Long-term Symptom Patterns, Endoscopic Findings, and Gastric Histology in Helicobacter pylori-Infected and -Uninfected Patients

Abstract

There is a paucity of data on the long-term behavior of dyspepsia, endoscopic findings, and gastroduodenal histology in patients with or without Helicobacter pylori colonization. We evaluated these parameters during a period of 7 to 19 years (average, 12.3 years) by baseline and follow-up studies. In 36 patients studied, the pattern of gastroduodenal dyspepsia and esophagogastroduodenoscopy findings remained essentially unchanged in 67% and 56% respectively. Dyspepsia patterns did not correlate significantly with either endoscopic or histologic findings, including the severity or location of gastritis in the fundus or antrum, or the presence or absence of H. pylori gastritis. Of 36 patients with adequate biopsies of the fundus and antrum, H. pylori colonization with gastritis was present in 73% but not in 27%. Progression to various degrees of atrophic gastritis was noted in 100% with, and in none without, H. pylori gastritis. In the fundus, atrophy progressed from 14% to 56%, but intestinal metaplasia did not change. In the antrum, atrophy increased from 22% to 64% and intestinal metaplasia increased from 17% to 36%. No patient demonstrated dysplasia, but severe atrophy was seen in the fundus (6%) and antrum (11%). Only two patients (5%) had severe loss of glandular elements and very low pepsinogen I, and thus can be considered to have developed advanced gastric atrophy.

Association of Helicobacter pylori infection with atrophic gastritis and intestinal metaplasia

“…Aging was the only a risk factor for atrophy in H. pylori infected patients, but it was no longer a risk factor for atrophy in patients without H. pylori infection. This result is consistent with previous studies including cross‐sectional studies 41–43 and long‐term follow up studies 44–46 . In contrast, aging was a common risk factor for intestinal metaplasia in both patients with and without H. pylori infection.…”

Evidence-Based Recommendations for Short- and Long-Term Management of Uninvestigated Dyspepsia in Primary Care: An Update of the Canadian Dyspepsia Working Group (CanDys) Clinical Management Tool

“…Patients with GERD who require long-term acid suppression, especially with a PPI, and who are infected with H pylori, have a worsening of gastritis in the body of the stomach (141). This deterioration of histological gastritis is not seen in H pylori-negative patients taking PPIs or in those in whom H pylori infection has been cured (142)(143)(144)(145)(146)(147). Several randomly assigned controlled trials (148,149), however, have shown that cure of the H pylori infection leads to regression of the body gastritis.…”

Personal view: to treat or not to treat? Helicobacter pylori and gastro‐oesophageal reflux disease — an alternative hypothesis

“…Gastric cancer is known to be associated only with pangastritis or a corpus‐predominant pattern 66 ,. 67 …”

“…This pattern of gastritis is the precursor of gastric cancer 66 ,. 67 If, however, H. pylori is eradicated, inflammation disappears and the progress to atrophy is arrested or reversed 78 . Acid suppression in a patient with a normal stomach does not lead to either gastritis or atrophy.…”

“…Gastric cancer is known to be associated only with pangastritis or a corpuspredominant pattern. 66,67 The epidemiology of H. pylori-associated disease has changed dramatically since the 19th century. Duodenal ulcer, which was rare until 1890, took over from gastric ulcer in the early 20th century in Europe, perhaps reflecting the increase in acid secretion in the population.…”