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Korean J Helicobacter  Up Gastrointest Res > Volume 26(3); 2026 > Article
Im: Autoimmune Gastritis: An Evolving Entity
Autoimmune gastritis (AIG) has long occupied an awkward place in clinical practice. For most of the 21th century, it was viewed mainly through its hematologic endpoint—pernicious anemia—and seen as a rare, late diagnosis of limited relevance to the endoscopist. That perception has changed. AIG is now found earlier and more often, frequently in patients who have no symptoms or who present only with iron-deficiency anemia, and it is increasingly recognized as a corpus-restricted gastric disease with meaningful neoplastic implications [1,2].
In this issue of the Korean Journal of Helicobacter and Upper Gastrointestinal Research [3], trace this shift through a hybrid bibliometric-conceptual analysis of AIG research from 1995 to 2025. Across 1298 articles from 5608 authors in 45 countries, annual output rose from 24 in 1995 to 86 in 2025, and the focus of the field changed clearly over time. Early studies centered on pernicious anemia, gastric autoimmunity, and chronic gastritis, whereas recent studies focus on endoscopic recognition, biomarker-based diagnosis, gastric neuroendocrine tumors (NETs), and neoplastic risk. Co-citation analysis frames this as a movement from immunologic and pathophysiologic investigation toward clinically oriented disease recognition and surveillance [3].
This shift reflects a real change in daily practice. Corpus biopsy is still the diagnostic standard, but serologic and functional markers—the pepsinogen I/II ratio, serum gastrin, and anti-parietal cell and intrinsic factor antibodies—now allow corpus-predominant atrophy to be suspected before or alongside endoscopy [2,4], and artificial intelligence tools that help detect corpus atrophy, noted here as one of the newest topics, point toward earlier detection [3]. This change matters most for cancer risk. Hypergastrinemia can lead to indolent type 1 gastric NETs, while corpus atrophy and intestinal metaplasia raise the risk of gastric adenocarcinoma—if still debated [2,5]. Because no treatment reverses the disease itself, management focuses on correcting iron and vitamin B12 deficiency and on regular endoscopic surveillance with adequate corpus sampling [4].
For readers of this journal, the analysis carries a pointed regional message. Despite the significant contributions Asian researchers are making to the field of gastrointestinal research, their integration into the international AIG research network, which is centered on European and North American groups, remains limited [3]. This is important because most diagnostic thresholds and surveillance recommendations in use came from studies in Western populations. In Korea, where the incidence of Helicobacter pylori–associated atrophy and gastric cancer is notably high, distinguishing AIG from advanced H. pylori–induced atrophic gastritis, validating serologic cutoff values tailored to the local context, and clarifying the neoplastic risk attributable to autoimmunity against a higher infection-related baseline are all urgent questions.
The method has limitations the authors acknowledge—a single database, English-language bias, and reliance on citation patterns rather than clinical significance—so bibliometric prominence should not be mistaken for clinical truth. Even so, the regional gap is better read as an opportunity than a shortcoming: Korean and Asian cohorts, with high endoscopy volumes, systematic biopsy protocols, and well-established cancer registries, are well positioned to fill it. For the practicing gastroenterologist, the real message is not the citation counts but the direction they show—unexplained iron deficiency, incidental corpus-predominant atrophy, or a small fundic NET is now a reason to consider AIG and to ask what surveillance it warrants.

Notes

Availability of Data and Material

Data sharing not applicable to this article as no datasets were generated or analyzed during the study.

Conflicts of Interest

Chan-Muk Im, a contributing editor of the Korean Journal of Helicobacter and Upper Gastrointestinal Research, was not involved in the editorial evaluation or decision to publish this article.

Funding Statement

None

Acknowledgements

None

REFERENCES

1. Lenti MV, Miceli E, Vanoli A, Di Sabatino A. Autoimmune gastritis: emerging insights and clinical management. Nat Rev Gastroenterol Hepatol 2026;23:641–654.
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2. Soykan İ, Er RE, Baykara Y, Kalkan C. Unraveling the mysteries of autoimmune gastritis. Turk J Gastroenterol 2024;36:135–144.
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3. Ahn YH. The evolution of autoimmune gastritis research (1995–2025): a hybrid bibliometric–conceptual synthesis. Korean J Helicobacter Up Gastrointest Res 2026;26:314–323.
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4. Shah SC, Piazuelo MB, Kuipers EJ, Li D. AGA clinical practice update on the diagnosis and management of atrophic gastritis: expert review. Gastroenterology 2021;161:1325–1332.e7.
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5. Kishikawa H, Nakamura K, Ojiro K, et al. Relevance of pepsinogen, gastrin, and endoscopic atrophy in the diagnosis of autoimmune gastritis. Sci Rep 2022;12:4202.
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