Introduction

Helicobacter pylori is a slowly growing, gram negative microaerophilic bacterium that colonises the gastric mucosa. Cross-sectional epidemiological studies from both developed and developing countries suggest that the prevalence of H. pylori infection worldwide is declining, and may even be less than 10% in ‘westernised’ countries.1 ,2 H. pylori infection is acquired during the first decade of life and infection usually persists without treatment. Spontaneous clearance has been reported, although co-incidental antibiotic exposure may influence such ‘clearance’. H. pylori is the causative agent for diseases including peptic ulcer disease (PUD), chronic gastritis, gastric mucosa associated lymphoid tissue lymphoma and is the single-most important risk factor for developing gastric cancer.3 ,4 Putative extraintestinal associations have included refractory iron deficient anaemia, short stature and idiopathic thrombocytopenic purpura, although data supporting these associations in children must be interpreted with caution.4 ,5 The majority of children infected with H. pylori are asymptomatic. Following successful treatment, the risk of true reinfection in childhood is extremely low, at least in developed countries.6 Recrudescence describes re-colonisation with the same strain within 12 months, while re-infection refers to colonisation with a new strain, more than 12 months after eradication. Clinicians must carefully bear in mind these salient aspects of the pathogenesis and natural history of H. pylori-associated diseases as they consider whether testing their patients for H. pylori is indicated.