Proton pump inhibitors and H. pylori infection: Why the concern?

Abstract

Proton pump inhibitor therapy, even on a short-term basis, is associated with a decrease in antral gastritis and an increase in gastritis of the body. On a long-term basis, some series show the development of atrophic gastritis and some show none or hardly any. All studies fail to show or to report any significant increase in the prevalence of intestinal metaplasia with long-term PPI therapy. If one wants to determine whether PPIs cause atrophic gastritis with intestinal metaplasia, then the angularis primarily and the gastric antrum secondarily need to be studied because that is where most IM resides in the intestinal types of cancer. Instead of focusing on the angularis and antrum, the studies have evaluated biopsies from the gastric body, the least likely spot to be intestinalized in association with the intestinal type of gastric cancer [11]. H. pylori is associated with both intestinal and diffuse types of gastric cancer. Obtaining an answer to the question of whether PPI therapy or any other type of therapy increases gastric cancer risk in H. pylori-positive patients will require epidemiologic studies in which cancer is the end point. Intermediate theoretic markers are not available for diffuse cancers. If intermediate markers are used for the intestinal type of gastric cancer, then atrophic gastritis with intestinal metaplasia might provide some insight on theoretical grounds. However, the published long-term studies to date have not addressed that question because of where they have focused the biopsy sampling, and/or because of failure to report data on intestinal metaplasia.

Helicobacter pylori‐Induced Damage to the Gastric Mucosa is Not Modulated by Previous Vagotomy or Medical Treatment of Peptic Ulcer Disease: A Comparative Study of Vagotomized Patients, Medically Treated Peptic Ulcer Patients and Community Control Subjects

“…The frequency of intestinal metaplasia found in H. pylori-positive subjects in this study at the different biopsy sites is in accordance with the findings of Eidt and Stolte [18]. It should be reminded that it is not the gastric corpus but the gastric antrum and angulus that is the predominant location for H. pyloriassociated premalignant changes [33], and that it is not the gastritis or atrophy per se that is associated with increased risk of developing gastric cancer, but the severity of the atrophy and only atrophy associated with intestinal metaplasia [34,35].…”

Current practice in the use of antiplatelet agents in the peri-operative period by UK vascular surgeons

“…Some concern must also be voiced over the long-term effect of gastric acid suppression with proton pump inhibitors and H2 blockers. 16,17 Discontinuing antiplatelet therapy completely cannot be recommended as it is preferable that these patients continue antiplatelet therapy for prophylaxis against secondary vascular events.…”

The Risk of Gastric Cancer in Patients with Duodenal and Gastric Ulcer: Research Progresses and Clinical Implications

“…It seems that it remains too early for assessing such risk as it is just over 15 years since first PPI came to the market and only very small proportion of patients are on PPIs for longer than few years [54][55][56]. It is generally accepted, however, that PPI treatment can lead to a change in the distribution of H. pylori in the stomach from an antral to a predominantly corpus localization [57,58]. Most studies have found an annual increase in corpus atrophy in H. pylori-infected patients on PPIs compared with those receiving no treatment [59][60][61].…”