Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2022 Jun;27(3):e12885.
doi: 10.1111/hel.12885. Epub 2022 Mar 20.

Atrophic gastritis in Helicobacter pylori-infected children

Affiliations

Atrophic gastritis in Helicobacter pylori-infected children

Hsuan Hsieh et al. Helicobacter. 2022 Jun.

Abstract

Background: Helicobacter pylori infection is the leading cause of peptic ulcer and chronic gastritis and may initiate gastric carcinogenesis following the Correa cascade. Another lineage of metaplasia, spasmolytic peptide-expressing metaplasia (SPEM) has recently been found to be an alternative precursor to gastric cancer. To date, few reports have investigated gastric precancerous lesions among children with H. pylori infection. This study aimed to evaluate the histopathological pattern of H. pylori atrophic gastritis in children and the extent of precancerous lesions.

Materials and methods: This study enrolled pediatric patients with H. pylori infection from 1998 to 2019. During esophagogastroduodenoscopy examinations, biopsy fragments were collected from the gastric antrum and corpus for rapid urease test, culture, and histology evaluation. The presence and degree of chronic inflammation, activity of gastritis, H. pylori density, atrophy, and intestinal metaplasia (IM) were assessed according to the modified Updated Sydney System. Trefoil factor 2 (TFF2) immunohistochemistry was also performed to assess SPEM in the gastric tissues collected from each case using rabbit anti-human TFF2 antibodies.

Results: A total of 92 children with H. pylori infection and adequate gastric mucosa biopsies were enrolled. Esophagogastroduodenoscopy showed that 39 (42.4%) had duodenal ulcers, 11 (12.0%) had gastric ulcers, 41 (44.6%) had gastritis, and 1 (1.1%) had negative findings. Mild-to-moderate IM was identified in 4 patients (4.3%). SPEM was found in 8 patients (8.7%) with a significantly higher incidence among female patients (15.8% vs. 8.7%, p = .031). Gastric glandular atrophy presented in 28 patients (30.4%), and high-grade atrophy was more common in female patients (3.2% vs. 1.9%, p = .031).

Conclusions: The prevalence rates of atrophic gastritis in the children with H. pylori infection were 30.4% for gastric glandular atrophy, 4.3% for IM and 8.7% for SPEM. SPEM and high-grade atrophy were more common in female patients.

Keywords: Helicobacter pylori; atrophys; child; intestinal metaplasia; spasmolytic peptide-expressing metaplasia.

PubMed Disclaimer

References

REFERENCES

    1. Correa P. A human model of gastric carcinogenesis. Can Res. 1988;48:3554-3560.
    1. Uemura N, Okamoto S, Yamamoto S, et al. Helicobacter pylori infection and the development of gastric cancer. N Engl J Med. 2001;345:784-789.
    1. Chen H-N, Wang Z, Li X, Zhou Z-G. Helicobacter pylori eradication cannot reduce the risk of gastric cancer in patients with intestinal metaplasia and dysplasia: evidence from a meta-analysis. Gastric Cancer. 2016;19:166-175.
    1. Whitney AE, Guarner J, Hutwagner L, Gold BD. Helicobacter pylori gastritis in children and adults: comparative histopathologic study. Ann Diagn Pathol. 2000;4:279-285.
    1. Ricuarte O, Gutierrez O, Cardona H, Kim JG, Graham DY, El-Zimaity HM. Atrophic gastritis in young children and adolescents. J Clin Pathol. 2005;58:1189-1193.

LinkOut - more resources