Reflux in Untreated Achalasia Patients

Jp, Shoenut; Ab, Micflikier; Cs, Yaffe; B, Den Boer; Jm, Teskey

doi:10.1097/00004836-199501000-00004

Cited by 41 publications

(22 citation statements)

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“…10,17,21,22 Conversely, patients with achalasia are insensitive to acid in the esophagus. 23 Fisichella et al 8 reported data from 145 untreated achalasia patients. Among them, ambulatory pH monitoring was performed for 54 patients.…”

Section: Does Reflux Occur In Achalasia?mentioning

confidence: 99%

Is Gastroesophageal Reflux Disease and Achalasia Coincident or Not?

Jung

Park

2017

J Neurogastroenterol Motil

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Achalasia and gastroesophageal reflux disease (GERD) are on opposite ends of the spectrum of lower esophageal sphincter dysfunction. Heartburn is the main symptom of GERD. However, heartburn and regurgitation are frequently observed in patients who have achalasia. The diagnosis of achalasia might be delayed because these symptoms are misinterpreted as gastroesophageal reflux. Here, we reviewed the clinical characteristics of patients with the erroneous diagnosis of GERD who actually had untreated achalasia.

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Section: Does Reflux Occur In Achalasia?mentioning

confidence: 99%

Is Gastroesophageal Reflux Disease and Achalasia Coincident or Not?

Jung

Park

2017

J Neurogastroenterol Motil

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“…Circumstantial evidence for such a functional impairment comes from the observation that patients with achalasia are often poorly cognizant of either retained food in the esophagus or esophageal distension. Furthermore, uncontrolled studies have reported that achalasia patients have diminished perception of acid reflux events both before and after treatment of their achalasia (20). In contrast, however, chest pain does occur in patients with achalasia with some frequency.…”

mentioning

confidence: 99%

Diminished mechanosensitivity and chemosensitivity in patients with achalasia

Brackbill

Shi

Hirano

2003

American Journal of Physiology-Gastrointestinal and Liver Physi

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.-The pathogenesis of achalasia involves the degeneration of enteric and autonomic nervous systems with resultant effects on esophageal motility. The neural degeneration could affect visceral sensation in achalasia. The aim of this study was to examine mechanosensitivity and chemosensitivity in patients with achalasia. Perceptual responses to esophageal distension and acid perfusion were assessed in nine achalasia patients and nine healthy subjects. Mechanosensitivity was evaluated using a barostat with a doublerandom staircase distension protocol. Responses were graded as follows: 0, no sensation; 1, initial sensation; 2, mild discomfort; 3, moderate discomfort; and 4, pain. Chemosensitivity was graded along a visual analog scale after perfusion of saline and 0.1 N HCl. Barostat pressure-volume relationships were used to report esophageal body compliance. Barostat pressures for initial sensation and mild discomfort were not significantly different for patients and controls. The pressures for moderate discomfort (37.9 Ϯ 3.5 vs. 25.7 Ϯ 2.4 mmHg; P Ͻ 0.05) and pain (47.8 Ϯ 2.3 vs. 32.2 Ϯ 3.5 mmHg; P ϭ 0.002) were significantly higher in achalasics than controls. Seven of the eight achalasia patients never reached pain thresholds at the maximum distension pressure (50 mmHg). Sensation to acid perfusion was significantly lower in achalasics compared with controls (2.2 Ϯ 1.2 vs. 6.7 Ϯ 1.7 cm; P Ͻ 0.05). Compliance was significantly increased in patients with achalasia compared with controls. We conclude that both mechanosensitivity and chemosensitivity are significantly diminished in achalasia patients compared with controls. Also, initial sensation and pain sensation are differentially affected in achalasics. These findings suggest that neuropathic defects in achalasia may manifest themselves in visceral sensory and motor dysfunction. motility; esophageal motility disorders; visceral sensitivity; noncardiac chest pain ACHALASIA IS AN ESOPHAGEAL motility disorder characterized histopathologically by degeneration of ganglia of the myenteric plexus. The pathology may follow a continuum ranging from inflammation of the myenteric plexus with neuronal degeneration to complete aganglionosis (7). Loss of neurons within the dorsal motor nucleus and degenerative changes of vagal nerve fibers have also been described. The resulting motor deficits have been well characterized by manometry and include aperistalsis of the esophageal body and failure of the lower esophageal sphincter (LES) to relax with deglutition although manometric variability has been described (10). Functional obstruction of the LES leads to impaired esophageal emptying that is manifest clinically as progressive dysphagia, regurgitation, and weight loss. Serious complications of retained material in the esophagus exist, including stasis mucosal injury, chronic aspiration, and delayed transit of nutrients and medications.In contrast to the pathophysiology of motor dysfunction, little is known about the integrity of esophageal sensory perception in patients wit...

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“…However, there are a few reports where gastroesophageal reflux has been well documented to occur in patients prior to the development achalasia [4,6]. In our clinic, in the past 15 years we operated on 40 patients with achalasia and in 4 patients among them (10%) the etiologic role of reflux arose.…”

Section: Discussionmentioning

confidence: 96%

“…In our clinic, in the past 15 years we operated on 40 patients with achalasia and in 4 patients among them (10%) the etiologic role of reflux arose. Other reports showed that approximately 10-20% of untreated achalasia patients had abnormal acid exposure on pH monitoring [5][6][7]. Question rises how reflux can occur in untreated achalasia patients, as the two diseases represent opposite ends of abnormal LES function.…”

Section: Discussionmentioning

confidence: 99%

GERD: A Debated Background of Achalasia

Bognár¹,

Horváth²

2016

J Gastrointest Dig Syst

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Achalasia is a primary esophageal motility disorder of unknown etiology, characterized by aperistalsis of the esophageal body and impaired lower esophageal sphincter (LES) relaxation. Available data suggest that the disease is multifactorial, but the exact initiating factors that may play a role in the development of the disease remain unclear. Case presentation: We report the case of a 65 year-old woman who had typical reflux symptoms with heartburn and regurgitation for about seven years. During the year before her admission to our clinic her reflux symptoms resolved and dysphagia developed. Endoscopy revealed esophageal dilatation with erosive esophagitis, narrowed cardia and hiatal hernia. Barium swallow test, manometry and 24 hour pH monitoring confirmed the development of achalasia with accompanying gastroesophageal reflux disease (GERD). The patient underwent laparoscopic surgery, the hiatal hernia was reconstructed and a Heller's myotomy with a 360 degree Nissen fundoplication was performed. At the 3-year follow-up the patient was symptom free. Conclusion: Based on our experience and the review of the literature we believe that there is a cause-and-effect relationship between gastroesophageal reflux and the development of achalasia. In these cases a laparoscopic Heller's myotomy completed with a 360 degree Nissen fundoplication should be the recommended surgical treatment to minimize the possibility of postoperative reflux disease.

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Reflux in Untreated Achalasia Patients

Cited by 41 publications

References 0 publications

Is Gastroesophageal Reflux Disease and Achalasia Coincident or Not?

Is Gastroesophageal Reflux Disease and Achalasia Coincident or Not?

Diminished mechanosensitivity and chemosensitivity in patients with achalasia

GERD: A Debated Background of Achalasia

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