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Association between Helicobacter pylori infection and gastrointestinal malignancy

Section Editor
Mark Feldman, MD, MACP, AGAF, FACG
Deputy Editor
Shilpa Grover, MD, MPH, AGAF


Since the discovery of Helicobacter pylori in the 1980s, much has been learned about this gram-negative spiral bacteria and its associated disease states. In 1994, the National Institutes of Health Consensus Conference recognized H. pylori as a cause of gastric and duodenal ulcers. Later that year, the International Agency for Research on Cancer declared H. pylori to be a group I human carcinogen for gastric adenocarcinoma [1]. There is also evidence that H. pylori infection is a risk factor for gastric mucosa-associated lymphomas (MALT lymphomas). (See "Clinical presentation and diagnosis of primary gastrointestinal lymphomas".)

Despite these clear associations, there is marked individual variability in the outcomes of H. pylori infection, with most patients having a non-neoplastic rather than neoplastic process. H. pylori infection is associated with a complex interaction between genetic, environmental, and bacterial factors, which potentially explains the different outcomes possible following infection. Until these factors are better defined and their interactions better understood, practitioners should limit testing for and treating H. pylori to those situations where there is evidence to support a clinical benefit.


Gastric cancer is one of the most common causes of cancer-related death in the world [2] (see "Epidemiology of gastric cancer"). Gastric cancers can be categorized by site of occurrence: gastroesophageal junction, proximal stomach, and distal stomach (body and antrum). In the 1930s in the United States, distal cancers were the most common. Over the subsequent 70 years, the incidence of gastric cancer has fallen primarily due to a reduction in distal cancers. In comparison, an increase in the incidence of gastroesophageal junction and proximal cancers has been noted during the past several decades [3,4]. These observations suggest that gastroesophageal and proximal gastric cancers share a common pathogenesis, which is distinct from that of distal cancers [5].

Adenocarcinomas, which accounts for more than 90 percent of tumors arising in the stomach, are of two distinct morphologic types: intestinal-type and diffuse. A sequence of steps with phenotypic changes in the gastric mucosa has been hypothesized as a model for carcinogenesis of intestinal type adenocarcinomas: superficial gastritis; chronic atrophic gastritis; intestinal metaplasia (picture 1); dysplasia; and finally carcinoma (algorithm 1) [6]. No similar sequence has been described for the diffuse type. (See "Pathology and molecular pathogenesis of gastric cancer".)

H. pylori can cause chronic active gastritis and atrophic gastritis, early steps in the carcinogenesis sequence [7,8]. In animal models, H. pylori infection has induced gastric adenocarcinoma [9]. Furthermore, a number of studies in humans have demonstrated a clear association between H. pylori infection and gastric adenocarcinoma [10-12]. The link has been demonstrated in both the intestinal and diffuse subtypes of gastric cancer [10,13].

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Literature review current through: Sep 2017. | This topic last updated: May 03, 2016.
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