Antral Atrophy,Helicobacter pyloriColonization, and Gastric pH

Abstract

The association between the topographic distribution of Helicobacter pylori colonization, inflammation and atrophy of the gastric mucosa, and fasting gastric pH was studied in a population with high prevalence of multifocal atrophic gastritis. Increasing atrophy of the antrum was associated with decreasing H pylori colonization of the antrum itself, but increasing colonization of the corpus. Advanced atrophy was associated with high fasting gastric pH. However, after therapeutic eradication of H pylori, inflammation subsided and gastric pH decreased indicating improved acid secretion despite persistent atrophy. The authors propose that antral atrophy fosters the colonization of oxyntic mucosa by H pylori, thus impairing acid secretion and causing hypochlorhydria that may further promote colonization of the oxyntic mucosa. Eradication of H pylori significantly improves hypochlorhydria. It m:iy restore acid secretion in most patients, regardless of the presence of atrophy, which is an effect that may be of great benefit in halting the process of gastric carcinogenesis. Inconsistent findings have been published regarding the effects of Helicobacter pylori on gastric acidity and acid secretion. "14 Most studies are based on a very small number of observations, deal only with duodenal ulcer patients or asymptomatic volunteers, and do not consider the type of gastritis, the presence of atrophy, or the effect of Hpylori colonization in the different specialized areas of the gastric mucosa.Helicobacter pylori infection causes hypergastrinemia and hyperacidity, which is a mechanism that has been related to the etiology of duodenal ulcers, in at least in some individuals. 4715 However, at Charity Hospital in New Orleans, H pylori infection is often associated with hypochlorhydria. Hypochlorhydria is thought to be a consequence of atrophic gastritis and has been related to the etiology of gastric cancer. 16 We examined the associations among the presence, abundance, and topographic distribution of H pylori infection in the gastric mucosa, mucosal atrophy, and fasting gastric pH in patients referred for endoscopy. MATERIALS AND METHODSSubjects of this study were referred for endoscopy at Charity Hospital in New Orleans, had not taken antibi- otics, bismuth, or drugs that inhibit acid secretion during the previous 2 weeks and gave a written informed consent. This study was approved by the Louisiana State University Medical School Institutional Review Board.Patients were examined after overnight fast. Immediately after passing the endoscope into the stomach, up to 50 rnL of gastric juice were aspirated into a sterile container. Gastric juice pH was measured with a calibrated digital pH meter soon thereafter. Two antral biopsies (distal greater curvature and lesser curvature adjacent to the incisura angularis) and one biopsy from the gastric corpus (mid anterior wall) were fixed in buffered formalin and embedded in paraffin. Reported history of peptic ulcers and endoscopic observation of peptic ulcers were registered.Paitient...

Association of Gastric Mucosal Injury Severity with Platelet Function and Gastric pH during Low-Dose Aspirin Treatment

“…However, this technique is relatively invasive and is difficult to be routinely performed for all patients with acid-related disorders. For this reason, we measured the pH of gastric juice samples collected by aspiration during endoscopy, as this approach has also been used to evaluate acid secretion [23,24,25]. Using one-point measurements, we found that gastric juice pH was significantly associated with gastric mucosal injury induced by LDA.…”

Pathogenesis ofHelicobacter pyloriInfection

“…This is illustrated by various observations. Firstly, H. pylori corpus gastritis is often associated with hypochlorhydria, and eradication therapy leads to increased acid secretion in these subjects (158,533). Secondly, H. pylori corpus gastritis augments the acid-suppressive effects of PPIs (663).…”

Helicobacter pylori Eradication Prevents Extension of Intestinalization Even in the High-Risk Group for Gastric Cancer

“…We speculated that eradication may prevent extension of intestinalization even in the high-risk group for gastric cancer. It is reported that CDX2 expression and intestinal trans-differentiation in the gastric mucosa can be suppressed by an increase in acid secretion that often follows H. pylori eradication presumably due to removal of the postulated acid inhibitory factors [29,30,31,32]. Further studies are required to elucidate the molecular mechanisms how eradication suppress aberrant CDX2 expression.…”