Optimizing Surveillance Strategies for Autoimmune Gastritis with Risk Factors: Insights from Stage IV OLGIM and Prior Gastric Cancer

By: Rex Wiig, Engineer, Author, and Autoimmune Advocate

Abstract

Autoimmune gastritis (AIG) is a chronic inflammatory condition leading to oxyntic gland loss, achlorhydria, and increased risk of gastric neoplasia. Patients with Stage IV OLGIM and prior gastric adenocarcinoma face particularly high risk, yet surveillance guidance remains poorly defined. Existing guidelines from AGA and ESGE exclude many AIG-associated cases. This paper integrates literature review and modeling of miss-rate, histologic stage, and risk kinetics to propose a personalized surveillance paradigm for AIG patients with advanced disease. We conclude that 6–9 month endoscopic intervals are more appropriate than the conventional 12-month schedule in this subgroup.

1. Introduction

Autoimmune gastritis (AIG)—also called autoimmune metaplastic atrophic gastritis (AMAG)—is characterized by immune-mediated destruction of parietal cells, leading to achlorhydria, hypergastrinemia, intrinsic factor deficiency, and B12 malabsorption1,2. Although uncommon (~1–1.5%), AIG predisposes to gastric adenocarcinoma and neuroendocrine tumors3–5. Guidelines such as the AGA CPU and ESGE MAPS provide general recommendations but largely exclude AIG and prior gastric cancer cases.6–8

2. Literature Review

The risk of gastric neoplasia in AIG has been confirmed in recent meta-analyses showing up to 11-fold increased risk9. OLGA and OLGIM stages III–IV confer the highest risk of malignancy10,11, but most data derive from H. pylori-driven disease, not autoimmune forms.

Current guidelines provide inconsistent intervals: AGA CPU suggests individualized assessment; ESGE MAPS II recommends 3–5 years, shortened to 1–2 years for severe atrophy or family history6,7,12. None define a standard interval for AIG with prior cancer.

3. Risk Stratification and Interval Modeling

Miss rates for early gastric neoplasia remain 9–14% even in expert centers13. Flat fundic mucosa in AIG further increases this miss probability, reducing curative windows for EMR. Therefore, intervals must balance statistical, procedural, and life-consequence risk.

Assuming a 10% miss rate per exam, cumulative undetected risk doubles within two 18-month cycles, supporting a 6–9 month interval for high-risk Stage IV OLGIM with prior adenocarcinoma.

4. Serologic Plateau ≠ Stability

In advanced AIG, stable high gastrin and low pepsinogen reflect end-stage mucosal failure, not remission. Once oxyntic mucosa is extinct, biomarkers plateau but the carcinogenic environment persists.14,15 Unlike H. pylori-driven gastritis, where eradication can induce mucosal healing and reduce risk, AIG represents an irreversible state requiring continuous vigilance.16

5. Discussion

Most data supporting 12-month intervals stem from incidental GIM cohorts such as Reddy et al. and Song et al., which exclude prior cancer and rarely phenotype AIG17,18. Consequently, these intervals are extrapolative and not evidence-based for AIG. AIG represents a fundamentally different biological context—autoimmune, not infectious—and carries persistent oncogenic risk even after histologic plateau.9,14

Our model contrasts ascending cumulative autoimmune risk with descending recurrence risk typical of non-AIG post-remission surveillance. The intersection near 12 months suggests earlier (6–9 month) surveillance may capture otherwise missed lesions.19,20

6. Conclusion

Twelve-month surveillance intervals are derived from non-AIG or incidental GIM cohorts that exclude pre-cancer cases. For AIG with Stage IV OLGIM, achlorhydria, and prior adenocarcinoma, this interval may be inadequate. In such patients, serologic plateaus mark irreversible atrophy, not healing, distinguishing AIG from healable H. pylori gastritis. A 6–9 month surveillance schedule is therefore justified for optimal neoplasia detection and patient safety.

References

1. Rustgi SD, et al. Autoimmune gastritis: pathophysiology and clinical management. *Clin Gastroenterol Hepatol*. 2021;19:1807–1817.

2. Shah SC, et al. AGA Clinical Practice Update on the Diagnosis and Management of Atrophic Gastritis. *Gastroenterology*. 2021;161:1325–1332.

3. Chen C, et al. Incidence of gastric neoplasms in autoimmune metaplastic atrophic gastritis: a meta-analysis. *J Clin Med*. 2023;12:1062.

4. Du S, et al. Gastric intestinal metaplasia subtype and cancer risk. *Clin Transl Gastroenterol*. 2021;12:e00409.

5. Shao L, et al. Meta-analysis: GIM risk stratified by subtype and location. *Int J Cancer*. 2018;143:1671–1677.

6. Gupta S, et al. AGA Guideline on Management of Gastric Intestinal Metaplasia. *Gastroenterology*. 2020;158:693–702.

7. Pimentel-Nunes P, et al. MAPS II: ESGE guidelines on precancerous stomach lesions. *Endoscopy*. 2019;51:365–388.

8. Pimentel-Nunes P, et al. MAPS III Update: ESGE 2025 revision. *Endoscopy*. 2025;57:in press.

9. Castellana M, et al. Clinical review of autoimmune atrophic gastritis. *Nutrients*. 2024;16:1224.

10. Yue H, et al. The significance of OLGA/OLGIM staging in gastric cancer risk. *Gastric Cancer*. 2018;21:579–587.

11. Correa P, et al. Atrophic gastritis and intestinal metaplasia: risk models. *Cancer Epidemiol Biomarkers Prev*. 2015;24:609–616.

12. Dinis-Ribeiro M, et al. European guidelines for gastric atrophy and metaplasia. *Endoscopy*. 2012;44:74–94.

13. Ebigbo A, et al. Miss rate for early gastric cancer using HD endoscopy. *Gastrointest Endosc*. 2020;91:1432–1440.

14. Neumann WL, et al. Autoimmune gastritis and neoplasia. *Autoimmun Rev*. 2013;12:459–466.

15. Rugge M, et al. Histologic staging and cancer risk in autoimmune gastritis. *Am J Surg Pathol*. 2020;44:557–564.

16. Sugano K, et al. H. pylori eradication and regression of gastritis. *Gut*. 2012;61:510–516.

17. Reddy KM, et al. Risk of gastric cancer among patients with GIM. *Clin Gastroenterol Hepatol*. 2016;14:1425–1432.

18. Song H, et al. Cancer risk in gastric intestinal metaplasia: a population study. *BMJ*. 2015;351:h3867.

19. Esposito G, et al. Surveillance in autoimmune and multifocal atrophic gastritis. *Dig Liver Dis*. 2021;53:162–169.

20. Shah SC, et al. Gastric intestinal metaplasia surveillance strategies: current perspectives. *Gastroenterology*. 2022;162:1545–1556.

Permission is granted to share this article for educational or patient-advocacy use only if unaltered and properly attributed to the author.
All other rights reserved worldwide.“Written by Rex Wiig, © 2025 Subsurface Press™. Used with permission.”