Preventing Metachronous Gastric Cancer after the Endoscopic Resection of Gastric Epithelial Neoplasia: Roles of Helicobacter pylori Eradication and Aspirin

Abstract

Whether Helicobacter pylori eradication actually reduces the risk of metachronous gastric cancer (MGC) development remains a controversial question. In this review, we addressed this topic by reviewing the results of clinical investigations and molecular pathological analyses of the roles of H. pylori eradication and aspirin administration in the prevention of MGC. In regard to the clinical studies, the results of meta-analyses and randomized control trials differ from those of retrospective studies: the former trials show that H. pylori eradication has a preventive effect on MGC, while the latter studies do not. This discrepancy may be at least partly attributable to differences in the follow-up periods: H. pylori eradication is more likely to prevent MGC over a long-term follow-up period (≥5 years) than over a short-term follow-up period. In addition, many studies have shown that aspirin may have an additive effect on MGC-risk reduction after H. pylori eradication has been achieved. Both H. pylori eradication and aspirin use induce molecular alterations in the atrophic gastritis mucosa but not in the intestinal metaplasia. Unfortunately, the molecular pathological analyses of these interventions have been limited by short follow-up periods. Therefore, a long-term prospective cohort is needed to clarify the changes in molecular events caused by these interventions.

Keywords: Aspirin; Eradication; Helicobacter pylori; Pathology; Stomach neoplasms; molecular.

Fig. 1

Biopsy specimens obtained from the gastric mucosa. Various numbers (small to large) of intestinal metaplastic glands are included in the samples (H&E, ×200).

Fig. 2

Schematic of the association between gastric cancer (GC) risk and the effects of Helicobacter pylori eradication and aspirin/nonsteroidal anti-inflammatory drugs (NSAIDs). H. pylori eradication when the patient is in his or her 40s or prior to the “decreased reversibility of the gastric mucosa” may suppress GC development. With regard to the reduction in metachronous GC (MGC) risk, the treatment may be effective from a long-term perspective. Long-term aspirin/NSAID use may have additional effects in reducing MGC risk after H. pylori eradication. OLGA, operative link on gastric atrophy; OLGIM, operative link on gastric intestinal metaplasia.