Helicobacter pylori - Associated Dyspepsia in Paediatrics

Helicobacter pylori ubiquitously infects the human gastric mucosa since time immemorial,predictably before the man’s diaspora out of East Africa around 58,000 years ago [1].Colonization may have been somehow beneficial for human carriers, allowing the coevolutionof this gram-negative bacterium and its host over the centuries. Yet, at leastnowadays [2], this may not be a peaceful association, with infection almost invariablycausing an acute host immune response. However, in a fully adapted manner, H. pyloriavoids recognition and, thus, clearance, by the host immune system, with both infectionand the consequent gastritis persisting throughout the patients’ life. The clinical outcomeof this persistence is dependent on a sophisticated crosstalk between the host and thepathogen. If often asymptomatic, the H. pylori-associated non-ulcer dyspepsia is clearly thestrongest aetiological factor for severe gastric diseases that will develop late in adult life ina minority of infected patients, i.e., peptic ulcer disease, both gastric and duodenal ulcers,and gastric cancer, namely, adenocarcinoma and mucosa associated lymphoid tissue(MALT) lymphoma (reviewed in [3]). Peptic ulcer disease rarely occurs soon after H. pyloriinfection [4-8] that generally starts in childhood; this presumably reflects marked differencesin the virulence [9-16] and/or in the susceptibility of young patients [17-19].This chapter, focussing on the paediatric population, seeks to explore: the prevalence of H.pylori infection; the molecular mechanism used by H. pylori during colonization and infection;the role of this bacterium in the development of peptic ulcer-related organic dyspepsia; andthe genetic/proteome profile of the H. pylori-strains associated with peptic ulcer disease.BNP Paribas, Sociedade Portuguesa de Gastrenterologi