Helicobacter pylori Infection and Gastric Adenocarcinoma

Abstract

Gastric adenocarcinoma is the second leading cause of cancer-related mortality worldwide. Infection with Helicobacter pylori is the strongest recognized risk factor for gastric adenocarcinoma. This bacterial species colonizes the stomach of more than half of the world's population; however, only a very small proportion of infected subjects develop adenocarcinoma. H. pylori causes a chronic gastritis that may last decades, and a multistep precancerous process is recognized for the most frequent histologic type of gastric adenocarcinoma: the intestinal type. The severity and long-term outcome of this infection is modulated by an increasing list of bacterial, host, and environmental factors, which interplay in a complex manner. Identification of individuals at high risk for gastric cancer that may enter a surveillance program and intervention during the precancerous process is the most suitable strategy for decreasing mortality due to this malignancy.

Figure 1. Photomicrographs of Gastric Adenocarcinoma of the Intestinal and Diffuse Types (Lauren Classification)

A: Intestinal type. The tumor cells are cohesively arranged, forming irregular glandular structures infiltrating the stroma (H&E, ×200). B: Diffuse type. Single tumor cells infiltrate diffusely the stroma. In this subtype, the signet-ring cell adenocarcinoma, the intracytoplasmic mucin compresses the nucleus against the periphery of the cell, giving it its characteristic signet-ring appearance (H&E, ×400).

Figure 2. Histologic Section of Human Gastric Mucosa Colonized by Helicobacter pylori

Abundant microorganisms (black staining) are seen attached to the epithelial cells and surrounding mucus layer (modified Steiner silver stain, ×400).

Figure 3. Photomicrographs of Sequential Steps in the Gastric Mucosa for the Development of Adenocarcinoma

A) Normal gastric antral mucosa. B) Non-atrophic gastritis. Abundant inflammatory cells are seen in the lamina propria and the glands are well conserved. C) Multifocal atrophic gastritis, with prominent loss of deep glands. D) Intestinal metaplasia of the complete type, with well-formed goblet cells and brush border. E) Dysplasia, low-grade. Epithelial cells with enlarged, hyperchromatic and pseudostratified nuclei that maintain the polarity respect to the basement membrane. F) Adenocarcinoma of the intestinal type (H&E, ×200).