Esophageal Dysmotility in Patients Who Have Eosinophilic Esophagitis
Section snippets
Dysphagia
Intermittent dysphagia and food impactions are the most common presenting symptoms associated with EE in older children and adults. In a report of 103 children, 26% of patients (mean age, 13 years) presented with dysphagia and 6.8% (mean age, 16 years) presented with food impaction [1]. Other pediatric series have found that food impaction was the initial presenting symptom in up to 20% of the patients [2]. In adults, the main presenting symptom is dysphagia, which has been reported in 29% to
Etiopathogenesis of esophageal dysmotility
The etiopathogenesis of esophageal dysmotility is not well understood. It may be related to the eosinophilic infiltration of the esophageal mucosa and its interactions with the microenvironment. Studies in which full-thickness biopsies were performed in patients who had EE found eosinophilic infiltration in all esophageal layers [7], [8], [9], [10], [11].
The exact mechanism by which eosinophilic infiltration may produce esophageal dismotility is not certain, but several speculations exist.
Stationary esophageal manometry
Esophageal motility has not been well characterized in patients who have EE. The results of stationary manometry are varied and include findings ranging from normal peristalsis to ineffective peristalsis (particularly after meals), including simultaneous and high-amplitude esophageal body contractions, achalasia, diffuse esophageal spasms, tertiary contractions, aperistalsis, nonspecific motor disorders, nutcracker esophagus, and high-amplitude contractions, particularly in the lower esophagus
Studies with high-resolution manometry
High-resolution manometry offers some advantages over standard manometry; the catheters have more recording sites and less space between them, allowing the clinician to define the intraluminal pressures completely and to reduce movement-related artifacts [29], [30]. The technology allows seamless, dynamic representation of peristalsis at every axial position within and across the esophagus, although the role of this additional data in clinical management is unclear [29], [30]. Recent studies
Studies with combined esophageal impedance and manometry
Technological advances have allowed the pairing of impedance sensors with pressure sensors in a single catheter. The addition of impedance provides insight into the transit of liquid, viscous, and solid food in the esophagus and its relationship with esophageal peristalsis. The sensors provide information about the transit time of substances down the esophagus and can identify areas of the esophagus that retain ingested contents, suggesting impaired motility. Studies in adults showed that
Studies with prolonged esophageal manometry
The majority of patients who have EE and dysphagia have normal esophageal stationary manometry. Although this result may reflect a limitation of the technology, other possibilities explaining the normal results include the study's short duration, its performance during fasting rather than meal periods, and the lack of symptoms that typically occur during the short study duration. Prolonged esophageal manometry, conducted over 24 hours, allows the clinician to measure motility during meal
Effect of treatment on esophageal motility abnormalities
It is not clear if nonspecific motor abnormalities are responsible for the dysphagia, and it has been suggested the abnormalities found during stationary manometry may be nonspecific. Three case reports and one prospective study tried to establish if the motor abnormalities would disappear after successful treatment (Table 3). In one case report of a patient who had achalasia and EE, normal peristalsis returned after myotomy. Two other patients experienced resolution of nonspecific motor
Other possible explanations for the dysphagia
It often is difficult to determine if subtle motor abnormalities are responsible for symptoms; adult studies have shown that nonspecific motor disorders do not consistently result in functional abnormalities [35]. As mentioned previously, patients who have EE have a high incidence of esophageal narrowing and strictures that may represent diffuse thickening of the muscularis propria or a functional constriction related to the marked infiltration of the myenteric plexus [11]. It also has been
Summary
The ethiopathogenesis of the dysphagia in patients who have EE is probably multifactorial. Primary motility disorders such as achalasia or diffuse esophageal spasms, as well as nonspecific motility disorders including abnormal peristalsis and high-amplitude contractions, have been described. These abnormalities probably result from the interactions between eosinophils and mast cells with the esophageal microenvironment. Even though some of the observed motility abnormalities improve after
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2021, Clinical Gastroenterology and HepatologyCitation Excerpt :However, dysphagia may occur even without endoscopic findings, when the mechanism is unclear. In these circumstances the possibility that a hidden esophageal motility disorder, including achalasia, could be involved in symptom generation has been increasingly recognized4,12–15 and reported in up to 40% of EoE patients, although supporting data are limited to case reports and small retrospective series.13,14,25–27 We confirm a similar frequency of motility disorders (38%), with 16% demonstrating major motility disorders according to Chicago Classification version 3.0.
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2019, Human PathologyCitation Excerpt :The latest therapy option is per oral endoscopic myotomy [7]. Esophageal biopsies are taken during upper endoscopy to rule out other causes for the patients' symptoms, such as severe reflux disease with concomitant destruction of the motor function of the organ with or without Barrett esophagus [8], esophageal cancer [9], fungal infection [10], or eosinophilic esophagitis [11,12]. The etiology of idiopathic achalasia remains unknown, but a variety of possible pathogenetic mechanisms have been proposed including genetic disposition, neurodegeneration triggered by viral infection, or other related degenerative factors including autoimmune processes [2,13-15].
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This work was supported in part by the Pappas Foundation and by NIH grant 1K23DK073713-01A1.