Helicobacter pylori

Question 1

Gastritis
CLINICAL PRESENTATION
Gastritis represents a nonspecific inflammation of the
mucosal surface of the stomach. Clinically, the three most
common causes of gastritis are Helicobacter pylori, nonsteroidal
anti-inflammatory drugs (NSAIDs), and stress-related
mucosal changes.

Answer 1

Helicobacter pylori
Helicobacter pylori are curved, flagellated, gram-negative
rods found only in gastric epithelium or in gastric metaplastic
epithelium. It is the most common worldwide microbial
infection, with an estimated 50% of the world’s population
being infected. H. pylori organisms clearly cause histologic
gastritis and are found in 50% to 95% of patients with gastroduodenal
ulcers. However, only a minority of patients
with H. pylori gastritis develop peptic ulcer disease (PUD)
or gastric cancer. In the Western world, a clear age-related
prevalence of H. pylori infection exists in healthy individuals,
increasing from 10% in those younger than 30 years to 60%
in those older than 60 years, and the mode of transmission
appears to be by the fecal-oral route. Improvements in sanitation
and standards of living have been associated with a
decline in the rate of infection. H. pylori colonization is more
common in individuals in lower socioeconomic strata compared
with other groups. In the developing world, infection
is far more common, with more than 80% of the population
being infected by age 20 years. H. pylori infection is typically
lifelong, unless antimicrobial treatment is instituted.

Question 2

H. pylori organisms reside in the mucus layer overlying
gastric epithelium and are characterized as noninvasive
organisms. Factors important in the organism’s ability to
colonize the stomach include its motility, production of
urease, and bacterial adherence. Ammonia generated from
urea by H. pylori urease neutralizes acid, creating a more
hospitable microclimate in which the bacteria can survive.
H. pylori also have the ability to bind specifically to gastrictype
epithelium, which prevents the organisms from being
shed during cell turnover and mucus secretion or gastric
motility. Tissue injury is mediated by the production of lipopolysaccharide,
leukocyte-activating factors, and CagA and
VacA proteins, which have been associated with cytotoxic
effects, inflammation, and cytokine activation. Colonization
causes acute and chronic inflammation consisting of neutrophils,
plasma cells, T cells, and macrophages accompanied
by varying degrees of epithelial cell injury, all of which
resolve after treatment.

Answer 2

Although predicting the ultimate outcome of H. pylori
infection is impossible, the clinical manifestations can be
correlated with various distributions of gastric histopathologic
states. Antral-predominant H. pylori gastritis is associated
with duodenal ulcers, whereas corporal and fundic
colonizations are more likely to cause atrophic gastritis.
Other important factors that may influence the outcomes
of the infection include the host response, environmental

Question 3

factors, and age at the time of infection. Virtually all patients
with H. pylori infection have a chronic superficial gastritis;
however, duodenal and gastric ulcers develop in only 20%
of infected patients. Patients with H. pylori infection and
severe atrophic gastritis, corpus-predominant gastritis, or
both, along with intestinal metaplasia, are at increased risk
for intestinal-type gastric cancer. Finally, the mucosal lymphocytic
response to H. pylori infection may lead to a monoclonal
B-cell proliferation in mucosa-associated lymphoid
tissue (MALT). MALT lymphomas, also known as maltomas,
are rare, with about 1 in 1 million infected patients
developing the disease. Complete histologic regression has
been demonstrated in 50% to 80% of maltomas following
eradication of H. pylori. Flat, localized, nonbulky lesions of
the distal stomach are associated with greater rates of cure
after antibiotic therapy.

Answer 3

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