Abstract
Objectives
We aimed to evaluate the histopathological characteristics of chronic gastritis in dyspeptic patients without visible mucosal lesions in different age groups and different biopsy sites.
Methods
Patients who underwent upper endoscopy for the investigation of dyspepsia as the sole indication were recruited. We selected data from patients without visible mucosal lesions for the study. Gastric biopsy specimens were evaluated by Update Sydney classification according to age, Helicobacter pylori (Hp), and biopsy sites.
Results
A total of 626 patients were retrospectively studied. 58.2% had histopathological features of chronic gastritis, while 41.8% had normal gastric mucosa. The prevalence of glandular atrophy, intestinal metaplasia, and Hp infection was 36.7, 19.3 and 36.6%. Complete and incomplete metaplasia was found to be 17.0 and 2.2%. The mean score of chronic inflammation, neutrophil activity, glandular atrophy, and intestinal metaplasia was significantly higher in the antrum than in the corpus. The positivity of gastritis increases with age; however, Hp positivity decreased considerably with advanced age. Concerning gastritis’s topography, antral-predominant gastritis and corpus-predominant gastritis increased with age. The prevalence of glandular atrophy and intestinal metaplasia markedly increased with age, especially after age 50. Gastric atrophy and intestinal metaplasia were significantly higher in patients positive for Hp than in negative patients.
Conclusion
Overall chronic gastritis is common in dyspeptic patients without visible lesions. Prevalence, grading, and severity of chronic gastritis increase with age and Hp infection. Temporal changes of the gastric mucosa are caused by aging rather than by Hp alone.
Acknowledgments
The authors thank Mrs. Patumrat Sripan, Research Institute for Health Sciences, Chiang Mai University, for her guidance in regression analysis and statistical computing.
Ethics approval
This study was approved by the Institutional Review Board for Chiang Mai University (MED-2558-07016).
Author contributions
T.C. contributed to the study conception and design; acquisition, analysis, and interpretation of data; drafted the manuscript and revised it critically for valuable intellectual content; and gave the final approval for publication. T.C. and P.J. undertook the endoscopic assessments and performed data collection. N.C. performed data collection and statistical analysis. N.L. helped with the pathologic evaluations. All authors have seen and approved the final version of the report.
Disclosure statement
The authors declare that there is no conflict of interest regarding the publication of this paper.
Data availability statement
The datasets used and analyzed during the current study are available from the corresponding author on reasonable request.