Gastritis is an inflammatory process
associated with gastric mucosal injury. It is usually classified
by histologic features (atrophic or non-atrophic, chemical, granulomatous,
eosinophilic, lymphocytic, etc.), time course (acute versus chronic),
etiology (Helicobacter pylori, bile,
non-steroidal anti-inflammatory drugs (NSAIDs), Crohn’s
disease, etc.), and proposed pathophysiology.
Peptic ulcers are deep mucosal ulcerations that penetrate into
the muscularis mucosa of the stomach or duodenum. Peptic erosions are superficial mucosal
lesions; they do not involve the muscularis mucosa. Peptic ulcers
and erosions are relatively uncommon in children, found in less
than 25% of children undergoing upper gastrointestinal
endoscopy for abdominal pain.1H.
pylori is by far the most common etiology for gastritis and
peptic ulcer disease (PUD) in the pediatric age group.
The Role of H. pylori in Peptic Disease
H. pylori is a Gram-negative spiral
organism that colonizes the gastric mucosa of humans. The bacteria live
in the gastric mucus and cause chronic gastritis, duodenal ulcers,
and, to a lesser extent, gastric ulcers. Infection with H. pylori is strongly associated with
gastric adenocarcinoma and mucosal-associated lymphomas (MALT) in
H. pylori is almost always acquired
in childhood (usually before 10 years of age), and if untreated,
infection is lifelong.2 It is estimated that 50% of
the world’s population is infected with this organism.
Infection with H. pylori is prevalent
in developing countries where about 80% of children are
colonized. The highest rates of H. pylori prevalence
are in Eastern Europe, Asia, and many developing countries. The
organism is also prevalent in selected populations in the United
States (e.g., Native Americans, African Americans, and Hispanics).
Lifetime risk of developing PUD from H.
pylori infection is 10–15%, while gastric
cancer develops in less than 1%.3
The route of transmission of H. pylori remains
incompletely defined. Infection is thought to result from direct
human-to-human contact via fecal–oral, oral–oral,
or gastro-oral routes.4 Contaminated water can also be
a reservoir. Low socioeconomic status, poverty, crowding, and poor
hygiene are considered as major risk factors for this infection.
Twenty-one percent of children whose mothers are infected with H. pylori acquire the infection, compared
to 3% of children whose mothers are not infected, confirming
that H. pylori-infected mothers are
a key source of infection.5H.
pylori infection is uncommon in children from developed countries
(10%) and the number of symptomatic cases seems to be decreasing.
of H. pylori-Associated Peptic Disease
Adherence of H. pylori to gastric
epithelial cells facilitates access to nutrients and delivery of
effector molecules that are essential for the development of the
disease.6 The main virulence determinant of H. pylori is a 40-kb genomic “pathogenicity
island” called cytotoxin-associated gene or cag. Cag-positive
strains are closely associated with PUD and gastric cancer7;
patients infected with cag-negative
strains tend to have less severe disease. Genes in the cag pathogenicity ...