has emerged as a comorbidity of COPD. GERD may be diagnosed by both symptomatic approaches (including both typical and atypical symptoms) and objective measurements. Based on a mix of diagnostic approaches, the prevalence of GERD in COPD ranges from 17% to 78%. Although GERD is usually confined to the lower esophagus in some individuals, it may be associated with pulmonary microaspiration of gastric contents. Possible mechanisms that may contribute to GERD in COPD originate from gastroesophageal dysfunction, including altered pressure in the lower esophageal sphincter (which normally protect against GERD) and changes in esophageal motility. Proposed respiratory contributions to the development of GERD include respiratory medications that may alter esophageal sphincter tone and changes in respiratory mechanics, with increased lung hyperinflation compromising the antireflux barrier. Although the specific cause and effect relationship between GERD and COPD has not been fully elucidated, GERD may influence lung disease severity and has been identified as a significant predictor of acute exacerbations of COPD. Further clinical effects could include a poorer health-related quality of life and an increased cost in health care, although these factors require further clarification. There are both medical and surgical options available for the treatment of GERD in COPD and while extensive studies in this population have not been undertaken, this comorbidity may be amenable to treatment.
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            The relationship between gastroesophageal reflux disease and obstructive sleep apnea.

            There has been an accumulating body of research concerning the extraesophageal complications of gastroesophageal reflux disease over the past decade. Given the cardiological, pulmonological, laryngeal, and dental aspects of such complications, an interdisciplinary approach is required. The most recognized manifestations are noncardiac chest pain, bronchial asthma, chronic bronchitis, chronic cough, and posterior laryngitis, as well as the acidic damage of dental enamel. This article focuses on the potential relationship between reflux disease and obstructive sleep apnea, which has been raised only more recently. Because of the decrease of primary peristalsis and the reduced production of saliva, as well as the diminished acid and volume clearance of the esophagus, sleeping can be considered as a risk factor of the reflux event by itself. Moreover, it should also be taken into account that the transdiphragmatic pressure increases in parallel with the growing intrathoracic pressure generated during obstructive apnea episodes. This has a non-negligible effect on the phrenoesophageal ligament, which is connected to the lower esophageal sphincter. Repetition of the pressure changes results in insufficiency of the cardia. While this pressure change produces a considerable suction effect, further reducing the clearing mechanism of the gastric volume, lower esophageal sphincter insufficiency can directly lead to reflux disease. The challenge for gastroenterologists is to gain further insight into this relationship and to play a more active role in the complex therapy of the disease, as well as to develop a new diagnostic approach towards the severe forms of gastroesophageal reflux disease.
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              Mechanism of gastroesophageal reflux in patients with obstructive sleep apnea syndrome.

              It has been reported that the prevalence of gastroesophageal reflux (GER) disease is high in patients with obstructive sleep apnea (OSA). End-inspiratory intra-esophageal pressure decreases progressively during OSA, which has been thought to facilitate GER in OSA patients. The aim of our study was to clarify the mechanisms of GER during sleep (sleep-GER) in OSA patients. Eight OSA patients with reflux esophagitis (RE), nine OSA patients without RE, and eight healthy controls were studied. Polysomnography with concurrent esophageal manometry and pH recording were performed. Significantly more sleep-GER occurred in OSA patients with RE than without RE or in controls (P < 0.05). The severity of OSA did not differ between OSA patients with RE and without RE. Sleep-GER was mainly caused by transient lower esophageal sphincter relaxation (TLESR), but not by negative intra-esophageal pressure during OSA. During OSA gastroesophageal junction pressure progressively increased synchronous to intra-esophageal pressure decrease. OSA patients had significantly more TLESR events during sleep related to preceding arousals and shallow sleep, but the number of TLESR events was not related to RE. In OSA patients, sleep-GER was mainly caused by TLESR, but not by negative intra-esophageal pressure due to OSA.
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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
                2016
                27 January 2016
                : 11
                : 147-150
                Affiliations
                Department of Pulmonary Medicine, Hitachinaka Medical Education and Research Center, University of Tsukuba, Ibaraki, Japan
                [1 ]Department of Respiratory Medicine, West Park Healthcare Centre, Toronto, ON, Canada
                [2 ]Department of Physical Therapy, University of Toronto, Toronto, ON, Canada
                [3 ]Institute for Breathing and Sleep, Austin Health, Melbourne, VIC, Australia
                [4 ]Department of Medicine, University of Toronto, Toronto, ON, Canada
                Author notes
                Correspondence: Shinji Teramoto, Hitachinaka Medical Education and Research Center, University of Tsukuba, 20-1 Hitachinaka-shi, Ibaraki, 312-0057, Japan, Tel +81 29 354 5111, Fax +81 29 354 5926, Email shinjit-tky@ 123456umin.ac.jp
                Correspondence: Annemarie L Lee, Department of Respiratory Medicine, West Park Healthcare Centre, 82 Buttonwood Avenue, Toronto, ON, M6M 2J5, Canada, Tel +1 416 243 2653, Fax +1 416 243 3747, Email annemarie.lee@ 123456westpark.org
                Article
                copd-11-147
                10.2147/COPD.S99663
                4734722
                26869780
                © 2016 Teramoto. 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.

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                Respiratory medicine

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