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This article summarises the epidemiology and pathophysiology of Helicobacter pylori related disease in childhood, to enable the general paediatrician to develop an informed and evidence based approach to management.
H pylori is a unique bacterial pathogen:
it is widespread, so that around 50% of people throughout the world are colonised
it occupies an inhospitable niche (H pylori survives gastric acidity even down to pH of < 2)
colonisation is chronic and may be lifelong.
H pylori was first conclusively identified as a human pathogen, and an aetiological agent of acute gastritis, in 1984.1 The discovery that this bacterium is the cause of most peptic ulcer related disease in adult life has been arguably the most important advance in gastroenterology in recent decades. Approximately 0.5% of the UK population (around 290 thousand people, 20% of all general practice workload) are on long term acid suppression because of peptic ulcer related disease attributable to chronic H pylori infection.
H pylori are Gram negative spiral organisms (fig 1) that live within and beneath the mucus layer of the human stomach. They do not invade the host and can only survive adherent to gastric type mucosa. H pylori utilises a urea splitting enzyme (urease) to neutralise gastric acidity, as it traverses the gastric lumen. Urease negative mutants do not readily colonise animal models of infection.2
Two complete genomes for H pylori have been described.3,4 Among the genes that have excited considerable interest (which include BabA, IceA, neutrophil activating protein, and various flagella and heat shock proteins) are two principle virulence determinants known to play a role in disease causation; the cag pathogenicity island (CagA PAI which codes for several genes including cagA) and vacA (coding for vacuolating …
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