Background and objectives: It is known that Helicobacter pylori can be acquired in early childhood. There is not enough data to know whether or not infected children should be treated. A better knowledge of the natural outcome and implications of H pylori infection may provide evidence that eradication therapy is beneficial in childhood. This prospective study looks at clinical symptoms, endoscopic, microbial, and histologic changes during a 2-year period in infected asymptomatic children. It is hoped that some prognostic indicators will be found that select out the children that later need therapy.
Patients and methods: During epidemiologic study of the prevalence of H pylori infection, 18 children aged 7 +/- 4 years (mean +/- 1 SD) were discovered to have H pylori infection and enrolled in the 2-year follow-up study. These patients had received no eradication therapy because they were asymptomatic. The follow-up for each patient consisted of an initial assessment, a clinical examination every 6 months, and an endoscopic reevaluation at the end of the first and second years. Gastric mucosal samples were analyzed for bacteriologic and histologic changes. Various factors were initially recorded: individual factors included sex, age, and housing conditions; microbial factors included bacterial load and the presence of the CagA gene. Inflammatory changes were also noted, such as the presence of active gastritis and nodular formation, and these were correlated with the histology which was described using the Sydney classification. Typing polymerase chain reaction-restriction fragment length polymorphism was performed to check the persistence of the same strain of H pylori in each patient.
Results: All of the children were still infected after 2 years with the same strain as in the initial assessment with the exception of 1 child whose infection cleared spontaneously. The density of antral and fundal mucosal colonization with H pylori also remained stable. There were progressive inflammatory changes in this cohort, particularly between the first and second year (histologic score, 3.5 +/- 1.3 vs 5 +/- 1). Active antral gastritis occurred in 3 out of 14 and 1 out of 8 children during the first and second year, respectively. Gastritis became active in the fundus in 2 out of 14 and 2 out of 8 children during the same period. Increases in the histologic score were found particularly in male children, and children colonized by cagA- strains of H pylori during the follow-up. The frequency of nodular gastritis significantly rose from 11% (2 out of 18 children) to 64% (9 out of 14 children) after 1 year, and to 80% (8 out of 10 children) after 2 years.
Conclusion: These findings demonstrate a deterioration in the histologic features of the gastric mucosa of infected children despite stable H pylori colonization and the absence of symptoms.