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 coevolution of this gram-negative bacterium and its host over the centuries. Yet, at least nowadays [2], this may not be a peaceful association, with infection almost invariably causing an acute host immune response. However, in a fully adapted manner, H. pylori avoids recognition and, thus, clearance, by the host immune system, with both infection and the consequent gastritis persisting throughout the patients’ life. The clinical outcome of this persistence is dependent on a sophisticated crosstalk between the host and the pathogen. If often asymptomatic, the H. pylori-associated non-ulcer dyspepsia is clearly the strongest aetiological factor for severe gastric diseases that will develop late in adult life in a 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. pylori infection [4-8] that generally starts in childhood; this presumably reflects marked differen‐ ces in the virulence [9-16] and/or in the susceptibility of young patients [17-19].