Page 580 - Robbins Basic Pathology by Vinay Kumar, Abul K. Abbas, Jon C. Aster

566 C H A P T E R 14 Oral Cavity and Gastrointestinal Tract • Adhesins, which enhance bacterial adherence to surface
foveolar cells
Chronic Gastritis
• Toxins, such as that encoded by cytotoxin-associated
The symptoms and signs associated with chronic gastritis gene A (CagA), that may be involved in ulcer or cancer
typically are less severe but more persistent than those of development by poorly defined mechanisms
acute gastritis. Nausea and upper abdominal discomfort
may occur, sometimes with vomiting, but hematemesis is These factors allow H. pylori to create an imbalance between
uncommon. The most common cause of chronic gastritis is gastroduodenal mucosal defenses and damaging forces that
infection with the bacillus Helicobacter pylori. Autoimmune overcome those defenses. Over time, chronic antral H. pylori
gastritis, the most common cause of atrophic gastritis, repre- gastritis may progress to pangastritis, resulting in multifo-
sents less than 10% of cases of chronic gastritis and is the cal atrophic gastritis, reduced acid secretion, intestinal
most common form of chronic gastritis in patients without metaplasia, and increased risk of gastric adenocarcinoma in
H. pylori infection. Less common causes include radiation a subset of patients. The underlying mechanisms contributing
injury and chronic bile reflux. to this progression are not clear, but interactions between
the host immune system and the bacterium seem to be
Helicobacter pylori Gastritis critical.

The discovery of the association of H. pylori with peptic MORPHOLOGY
ulcer disease revolutionized the understanding of chronic
gastritis. These spiral-shaped or curved bacilli are present Gastric biopsy specimens generally demonstrate H. pylori
in gastric biopsy specimens from almost all patients with in infected persons (Fig. 14–14, A). The organism is concen-
duodenal ulcers and a majority of those with gastric ulcers trated within the superficial mucus overlying epithelial cells in
or chronic gastritis. Acute H. pylori infection does not
produce sufficient symptoms to require medical attention AB
in most cases; rather the chronic gastritis ultimately causes
the afflicted person to seek treatment. H. pylori organisms
are present in 90% of patients with chronic gastritis affect-
ing the antrum. In addition, the increased acid secretion
that occurs in H. pylori gastritis may result in peptic ulcer
disease of the stomach or duodenum; H. pylori infection
also confers increased risk of gastric cancer.

Epidemiology
In the United States, H. pylori infection is associated with
poverty, household crowding, limited education, African
American or Mexican American ethnicity, residence in
areas with poor sanitation, and birth outside of the United
States. Colonization rates exceed 70% in some groups and
range from less than 10% to more than 80% worldwide. In
high-prevalence areas, infection often is acquired in child-
hood and then persists for decades. Thus, the incidence of
H. pylori infection correlates most closely with sanitation
and hygiene during an individual’s childhood.

PAT H O G E N E S I S CD

H. pylori infection most often manifests as a predominantly Figure 14–14 Chronic gastritis. A, Spiral-shaped Helicobacter pylori
antral gastritis with high acid production, despite bacilli are highlighted in this Warthin-Starry silver stain. Organisms are
hypogastrinemia. The risk of duodenal ulcer is increased abundant within surface mucus. B, Intraepithelial and lamina propria neu-
in these patients, and in most cases, gastritis is limited to the trophils are prominent. C, Lymphoid aggregates with germinal centers
antrum. and abundant subepithelial plasma cells within the superficial lamina
propria are characteristic of H. pylori gastritis. D, Intestinal metaplasia,
H. pylori organisms have adapted to the ecologic niche recognizable as the presence of goblet cells admixed with gastric foveolar
provided by gastric mucus. Although H. pylori may invade the epithelium, can develop and is a risk factor for development of gastric
gastric mucosa, the contribution of invasion to disease patho- adenocarcinoma.
genesis is not known. Four features are linked to H. pylori
virulence:
• Flagella, which allow the bacteria to be motile in viscous

mucus
• Urease, which generates ammonia from endogenous

urea, thereby elevating local gastric pH around the organ-
isms and protecting the bacteria from the acidic pH of the
stomach