The roles of excessive gastro-oesophageal reflux, disordered oesophageal motility and decreased mucosal sensitivity in the pathogenesis of Barrettʼs oesophagus

Effects of low-power argon plasma coagulation thermoablation of Barrett??s epithelium on oesophageal motility

“…Their mean age was 63.4 years (SD 11, range 39-79). The mean BE length was 6.5 cm (SD 3.3, range [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19], and the mean LOS length was 2.8 cm (SD 1.32, range 1-6). Twenty-eight (85%) achieved macroscopic ablation of 90% or greater of the original Barrett's area assessed from grid drawings and photographs.…”

“…Patients with BE have increased oesophageal acid exposure compared with those with milder forms of reflux disease [2,3]. The duration of reflux episodes appears to be of greater importance than increased reflux frequency [4], as reflected in putative pathophysiological mechanisms [5]. BE patients have impaired oesophageal motility; a defective lower oesophageal sphincter (LOS) with reduced pressure, short overall and intra-abdominal sphincter length, and low amplitude peristaltic contraction in the distal oesophagus are the commonest reported abnormalities [6,7].…”

Esophageal motility and gastric acid secretion in patients with Barrett's esophagus

“…Acid refl ux episodes that persist for longer than 5 min occur more often in patients with BE than in patients without BE [13,14]. Longer duration of acid refl ux episodes results from low-amplitude esophageal contractions and/or nonpropagated peristaltic esophageal contractions.…”

“…The incidence of esophageal adenocarcinoma has been steadily increasing in the United States, and it now accounts for at least half of all esophageal cancer [5][6][7][8], compared with Japan where the incidence is still low. BE is characterized by excessive esophageal acid exposure in the majority of BE patients, compared with healthy subjects or patients with mild erosive esophagitis [9][10][11][12][13][14][15][16][17], although the difference in esophageal acid exposure between patients with BE and those with severe erosive esophagitis is less clear [16,17]. It is thought that excessive esophageal acid exposure results from gastric acid hypersecretion, the number of acid refl ux episodes and the length of time which is necessary to restore esophageal pH to normal after acid refl ux episodes.…”

Acid Suppression and Chemoprevention in Barrett’s Oesophagus

“…Duration and severity of intraoesophageal acid exposure correlates with the development of erosive oesophagitis and Barrett's metaplasia [43]. Barrett's patients have more frequent and prolonged episodes of acid exposure than those with GORD [44], and there is an increased risk of developing adenocarcinoma in patients with severe, frequent and prolonged duration of reflux [45]. This appears to be a dose-response relationship, so patients with intermittent mild reflux have an odds ratio of 1.6 of developing oesophageal cancer, increasing to 7.7 with recurrent reflux.…”