Helicobacter pylori

In recent years evidence has accumulated that infection of the gastric mucosa by the bacterium H. pylori is a causative factor in the development of ulcer disease. These spiral Gram-negative bacteria are found in the stomach of over 80% of patients with gastric or duodenal ulcers. Up to 90% of the population are infected with H. pylori by adult life in the Western world. The vast majority of individuals with a presence of the HP bacteria are usually healthy and asymptomatic and only a minority develop clinical disease (www.helico.com accessed 8 May 2004).

Pathophysiolgy of HP infection

The HP bacterium has many flagella attached to one end, making it highly mobile. It has adapted to the acidic nature of the stomach by burrowing beneath the mucosa of the stomach. Here the surface pH is close to neutral and any acidity is buffered by the organism's production of the enzyme urease. Urease produces ammonia from urea and raises the pH around the bacterium. Although it is non-invasive, the bacterium stimulates chronic gastritis by provoking a local inflammatory response in the underlying epithelium due to release of a range of cytotoxins. Once infection in the antrum is established, there is depletion of antral somatostatin and stimulation of gastrin release from G-cells. The subsequent increased flow of blood to the region (hypergastrinaemia) stimulates acid production by the parietal cells, leading to duodenal mucosal damage. Consequences of H. pylori infection include gastritis and gastric and duodenal ulcers.

Diagnosis of HP infection

Multiple methods are available for the detection of HP infection. Non-invasive methods include serology for antibody or antigen detection. Invasive procedures include biopsy during endoscopy for histology or rapid urease testing. These procedures are further examined in Chapter 10. For the latest information on HP consult the Heliobacter Foundation (www.helico.com accessed 8 May 2004).

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