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# Helicobacter pylori and the gastrointestinal system

## Problem

Helicobacter pylori is a Gram negative, microaerophilic bacterium characterized by its ability to survive in highly acidic conditions. This infectious pathogen, most commonly associated with Peptic Ulcer Disease (PUD), is responsible for the development of 70% of gastric ulcers, and an estimated 80-95% of duodenal ulcers, which may lead to the development of certain cancers. Once the bacteria reach the stomach, they burrow through the protective mucosal layer and adhere to the gastric epithelium, causing local cell destruction and inflammation.
Most commonly, H. pylori colonizes the antrum of the stomach—the distal end of the organ which is most closely associated with the opening to the small intestine, the pyloric sphincter.
Figure 1: Anatomical distribution of various secretory cell types throughout the stomach.
Due to the relatively localized nature of H. pylori infection, it is not surprising that on microscopic analysis of a stomach afflicted by PUD, a marked destruction in somatostatin-producing D-cells is noted. The decreased presence of D-cells relative to other cell types within the stomach is accompanied by measurable increases in gastric acid production, and a decrease in luminal pH. H. pylori is capable of surviving in these harsh conditions by two mechanisms. First, the mucous layer through which it burrows to reach the epithelial surface is characterized by a more neutral pH than the gastric lumen. Second, the organism is capable of producing the enzyme urease, the effect of which is to produce a more neutral environment in the area immediately surrounding the bacterium.
A strong association between chronic H. pylori infection and the development of gastric cancer has been demonstrated, though few studies have been able to accurately assess whether this risk is more strongly associated with specific microscopic subtypes of cancer or their anatomical distribution. Retrospective studies have been of limited use in this regard, as H. pylori does not colonize existing areas of cancer or atrophy, and thus such a model cannot fully assess the etiology of a long established gastric cancer.
A 2001 review of twelve prospective studies attempted to illustrate the association between gastric cancer risk and anatomical distribution (Cardia vs. non-Cardia) in patients with a known H. pylori infection. The results of this study are shown in Figure 2, which map the Odds Ratio (a measure of association between two variables, wherein a ratio not equal to “one” denotes some association) and 95, percent confidence interval for the relationship between cancer development and H. pylori for the given anatomical area.
Figure 2: Association between chronic H.pylori infection and the development of gastric cancers compared across twelve prospective studies. Matched Odds Ratio (OR) and 95, percent confidence intervals for association between H.pylori infection and non-cardia cancer (Panel A) and cardia cancer (Panel B). The area of the black squares is proportional to the study size. The white diamond shows the OR value for all studies combined, with 95, percent confidence interval represented by horizontal spread.
Data adapted from: Webb, P. M., Law, M., Varhese, C., & Forman, D. Gastric cancer and Helicobacter pylori : a combined analysis of 12 case control studies nested within prospective cohorts. Gut, 49, 347-353.
What is the most likely sequelae in generating the decreased luminal pH following the destruction of antral D-cells in H. pylori infection?