Helicobacter Pylori

Since its description in 1983, H. pylori has been implicated as a causative agent of gastritis, gastric adenocarcinomas, gastric B cell lymphoma, and peptic ulcer disease. In developed countries, the prevalence increases with age, whereas in developing countries, most children are infected by the age of 10 years. Transmission is believed to be by person-to-person spread, although the means of spread is unclear. Intrafamilial transmission is suggested by several epidemiologic studies.

The bacterium produces factors that allow it to colonize the gastric mucosa and, for some strains, gives it the ability to adhere to the epithelium. The flagella allow it to move quickly through the mucus layer to a region where the pH is neutral and thus favorable. The urease produced by H. pylori partly acts by producing ammonia from urea and locally neutralizing acid. Helicobacter pylori also produces factors that are associated with its virulence. The vacuolating toxin (vacA) causes vacuole formation in eukaryotic cells. Nearly half of the strains express vacA. Another protein, CagA, is often associated with more intense inflammation, duodenal ulceration, and gastric adenocarcinoma.

Acute infection with H. pylori induces a neutro-philic gastritis accompanied by transient hypo-chlorhydria. Chronic infection results in a chronic superficial gastritis characterized by neutrophils, eosinophils, and B and T lymphocytes. Inflammation is a result of bacterial products (e.g., VacA, CagA) and factors produced by gastric epithelial cells (e.g., cytokines). Most individuals with chronic infection remain asymptomatic. One in six chronically infected individuals will develop peptic ulcer disease. Atrophic gastritis, gastric lymphoma, and gastric adenocarcinoma are also thought to result from chronic infection, although these occur far less frequently.

Diagnosis of H. pylori infection can be made using an invasive endoscopic method or less-invasive breath tests and immunological assays (see Table 2). Endoscopy allows the collection of tissue biopsies that can subsequently be examined by histology, cultured for H. pylori, or measured for urease production. Histology with hematoxylin & eosin stain and special stains (Giemsa, Warthin-Starry) visualizes the bacteria as well as the surrounding inflammation. Culture is highly specific and it permits testing for antibiotic resistance, but its sensitivity is reduced by the risk of contamination. Urease tests on histological samples have a high sensitivity because the entire tissue sample is used to measure urease. Less-invasive tests that do not require gastric mucosal samples include ser-ology, urea breath tests, and stool antigen tests. Serology is used to measure serum IgG antibodies.

Table 2 Diagnostic tests for Helicobacter pylori

Diagnostic test

Notes

Histology

Invasive; requires biopsy

Urease test

Invasive; requires biopsy

Culture

Invasive; requires biopsy

Serology

Not suitable for follow-up studies

Urea breath test

Noninvasive; can be used to monitor

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