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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.

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The Role of H. pylori in Peptic Disease

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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 humans.4

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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

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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.

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Pathogenesis of H. pylori-Associated Peptic Disease

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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 ...

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