Defective Mucosal Movement at the Gastroesophageal Junction in Patients with Gastroesophageal Reflux Disease

Abstract

In non-GERD subjects, the gastric MMS moves rostrally into the distal esophagus during deglutitive inhibition and forms a barrier. This movement of the MMS is defective in patients with GERD.

Normal and abnormal physiology, pharmacology, and anatomy of the gastroesophageal junction high‐pressure zone

“…Furthermore, we believe that a large proportion of this increase in distensibility and lack of tone within the components of the GEJHPZ in GERD patients is due to excessive relaxation of the gastric clasp and gastric sling muscle fiber complex in response to nicotinic receptor stimulation, as demonstrated in patients with Barrett's esophagus. Finally, we have identified a unique mechanism involving the muscularis mucosa of the distal esophagus in which there is absent mucosal contraction during swallowing in patients with GERD . We believe that the mechanisms described above are pathophysiologic mechanisms that help explain the etiology of GERD in patients without hiatal hernia.…”

“…Finally, we have identified a unique mechanism involving the muscularis mucosa of the distal esophagus in which there is absent mucosal contraction during swallowing in patients with GERD. 25 We believe that the mechanisms described above are pathophysiologic mechanisms that help explain the etiology of GERD in patients without hiatal hernia. responsibility of the authors and does not necessarily represent the official views of the National Institute of Diabetes and Digestive and Kidney Diseases or the National Institutes of Health.…”

“…Several new pathophysiologic mechanisms for reflux have been discovered: (1) an attenuated pressure profile of the LECS, 23 (2) an absent pressure profile of the gastric clasp/gastric sling muscle complex, 23 (3) an increase in the distensibility of the smooth muscle components of the GEJHPZ in patients with gastroesophageal reflux disease (GERD), 24 (4) excessive relaxation of the gastric clasp and gastric sling muscle fiber complex to nicotinic stimulation in patients with Barrett's esophagus, 17 and (5) absent longitudinal muscularis mucosal contraction at the GEJHPZ during swallowing in patients with GERD. 25 Stein et al 26 used 3D computerized imaging of sphincter pressures obtained by a pullback of radially oriented pressure transducers and calculated the vector volume of the images in normal control subjects and in patients with GERD. The total and abdominal sphincter pressure vector volume was lower in 150 patients with increased esophageal acid exposure and decreased with increasing esophageal mucosal damage.…”

“…Using both simultaneous endoluminal ultrasound with manometry and transabdominal ultrasound to investigate the distal esophagus and proximal stomach in normal control subjects, we observed an increase in cross-sectional surface area of the mucosa/submucosa, along with an increase in the thickness of the muscularis mucosa during swallowing. 25 This occurs independently and before an increase in the cross-sectional surface area of the circular smooth muscle and longitudinal smooth muscle during swallowing. The mucosa/submucosa of the proximal stomach is pulled into the distal tubular esophagus independent of shortening of the muscularis propria.…”

“…Several new pathophysiologic mechanisms for reflux have been discovered: (1) an attenuated pressure profile of the LECS, (2) an absent pressure profile of the gastric clasp/gastric sling muscle complex, (3) an increase in the distensibility of the smooth muscle components of the GEJHPZ in patients with gastroesophageal reflux disease (GERD), (4) excessive relaxation of the gastric clasp and gastric sling muscle fiber complex to nicotinic stimulation in patients with Barrett's esophagus, and (5) absent longitudinal muscularis mucosal contraction at the GEJHPZ during swallowing in patients with GERD . Stein et al .…”