Is there a vicious cycle between obstructive sleep apnea and laryngopharyngeal reflux disease?
Introduction
Obstructive sleep apnea (OSA) is characterized by repetitive episodes of airflow obstruction during sleep, and the estimated prevalance rate is 4–9% in men and 2–4% in women [1]. Abnormalities in upper airway anatomy (tonsils, soft palate, base of tongue and/or hypopharynx) and neuromuscular control are the primary factors that contribute to upper airway collapsibility in OSA patients [2], [3].
OSA is associated with many diseases such as obesity, metabolic syndrome cardiovascular diseases (hypertension, ischemic heart disease, sudden death, etc.) and cerebrovascular diseases [4], [5], [6]. In addition, the association between OSA and reflux diseases is well-established [7], [8], [9], [10]. Reflux of gastric contents includes both gastroesophageal reflux (GER) and laryngopharyngeal reflux (LPR) disease. The distinction between the two is largely based on the location of the area which is injured, with GER disease defined by reflux solely into the esophagus and LPR disease defined by reflux to the larynx and pharynx, above the esophagus. LPR disease has been increasingly recognized as common and can contribute to or cause several diseases of the upper airway as chronic cough, laryngopharyngitis, asthma attacks, laryngospasm, subglottic stenosis, benign and malignant diseases of head and neck [11], [12]. Although there is agreement about the association between OSA and LPR disease, the precise pathophysiological mechanism is not understood completely. Some authors have postulated that reflux of gastric contents plays a role in the development of OSA and have obtained a significant improvement in the symptoms of OSA after an aggressive antireflux therapy [8], [13]. In contrast, others have argued that OSA contributes to reflux of gastric contents and have demonstrated improvements in reflux after treatment with CPAP [14], [15]. All of these studies support a possible bidirectional causative relationship between them. However, the pathophysiological mechanism underlying the relationship between OSA and reflux diseases, especially LPR disease has not been determined.
Section snippets
Hypothesis
It is hypothesized that the causative relationship between OSA and LPR disease depends on a vicious cycle (Fig. 1). The vicious cycle is initially triggered by respiratory efforts. As airflow obstruction develops in OSA, progressive increases in respiratory effort produce greater negative intrathoracic pressure. This negative intrathoracic pressure promotes reflux of gastric contents (acid, pepsin, etc.) into the esophagus, larynx and pharynx as the pressure overwhelms the ability of the lower
Evaluation of the hypothesis
The first step in evaluating this vicious cycle is examination of the association between increased respiratory effort and LPR disease. Airflow obstruction in OSA is associated with increased respiratory effort, which particularly occurs during the episodes of apnea, hypopnea and respiratory effort-related arousals (Fig. 1). Most published studies that have examined the association between OSA and reflux disease (both GER and LPR disease) have focused on the frequency of breathing disturbances
Conclusion
OSA and LPR disease may be related through a vicious cycle whereby increased respiratory effort specifically contributes to reflux of gastric contents that, in turn, contributes to progression of OSA by causing inflammation that directly narrows the upper airway and produces changes in upper airway mechanics through mucosal damage and sensory dysfunction.
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