Use of multiple channel pH monitoring for evaluation of ultra-distal reflux in patients after fundoplication for treatment of Barrett's esophagus

Seguro, Francisco Carlos Bernal da Costa; Santo, Marco Aurélio; Szachnowicz, Sérgio; Maluf‐Filho, Fauze; Kishi, Humberto S.; Falcäo, Angela; Nasi, Ary; Sallum, R. A. A.; Cecconello, Ivan

doi:10.1111/j.1442-2050.2010.01160.x

Cited by 3 publications

(1 citation statement)

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“…However, there are currently no data to support such speculation. It has, however, been demonstrated that acid exposure is significantly greater in the distal and intrasphincteric segment of the esophagus [42, 51-53]. Fletcher at al.…”

Section: The Acid Pocketmentioning

confidence: 99%

Mechanisms of Barrett's oesophagus (clinical): LOS dysfunction, hiatal hernia, peristaltic defects

Roman

Kahrilas

2015

Best Practice & Research Clinical Gastroenterology

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Summary Barrett’s esophagus, with the potential to develop into esophageal adenocarcinoma (EAC), is a major complication of gastroesophageal reflux disease (GERD). However, about 50% of patients developing EAC had no known GERD beforehand. Hence, while GERD symptoms, esophagitis, and Barrett’s have a number of common determinants (esophagogastric junction (EGJ) incompetence, impaired esophageal clearance mechanisms, hiatus hernia) they also have some independent determinants. Further, although excess esophageal acid exposure plays a major role in the genesis of long-segment Barrett’s esophagus there is minimal evidence supporting this for short-segment Barrett’s. Hence, these may have unique pathophysiological features as well. Long-segment Barrett’s seems to share most, if not all, of the risk factors for esophagitis, particularly high-grade esophagitis. However, it is uncertain if EGJ function and acid clearance are more severely impaired in patients with long-segment Barrett’s compared to patients with high-grade esophagitis. With respect to short-segment Barrett’s, the acid pocket may play an important pathogenic role. Conceptually, extension of the acid pocket into the distal esophagus, also known as intra-sphincteric reflux, provides a mechanism or acid exposure of the distal esophageal mucosa without the occurrence of discrete reflux events, which are more likely to prompt reflux symptoms and lead to the development of esophagitis. Hence, intra-sphincteric reflux related to extension of the acid/no acid interface at the proximal margin of the acid pocket may be key in the development of short segment Barrett’s. However, currently this is still somewhat speculative and further studies are required to confirm this.

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Section: The Acid Pocketmentioning

confidence: 99%

Mechanisms of Barrett's oesophagus (clinical): LOS dysfunction, hiatal hernia, peristaltic defects

Roman

Kahrilas

2015

Best Practice & Research Clinical Gastroenterology

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The Acid Pocket: A Target for Treatment in Reflux Disease?

Kahrilas

McColl

Fox³

et al. 2013

American Journal of Gastroenterology

133

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The nadir esophageal pH of refl ux observed during pH monitoring in the postprandial period is often more acidic than the concomitant intragastric pH. This paradox prompted the discovery of the " acid pocket " , an area of unbuffered gastric acid that accumulates in the proximal stomach after meals and serves as the reservoir for acid refl ux in healthy individuals and gastroesophageal refl ux disease (GERD) patients. However, there are differentiating features between these populations in the size and position of the acid pocket, with GERD patients predisposed to upward migration of the proximal margin onto the esophageal mucosa, particularly when supine. This upward migration of acid, sometimes referred to as an " acid fi lm " , likely contributes to mucosal pathology in the region of the squamocolumnar junction. Furthermore, movement of the acid pocket itself to a supradiaphragmatic location with hiatus hernia increases the propensity for acid refl ux by all conventional mechanisms. Consequently, the acid pocket is an attractive target for GERD therapy. It may be targeted in a global way with proton pump inhibitors that attenuate acid pocket development, or with alginate / antacid combinations that colocalize with the acid pocket and displace it distally, thereby demonstrating the potential for selective targeting of the acid pocket in GERD.

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