Helicobacter pylori
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Introduction
The Case of...
Epidemiology
H. pylori is thought to be the world's most common infection, with an estimated 50% infected. In the West, there is a clear age-related increase in prevalence, while in the developing world, over 80% are infected by age 20. Colonization is more common in people from lower socioeconomic backgrounds.
Classification and Characteristics
H. pylori are curved, flagellated, gram-negative rods. Factors helping it colonize the stomach include motility, production of urease, and bacterial adherence. Ammonia production by urease neutralizes acid.
Transmission and Infection
Mode of transmission appears fecal-oral, and occurs primarily in childhood. Adult acquisition is rare. Infection is typically lifelong unless treatment is done.
H. pylori are found only within gastric epithelium or in gastric metaplastic epithelium. Bacteria live in the mucus layer and are characterized as noninvasive.
Clinical Manifesations
Tissue injury is mediated by LPS, leukocyte-activating factors, and CagA and VacA proteins, associated with cytotoxic effects, inflammation, and cytokine activation.
H. pylori cause superficial gastritis in almost all those infected and peptic ulcer disease in 20% of those infected. An increased risk for gastric cancer is also present.
Acute and chronic inflammation consists of neutrophils, plasma cells, T cells, and macrophages, along with epithelial injury.
Infection in the stomach antrum can lead to duodenal ulcers due to increased gastrin expression by G cells, increased acid production by parietal cells, and duodenal ulceration.
Infection in the stomach body can lead to gastric ulcers and gastric cancers due to chronic gastritis.
Other possible associations occur with iron deficiency, immune thrombocytopeina, CAD, HT, SIDS, and migrane.
Diagnosis
Serological testing is noninvasive and can be used to detect initial infection, but because antibodies remain for several years, it is not useful for documenting cure.
13C or 14C-labeled urea breath testing is more accurate, though more expensive and less available. PPIs should not be taken for at least 14 days to avoid false-negative results.
Stool antigen testing can be useful. Endoscopic samples can be evaluated using the rapid urease test, with high sensitivity and specificity.
Histologic sampling from across the stomach can detect the bacteria, but even if they are hard to find, chronic, active gastritis is strongly suggestive of infection.
Treatment
Successful care requires at least 2 antimicrobial agents. Compliance is essential.
- PPI
- clarithromycin
- amoxycillin/metronidzine
PPI-BMT (80-85% cure rate)
- PPI
- bismuth
- metronidazole
- tetracycline
Resources and References
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